以下在纸的参考与初乳相关效力*:

LeFranc-Millot C, Vercaigne-Marko D, Wal J 。 - M, 等。 (1996) IgE 滴定量对迟钝的colostral G 免疫球蛋白和F(ab')2 片段的比较在患者清液过敏对牛奶。 内部曲拱过敏Immunol 。 110:156-162 。

Savilahti E, Tainio VM, Salmenpera L, Arjomaa P, Kallio M, Perheentupa J, Siimes MA 。 (1991) 低colostral IgA 与相关牛奶过敏。 Acta Pediatr 扫瞄。 80:1207-1213 。

Selo I, 宽容G, Bernard H, 等。 (1999) 对迟钝的B 乳球蛋白质的过敏: 人的IgE 特异性对tryptic 肽。 临床和实验性过敏。 29:1055-1063 。

Delespesse, G 。 多缩氨基酸因素从初乳。 美国专利#5,371,073 (1994) 。 IgE (免疫球蛋白被介入在过敏反应) 约束因素(IgE-bf) 并且IgE 遏抑器活动(IgE-SF) 被获得从初乳成功地使用对待过敏。

Collins, 上午, 等。 牛牛奶, 包括加热杀菌的牛奶, 包含抗体被指挥反对临床重要性变态反应原对人。 国际档案过敏和应用的免疫学96:362-367 (1991) 。 抗体出现反对许多最共同的过敏在人, 包括裸麦草花粉、房子尘土小蜘蛛、曲霉菌模子和麦子面筋, 被查出了在迟钝的初乳。

Elrod, KC, 等。 Lactoferrin, 一种有力tryptase 抗化剂, 被废除的后阶段导气管反应在过敏绵羊。 呼吸重要关心医学156 美国学报:375-381 (1997) 。 Tryptase, 消化酵素, 被牵连了以哮喘的各种各样的方面, 包括支气管狭窄和导气管hyperreactivity 。 Lactoferrin 被显示禁止tryptase 活动, 如此免除症状哮喘。

Goldman, AS, 等。 人的牛奶抗发炎物产。 Acta Paediatrica Scandinavica 75(5):689-695 (1986) 。 主要抗发炎组分发现了在人的牛奶(和迟钝的初乳) 包括anti-proteases, lactoferrin 、溶菌酶、分泌IgA, 和一定数量的抗氧剂, 包括半胱氨酸、ascorbate 、阿尔法维生素E 和β- 胡萝卜素。

Murphey, DK, Buescher, ES 。 人的初乳有抗发炎活动在炎症鼠皮肤下空气囊模型。 小儿科研究34(2):208-212 (1993) 。 在一个实验性动物模型使用皮肤下空气囊在鼠, 初乳显示了重大抗发炎活动。

Buescher, ES, McWilliams-Koeppen, P 。 可溶解肿瘤坏死因素阿尔法(TNF 阿尔法) 感受器官在人的初乳和牛奶里束缚对TNF 阿尔法和中立化TNF 阿尔法bioactivity 。 小儿科研究44(1):37-42 (1998) 。 初乳的能力调整激动反应是独特的。 它做这的方式的当中一个用是通过TNF-a 感受器官蛋白质, 被发现在初乳。 这些束缚对TNF-a, 撤消TNF-a 。 TNF-a 是整个激动小瀑布的活化计, 因此由控制它的活动, 初乳控制激动反应的程度, 可能关闭它一共。

"临床研究表示, IgE 被发现在迟钝的初乳, 也许负责对调控过敏反应," 根据Drs 。 Tortora 、Funke 和塑像在微生物学方面。

曲拱Immunol Ther Exp (Warsz) 。 1999;47(6):377-85 。

Amaducci L 。 (1988) Phosphatidylserine 在Alzheimer 的疾病的治疗: multicenter 研究的结果。 精神药理学公报。 24(1):130-4 。

Leszek J, Inglot 广告, Janusz M, Lisowski J, Krukowska K, Georgiades JA 。 (1999) Colostrinin: 富有脯氨酸的多缩氨基酸(PRP) 复合体与羊似的初乳被隔绝为Alzheimer 的疾病的治疗。 双- 盲目的安慰剂受控研究。 Archivum Immunologiae 和Therapiae Experimentalis 。 47(6):377-85 。

Leszek, J, 等。 Colostrinin. 富有脯氨酸的多缩氨基酸复合体从羊似的初乳- 它的效力的一项长期研究在Alzheimer 的疾病。 医学显示器8(10):P193-P196 (2002) 。 在一项较长期研究中, colostrinin 引起了改善或安定在患者介入研究。

Amaducci, L, 等。 对phosphatidylserine 的用途在Alzheimer 的疾病。 纽约科学院的史册640:245-249 (1991) 。 补充与phosphatidylserine, phospholipids 的当中一个发现了在生物油脂里, 并且导致在症状的改善在Alzheimer 的。

弯曲处, TH, 等。 phosphatidylserine 的作用在年龄伴生的记忆损伤。 神经学41(5):644-649 (1991) 。 有年龄伴生的记忆损伤病人显示了重大改善在记忆性能测试以phosphatidylserine 补充在一个12 个星期期间。

弯曲处, T, 等。 phosphatidylserine 的作用在Alzheimer 的疾病。 精神药理学公报28(1):61-66 (1992) 。 显示改善在Alzheimer 的症状以phosphatidylserine 补充12 个星期的其它研究。 损伤, 更加伟大改善, 建议及早phosphatidylserine 补充开始疾病其间, 更好结果将是。

十字架, CE, 等。 氧气基础和人的疾病。 史册内科107(4):526-545 (1987) 。 氧气自由基, 正常新陈代谢副产物, 被牵连了在疾病过程中范围从致癌作用到老化, 强调抗氧剂的重要性在与这些情况交战。

Ames, BN, 等。 氧化剂、抗氧剂, 和老化退化疾病。 国家科学院的行动美国90(17):7915-7922 (1993) 。 新陈代谢氧化剂副产物造成对DNA 、蛋白质和油脂的重大损伤。 这损伤导致老化和退化疾病与相关老化, 譬如癌症, 心血管疾病、免疫系统衰落、脑子官能不良和大瀑布。 抗氧化防御反对这些疾病下降以年龄, 需要抗氧剂的补充在饮食。

Ballard 和。 al 。 "促合成代理的作用在蛋白质故障。"Biochem J, 1983;210:243-249:

Gil, A 。 & Sanchez-Medina, F 。 "母牛的、山羊的和绵羊的牛奶酸可溶解核苷酸在哺乳期不同的阶段。"牛奶店研究学报, 1981;48:35-44 。

Ullman, 等。 "生长激素的作用在肌肉再生和IgF-1 集中在老鼠。"Acta Physiol Scand, 1990;140:521-525 。

县, C 。J 。, 等。 "IGF-1 的退化在成人鼠胃肠道由具体抗血清或饮食蛋白质酪蛋白限制。"内分泌学学报, 1995;146:215-225 。

Holbrook, N 。J 。 & Ikeyama, S 。 "与年龄有关的衰落在对氧化重音的多孔的反应: 成长因素信号路的链接以共同的瑕疵。"Biochem Pharmacol, 2002;64(5-6):999-1005 。

Playford, R 。J 。, 等。 "疗效食品的Co 管理, 迟钝的初乳, 减少在小肠渗透性的深刻nonsteroidal 抗发炎药物导致的增量。"Clin Sci (Lond), 2001;100(6):627-633 。

化学和生化, Hellbrunner Str 学院。 34, 5020 萨尔茨堡, 奥地利。 Univ 。- 教授。 Dr 。 阿尔伯特·Duschl 。

Elrod, KC, 等。 Lactoferrin, 一种有力tryptase 抗化剂, 被废除的后阶段导气管反应在过敏绵羊。 呼吸重要关心医学156 美国学报:375-381 (1997) 。 Tryptase, 消化酵素, 被牵连了以哮喘的各种各样的方面, 包括支气管狭窄和导气管hyperreactivity 。 Lactoferrin 被显示禁止tryptase 活动, 如此免除症状哮喘。

"糖蛋白在迟钝的初乳禁止导致胃溃疡Helicobacter 幽门细菌的附件。 初乳包含重大相当数量interleukin-10, 一个强的炎症禁止代理发现了重大在减少炎症在关节炎联接并且伤害区域, "写了Dr 。 Olle Hernell, 从Ulmea 大学, 瑞典, 在科学杂志里。

抗菌(Moldoveanu, Zina, 等, "牛奶抗菌物产; IgA _ 过氧化物酶Lactoferrin N 互作用"史册。Y 。 科学院, (1983) 卷。 409, 848-850 。

金, K 。 等, "人的初乳和牛奶的体外和活体内中立化的活动反对被净化的毒素A 和B 纺锤状细菌属传染病Difficle" 学报(1984) 卷。 150 (1) 57-61 。

Wada, N 。, 等, "中立化的活动反对纺锤状细菌属Difficile 毒素在被开化的Colostral 细胞" Infectioius Immunology 上层清液(1980) 卷。 29, 545-550) 。

McConnell, M 。A 。; 溪, H 。J 。L 。; Borissenko, M 。B 。; Buchan, G 。 免疫球蛋白的一项比较研究感觉和抗发炎活动在四奶制品里。 牛奶店科学学报。 出版物即将到来。

Borody, TJ, 等。 隧道视觉在肠。 消化疾病的中心(2001) 。 急燥的肠综合症状回顾, 包括ulcerative colitis 和Crohn 的疾病, 和它的原因论, 包括传染性代理譬如Shigella 和Campylobacter 。 食道的传染难对待因为抗菌疗法不是可利用的是有效的反对纺锤状细菌属孢子。 唯一迟钝的初乳证明了临床效力在根除小肠病原生物, 譬如rotavirus, 和也许帮助控制传染看在慢性混乱譬如急燥的肠综合症状由于生物有效部分的数量在初乳。 成长因素在初乳帮助愈合小肠侵蚀和溃疡。 它包含抗发炎因素和并且是营养富有。 初乳也许被使用单独或与其它抗发炎并且/或者免疫物质的组合。 未来研究应该集中于辨认免疫战略、新颖的交付bioactives 的系统和证明在初乳。

Playford, RJ, 等。 迟钝的初乳是防止NSAID 导致的食道损伤的疗效食品。 食道44:653-658 (1999) 。 虽然non-steroidal 抗发炎药物(NSAIDs) 是非常有效的在控制关节痛在关节炎, 他们的用途并且造成重大, 和有时致命, 食道损伤。 补充与初乳, 然而, 减少了和极大愈合了伤害由NSAIDs 造成。

Playford, RJ, 等。 疗效食品的Co 管理, 迟钝的初乳, 减少在小肠渗透性的深刻non-steroidal 抗发炎药物导致的增量。 临床科学100:627-633 (2001) 。 其它研究由Dr 。 Playford 在初乳的能力防止损伤由于NSAID 用途。 这项研究表示, 初乳并且防止在食道渗透性的增量由于NSAID 用途, 但是NSAID 用途单独没有初乳导致在渗透性的增量。

Goldman, AS, 等。 人的牛奶抗发炎物产。 Acta Paediatrica Scandinavica 75(5):689-695 (1986) 。 主要抗发炎组分发现了在人的牛奶(和迟钝的初乳) 包括anti-proteases, lactoferrin 、溶菌酶、分泌IgA, 和一定数量的抗氧剂, 包括半胱氨酸、ascorbate 、阿尔法维生素E 和β- 胡萝卜素。

Murphey, DK, Buescher, ES 。 人的初乳有抗发炎活动在炎症鼠皮肤下空气囊模型。 小儿科研究34(2):208-212 (1993) 。 在一个实验性动物模型使用皮肤下空气囊在鼠, 初乳显示了重大抗发炎活动。

Buescher, ES, McWilliams-Koeppen, P 。 可溶解肿瘤坏死因素阿尔法(TNF 阿尔法) 感受器官在人的初乳和牛奶里束缚对TNF 阿尔法和中立化TNF 阿尔法bioactivity 。 小儿科研究44(1):37-42 (1998) 。 初乳的能力调整激动反应是独特的。 它做这的方式的当中一个用是通过TNF-a 感受器官蛋白质, 被发现在初乳。 这些束缚对TNF-a, 撤消TNF-a 。 TNF-a 是整个激动小瀑布的活化计, 因此由控制它的活动, 初乳控制激动反应的程度, 可能关闭它一共。

Britigan, 是, 等。 lactoferrin 的角色作为一个抗发炎分子。 前进在实验性医学和生物357:143-156 (1994) 。 当lactoferrin 的角色在提供未指明的免疫很好被提供, 它并且充当在抗发炎反应的一个角色通过它的抗氧化作用。

Conneely, OM 。 lactoferrin 的抗发炎活动。 营养美国学院学报20(Suppl 。 5):389S-395S (2001) 。 Lactoferrin 禁止皮肤激动cytokine 生产和作为有力抗发炎蛋白质在炎症地方站点, 包括呼吸和胃肠道。

Shigenaga, MK, 等。 氧化损伤和线粒体朽烂在老化。 国家科学院的行动美国91(23):10771-10778 (1994) 。 主要源泉的氧化损伤是氧化剂由线粒体引起在身体的细胞。 线粒体作用下降以年龄, 包括被减少的膜流动性, 氢核漏出横跨内在线粒体膜, 和减少cardiolipin, 支持作用蛋白质在内在线粒体膜的重要油脂的水平。

Kurz, DJ, 等。 慢性氧化重音减弱telomere 正直和加速衰老起始在人的内皮细胞的细胞里。 细胞科学117 学报:2417-2426 (2004) 。 氧化重音由于氧化副产物积累与细胞衰老起始连接了在血管线路单元里由打乱的telomere 正直。 Telomeres 是"盯梢" 染色体, 长度的确定细胞分裂的数量细胞可能接受在到达它的极限之前。 谷胱甘肽, 强有力的自然抗氧剂, 是关键的在维护的telomere 正直。

Borissenko, M 。 谷胱甘肽: 强有力的抗氧剂被发现在初乳。 NZMP 2002 年8月。 谷胱甘肽和它的化工前辈是存在大量地在初乳。 因为谷胱甘肽直接地不被吸收, 谷胱甘肽生产在身体可能由补充只完成与它的祖先、胱氨酸、氨基乙酸和glutamic 酸, 在初乳上是丰富的。

Buescher, ES, McIlheran, SM 。 人的初乳抗氧化物产。 小儿科研究24(1):14-19 (1988) 。 初乳减少ferricytochrome C 在多形核白细胞(PMNs) 并且并且打乱是关键的在深刻炎症的PMN 呼吸爆炸斡旋PMNs 的其它新陈代谢和酶活动, 表示, 初乳是强有力的抗氧剂。

Buescher, ES, McIlheran, SM 。 Colostral 抗氧剂: 二活动的分离和描述特性在人的初乳。 小儿科胃肠病学和营养14(1) 学报:47-56 (1992) 。 初乳干涉PMN 呼吸爆炸产品的生产在二种方式、ascorbate 和尿酸里。

Boldogh, I, 等。 4HNE 斡旋的信号的模块化由富有脯氨酸的肽从羊似的初乳。 分子神经科学20(2) 学报:125-134 (2003) 。 Colostrinin 下来调控油脂过氧化, 禁止谷胱甘肽取尽和减少易反应的氧气种类的细胞内水平(ROS) 。 这是一种更多方式, 初乳展示抗氧化活动。

Wakabayashi, H, 等。 iron/ascorbate 导致的油脂过氧化的禁止由迟钝的lactoferrin 和它的acylated 衍生物N 终端肽。 Bioscience, 生物工艺学, 生化63(5):955-957 (1999) 。 Lactoferrin 并且充当在初乳的一个重要抗氧化角色由防止油脂过氧化。

Satue-Gracia, MT, 等。 Lactoferrin 在婴儿惯例: 对氧化作用的作用。 农业和食物化学48(10) 学报:4984-4990 (2000) 。 商业修改过的婴儿惯例根据牛奶比全脂牛奶极大有较少lactoferrin, 并且大豆惯例包含无, 即使lactoferrin 作为钢运输者蛋白质。 增加lactoferrin 来婴儿惯例导致增加的钢吸收的双重好处和作为抗氧化和抗菌延长惯例的保存性。

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Hofman Z, Smeets R, Verlaan G, Lugt R, Verstappen PA 。, 内部J 体育Nutr Exerc Metab 。 2002 年Dec;12(4):461-9 。 相关文章, 迟钝的初乳补充的作用在锻炼表现在精华曲棍球球员。 Numico 研究, Bosrandweg 20, 6704 酸碱度Wageningen, 荷兰。

Coombes JS, Conacher M, Austen SK, 马歇尔PA 。 Med Sci 炫耀Exerc 。 2002 年Jul;34(7):1184-8 。 相关文章, 链接, 药量作用口头迟钝的初乳在物理工作能力在骑自行车者。 人的运动研究学校, 昆士兰, 圣Lucia, 澳洲大学。

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Hwa V, Oh Y, Rosenfeld RG, 部门。 小儿科、俄勒冈健康科学大学, 波特兰, 俄勒冈, 胰岛素象成长因素约束蛋白质(IGFBP) superfamily 。 Endocr 牧师1999 Dec; 20(6):761-87 。

Buckley, J 。, 等。 "口头补充与迟钝的初乳增加垂直的跃迁表现。"提出了在欧洲学院体育科学, 罗马14-17 1999 的7月第4 每年国会年。

Mero, A 。, 等。 "迟钝的初乳补充的作用在清液IGF-I 、IgG 、激素, 和唾液IgA 在训练期间。"J Appl Physiol, 1997;83(4):144-1151 。

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Antonio, J, 等。 迟钝的初乳补充的作用在身体构成和锻炼表现在活跃人和妇女。 营养17(3):243-247 (2001) 。 活跃地训练男性和女性运动员被给了初乳补充或安慰剂8 个星期的期间。 主题接受初乳但不是安慰剂显示了在精瘦的身体大量的增量。

Brinkworth, GD, 等。 迟钝的初乳补充的作用在抵抗训练的和未受训练的肢体的构成在健康年轻人。 应用的生理9(11) 欧洲学报:53-60 (2004) 。 或迟钝的初乳或乳清蛋白质被给了是或在训练或不是在训练的年轻人。 那些在接受初乳的训练小组显示了在膀臂圆周和断面的显着更加巨大的增量与那些比较接受乳清, 当那些不是在训练没有显示变动。

Buckley, JD, 等。 迟钝的初乳在绝氧锻炼表现和血浆的作用胰岛素象成长因素I 。 体育科学21(7) 学报:577-588 (2003) 。 运动员在训练被给了或迟钝的初乳或安慰剂8 个星期。 那些接受初乳显示了在高峰绝氧力量的重大增量在安慰剂。

Coombes, JS, 等。 药量口头迟钝的初乳的作用在物理工作能力在骑自行车者。 医学和科学在体育和锻炼34(7):1184-1188 (2002) 。 剂量研究完成在训练骑自行车者显示了小但重大改善在时间试验在20 g 或60 g/day 药量。

Hofman, Z, 等。 迟钝的初乳补充的作用在锻炼表现在精华曲棍球球员。 体育营养和锻炼新陈代谢12(4) 国际学报:461-469 (2002) 。 初乳补充在精华曲棍球球员, 男性和女性, 导致改善冲刺表现在安慰剂。

Nieman, DC, 等。 补全和免疫球蛋白成水平在运动员和惯座控制。 运动医学10(2) 国际学报:124-128 (1989) 。 补全C3 和C4 但不是免疫球蛋白的血液水平减少了在休息、被分级的最大的锻炼和补救的期间在马拉松运动员里。

Nieman, DC, 等。 长耐力的作用运行在免疫系统参量和淋巴细胞起作用在老练的marathoners 。 运动医学10(5) 国际学报:317-323 (1989) 。 马拉松运动员体验正常免疫作用的中断在跑长的距离以后, 回到正常水平跟随21 个小时补救的情况。

Berk, LS, 等。 长的耐力的作用运行在NK 细胞在marathoners 。 医学和科学在体育和锻炼22(2):207-212 (1990) 。 在NK 细胞人口的重大减退在21 个小时以前看了在马拉松运动员里跟随三个小时最大的锻炼以前锻炼水平充分的补救。 这关联了以在氢化皮质酮水平的增量在锻炼期间。

Sparling, 铅, 等。 马拉松赛跑的选择的科学方面。 一次更新在可变的替换、免疫作用、心理因素和性别区别。 运动医学15(2):116-132 (1993) 。 对免疫系统的消极变动在长的距离赛跑期间增加上部呼吸传染的机会在这些运动员期间跟随锻炼。 适当的营养, 充分休息和适当以及其它措施可能变小风险恢复在锻炼之间。

室息, ER 。 初乳作为运动改进物和帮助为爱滋病。 营养科学新闻, 1996 年。 当漏的食道是对大家重要, 它是特别如此为需要运用所有营养素他们采取并且防止传染的运动员当他们的免疫系统被削弱跟随锻炼。 许多运动员遭受急燥的肠综合症状由于蛋白质补充的残缺不全的消化。 角色的初乳获得胰岛素象成长因素1 (IGF-1), 表皮成长因素(EGF), 小片被获得的成长因素(PDGF) 并且变换的成长因素beta (TGF ss) 在医治用的漏的食道被探索。

Buckley, JD, 等。 迟钝的初乳补充在耐力连续训练期间改进补救, 但不是表现。 科学和医学学报在体育5(2):65-79 (2002) 。 当补充与迟钝的初乳不增加IGF-1 的水平在血液或最初的表现, 表现在锻炼第二个圆极大改善。

弯曲处, C, 等。 迟钝的初乳补充增加s-IGA 的水平在长跑运动员里: 研究根据运动员在训练为2002 年Rotorua 马拉松。 未出版的研究。 马拉松运动员在训练被给了迟钝的初乳或安慰剂12 个星期在一项双重盲目的研究中。 那些在初乳小组比或安慰剂小组或惯座控制显示了更分泌IgA (s-IgA) 在他们的唾液。 初乳小组并且报告了上部呼吸传染的显着更低的率(URI) 在这个期间。

Kasemkijwattana, C, 等。 对成长因素的用途改进肌肉愈合在张力伤害以后。 临床整形术370:272-285 (2000) 。 肌肉伤, 譬如张力, 是共同在运动员。 对成长因素的用途, 譬如IGF-1, 在对待这样伤害被探索。

Molloy, T, 等。 成长因素的角色在腱和韧带愈合。 运动医学33(5):381-394 (2003) 。 五个不同成长因素、IGF-1 、TGF ss 、血管内皮细胞的成长因素(VEGF), 小片被获得的成长因素(PDGF) 并且基本的成纤维细胞成长因素(bFGF 的) 角色, 在医治用的腱和韧带伤害被探索。 每个充当在过程的一个另外但重要角色。

Sato, K, 等。 肌肉的改善愈合通过肌肉再生的纤维变性的改进和预防。 肌肉& 神经28(3):355-372 (2003) 。 IGF-1 可能改进肌肉再生在受伤的肌肉里。

梁, L, 等。 [ cytokines 的作用在腱伤害修理] Zhongguo Xiufu Chongjian Waike Zazhi (中国) 14(5):283-285 (2000) 。 Cytokines, 譬如成长因素, 可能加速腱修理。

Mero, A, 等。 对迟钝的初乳补充的IGF-I 、IgA, 和IgG 反应在训练期间。 应用的生理93(2) 学报:732-739 (2002) 。 初乳补充增加IGF-1 和IgA 的水平在训练运动员, 但IGF-1 在初乳不被吸收得原封。

Kuipers, H, 等。 口头迟钝的初乳补充的作用在清液胰岛素象成长因素我成水平。 营养18(7-8):165-172 (2002) 。 一项研究为国际奥林匹克委员会没有显示在血液IGF-1 或IGF-bp3 水平的增量在4 个星期时间以后。

Zimecki, M, 等。 富有脯氨酸的多缩氨基酸的作用(PRP) 在溶血贫血症的新西兰黑色(NZB) 老鼠发展和生存。 Archivum Immunologiae 和Therapiae Experimentalis 39(5-6):461-467 (1991) 。 Colostrinin (PRP) 增加了生存在老鼠易受影响溶血贫血症, 一种自动免疫的疾病。 它被假设colostrinin 导致减慢疾病的发展的遏抑器细胞。 这建议, colostrinin 也许有治疗价值在对待的自动免疫的疾病。

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Seifert J, Molkewehrum M, Oesser S, Nebermann L, Schulze C 。 Eur Surg 皇家经济学会。 2002 日01 Apr;34(1 2):68-72 。 相关文章, 链接, 内毒素钝化作用由enterally 另外构成应用的初乳。 外科手术的研究、部门和胸部手术, Kiel, 德国。

Bolke E, Jehle PM, Hausmann F, Daubler A, Wiedeck H, 斯坦贝奇G, Storck M, Orth K 。, 震动。 2002 年Jan;17(1):9-12 。 免疫球蛋白被丰富的初乳牛奶的相关文章、链接, Preoperative 口头应用和斡旋人反应在胃肠手术期间。 手术, 大学Ulm, 德国的部门。

Lilius EM, Marnila P 。 Curr Opin 传染Dis 。 2001 年Jun;14(3):295-300 。 相关文章, 链接, colostral 抗体的角色在微生物传染的预防。 生化的部门和食物化学, Turku, Turku, 芬兰大学。

Graczyk TK, Cranfield Bostwick EF 先生, 。, J Parasitol 。 2000 年Jun;86(3):631-2 。 相关文章, 链接, 成功的hyperimmune 迟钝的初乳治疗大草原显示器(Varanus exanthematicus) 被感染Cryptosporidium sp 。 分子微生物学和免疫学的卫生学部门, 学校和公共卫生, 琼斯霍浦金斯大学, 巴尔的摩, 马里兰21205, 美国。

Huppertz HI, Rutkowski S, Busch DH, Eisebit R, Lissner R, Karch H 。, J Pediatr Gastroenterol Nutr 。 1999 年Oct;29(4):452-6 。 相关文章, 链接, 迟钝的初乳改良腹泻在传染与diarrheagenic 大肠埃希氏菌, shiga toxin-producing E 。 杆菌, 和E 。 杆菌表达intimin 和hemolysin 。 儿童医院, 维尔茨堡, 德国大学。

Bitzan, M 。M 。; 金子, B 。D 。; Philpott, D 。J 。; Huesca, M 。; 谢尔曼, P 。M 。; Karch, H 。; Lissner, R 。; Lingwood, C 。A 。; Karmali, M 。A 。; Helicobacter 幽门和Helicobactor mustelae 的禁止束缚对油脂感受器官由迟钝的初乳。 传染病学报。 177:955-961, 1998 年4月。

Casswall TH, SA, 阿尔伯特MJ, Fuchs GJ, Bergstrom M, Bjorck L, Hammarstrom L Sarker 。, Aliment Pharmacol Ther 。 1998 年Jun;12(6):563-8 。 相关文章, 链接, Helicobacter 幽门传染的治疗在婴儿在农村孟加拉国与口头免疫球蛋白从hyperimmune 牛科动物初乳。 临床科学的部门, Huddinge 医院, Karolinska 学院, 瑞典。

Bitzan 毫米, 金子BD, Philpott DJ, Huesca M, 谢尔曼PM, Karch H, Lissner R, Lingwood 加州, Karmali MA 。 J 传染Dis 。 1998 年Apr;177(4):955-61 。 相关文章, 链接, Helicobacter 幽门和Helicobacter mustelae 的禁止束缚对油脂感受器官由迟钝的初乳。 Department of Clinical Pathology, Hospital for Sick Children, University of Toronto, Ontario, Canada.

Tacket CO, Binion SB, Bostwick E, Losonsky G, Roy MJ, Edelman R. Am J Trop Med Hyg. 1992 Sep;47(3):276-83. Related Articles, Links, Efficacy of bovine milk immunoglobulin concentrate in preventing illness after Shigella flexneri challenge. Department of Medicine, University of Maryland School of Medicine, Baltimore.

Flanigan T, Marshall R, Redman D, Kaetzel C, Ungar B. J Protozool. 1991 Nov-Dec;38(6):225S-227S. Related Articles, Links, In vitro screening of therapeutic agents against Cryptosporidium: hyperimmune cow colostrum is highly inhibitory. Department of Medicine, University Hospitals, Case Western Reserve University, Cleveland, OH.

Ushijima H, Dairaku M, Mukoyama A. Kansenshogaku Zasshi. 1991 Jan;65(1):54-60. Related Articles, Links,[Bacteriostatic activity of bovine colostrum][Article in Japanese],Department of Enteroviruses, National Institute of Health.

Stephan W, Dichtelmuller H, Lissner R. J Clin Chem Clin Biochem. 1990 Jan;28(1):19-23. Related Articles, Links, Antibodies from colostrum in oral immunotherapy. Biotest Pharma GmbH, Forschungsabteilung, Frankfurt.

Fayer R, Perryman LE, Riggs MW.J Parasitol. 1989 Feb;75(1):151-3. Related Articles, Links, Hyperimmune bovine colostrum neutralizes Cryptosporidium sporozoites and protects mice against oocyst challenge. Zoonotic Diseases Laboratory, United States Department of Agriculture, Beltsville, Maryland 20705.

McClead RE Jr, Butler T, Rabbani GH. Am J Med. 1988 Dec;85(6):811-6. Related Articles, Links, Orally administered bovine colostral anti-cholera toxin antibodies: results of two clinical trials. Department of Pediatrics, Ohio State University 43205.

Tacket CO, Losonsky G, Link H, Hoang Y, Guesry P, Hilpert H, Levine MM. N Engl J Med. 1988 May 12;318(19):1240-3. Related Articles, Links, Protection by milk immunoglobulin concentrate against oral challenge with enterotoxigenic Escherichia coli. Department of Medicine, University of Maryland School of Medicine, Baltimore.

Opdebeeck JP, Norcross NL. Am J Vet Res. 1985 Jul;46(7):1561-4. Related Articles, Links, Antibodies in bovine serum and lacteal secretions to capsular antigens of Staphylococcus aureus.

McClead RE, Gregory SA. Infect Immun. 1984 May;44(2):474-8. Related Articles, Links, Resistance of bovine colostral anti-cholera toxin antibody to in vitro and in vivo proteolysis.

McClead RE, Butler T, Rabbani GH. (1988) Orally Administered Bovine Colostral Anti-Cholera Toxin Antibodies: Results of Two Clinical Trials. The American Journal of Medicine. 85:811-816

Michalek SM, McGhee JR. (1977) Effective immunity to dental caries: passive transfer to rats to antibodies to streptococcus mutans elicits protection. Infection and Immunity. 17:644-650.

Ellison, RT III, Giehl, TJ. Killing of gram-negative bacteria by lactoferrin and lysozyme. Journal of Clinical Investigation 88(4):1080-1091 (1991). Lactoferrin and lysozyme act together to kill gram-negative bacteria, such as Vibrio cholerae (cholera), Salmonella typhimurium (food poisoning) and Eschericia coli. The lactoferrin attaches to and destroys the cell wall of the bacteria, allowing the lysozyme to enter and lyse (burst) the organisms.

Korhonen, H, et al. Milk immunoglobulins and complement factors. British Journal of Nutrition 84(Suppl.1):S75-S80 (2000). Bovine colostrum contains three main classes of immunoglobulin IgG (IgG1 75% and IgG2), IgM and IgA, plus hemolytic and bactericidal complement. Complement is a complex group of proteins which act in concert with antibodies to inactivate and/or kill pathogens.

Gopal, PK, and Gill, HS. Oligosaccharides and glycoconjugates in bovine milk and colostrum. British Journal of Nutrition 84(Suppl.1):S69-S74 (2000). Another way colostrum helps protect against infections is through the oligosaccharides and glycoconjugates it contains. These are complex sugars which compete for binding sites in the GI tract with pathogens.

Korhonen, H. Bactericidal effect of bovine normal and immune serum, colostrum and milk against Helicobacter pylori. Journal of Applied Bacteriology 78:655-662 (1995). The antibody-complement system found in bovine colostrum was also found to be bactericidal against H. pylori.

Korhonen, H, et al. Bactericidal effect of bovine normal and immune serum, colostrum and milk against Helicobacter pylori. Journal of Applied Bacteriology 78(6):655-662 (1995). Helicobacter pylori is a major cause of gastritis and ulcers in humans. Serum and colostrum from non-immunized Friesian cows were found to be highly bactericidal against H. pylori. Post-colostral milk did not show any bactericidal effect against H. pylori.

Bitzan, MM, et al. Inhibition of Helicobacter pylori and Helicobacter mustelae binding to lipid receptors by bovine colostrum. Journal of Infectious Disease 177(4):955-961 (1998). H. pylori and H. mustelae (a gastric pathogen of ferrets) are both bound by lipid receptors (phosphatidylethanolamine, gangliotetraosylceramide and gangliotriaosyl-ceramide) in the gut, allowing them to carry out their pathogenic activities. Bovine colostrum, however, was shown to prevent binding of the pathogens to these lipid receptors even though there was no detectable anti-H. pylori antibody activity in the colostrum.

Wada, T, et al. The therapeutic effect of bovine lactoferrin in the host infected with Helicobacter pylori. Scandinavian Journal of Gastroenterology 34(3):238-243 (1999). Mice infected with H. pylori were given a daily dose of bovine lactoferrin for 2-4 weeks. Their intestines were then examined for bacterial content. Numbers of H. pylori were reduced to 10% of pre-lactoferrin levels and greatly decreased the numbers of H. pylori bound to the intestinal wall. Serum antibody titer to H. pylori were reduced to practically zero, indicating that the immune response of the host was no longer recognizing H. pylori infection. Therefore it was deduced that lactoferrin has a direct antibacterial effect on H. pylori infection and prevents binding of the pathogen to the intestinal lining.

Casswall, TH, et al. Bovine anti-Helicobacter pylori antibodies for oral immunotherapy. Scandinavian Journal of Gastroenterology 37(12):1380-1385 (2002). Bovine colostrum with high titers against H. pylori was given to H. pylori infected mice. Comparison of treated mice with control mice showed a 50-66% cure rate for H. pylori infection in treated mice. Binding studies also showed that the colostrum prevented binding of the H. pylori.

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Ogra, PL, et al. Colostrum-derived immunity and maternal-neonatal interaction. Annals of the New York Academy of Sciences 409:82-95 (1983). Passive immunity to specific pathogens is passed from mother to infant via colostrum.

Brüssow, H., et al. Bovine milk immunoglobulins for passive immunity to infantile rotavirus gastroenteritis. Journal of Clinical Microbiology 25(6):982-986 (1987). Protection against rotavirus, a dangerous pathogen which can cause serious, even fatal diarrhea in infants, can be passed orally through milk or colostrum safely and effectively.

Ebina, T, et al. Passive immunizations of suckling mice and infants with bovine colostrum containing antibodies to human rotavirus. Journal of Medical Virology 38:117-123 (1992). Another study that confirmed that oral immunization via colostrum or milk against rotavirus was possible, safe and effective.

Stephan, W, et al. Antibodies from colostrum in oral immunotherapy. Journal of Clinical Chemistry and Clinical Biochemistry 28:19-23 (1990). An immunoglobulin preparation from pooled bovine colostrum was found to be very effective in treating severe diarrhea, such as often found in AIDS patients.

van Hooijdonk, AC, Kussendrager, KD, Steijns, JM. In vivo antimicrobial and antiviral activity of components in bovine milk and colostrum involved in non-specific defense. British Journal of Nutrition 84(Suppl.1):S127-S134 (2000). Lactoferrin and lactoperoxidase, both present in colostrum in large amounts, provide non-specific defense against a broad spectrum of pathogens, including bacteria and viruses. This is significant both for the protection of commercially important animals as well as humans.

Korhonen, H, et al. Bovine milk antibodies for health. British Journal of Nutrition 84(Suppl.1):S135-S146 (2000). Bovine colostrum provides safe, effective protection against many pathogens. This natural immune protection can be extended by hyperimmunizing cows against specific pathogens.

Solomons, NW. Modulation of the immune system and the response against pathogens with bovine colostrum concentrates. European Journal of Clinical Nutrition 56(Suppl.3):524-528 (2002). The ability of colostrum to protect infants against pathogens, specifically those which cause gastroenteritis and severe diarrhea, makes it an ideal, cheap, safe and effective means of protecting children in those parts of the world where medical assistance is lacking or substandard and could save thousands of lives each year.

Ho, PC, Lawton, JWM. Human colostral cells: Phagocytosis and killing of E. Coli and C. Albicans. Journal of Pediatrics 93(6):910 ?915 (1978). Cells found in colostrum are able to ingest and kill both E. coli and Candida.

Majumdar, AS, et al. Protective properties of anti-cholera antibodies in human colostrum. Infection and Immunity 36:962-965 (1982). Colostrum was able to prevent infection with cholera. Colostrum samples from India, where cholera is common, had much higher levels of anti-cholera IgA than those from Sweden, where cholera is rare.

Funatogawa, K, et al. Use of immunoglobulin enriched bovine colostrum against oral challenge with enterohaemorrhagic Eschericia coli O157:H7 in mice. Microbiology and Immunology 46(11):761-766 (2002). Colostrum can prevent infection against food-borne pathogens by preventing them from binding to the intestinal lining.

Widiasih, DA, et al. Passive transfer of antibodies to Shiga toxin-producing Eschericia coli O26, O111 and O157 antigens in neonatal calves by feeding colostrum. Journal of Veterinary Medicine 66(2):213-215 (2004). Feeding colostrum to calves provided protection against Shiga toxin-producing E. Coli, a particularly deadly strain of E. coli.

Acosta-Altamirano, G, et al. Anti-amoebic properties of human colostrum. Advances in Experimental Medicine and Biology 216B:1347-1352 (1987). In addition to its effectiveness against bacterial, viral and fungal infections, colostrum also provides protection against amoebic pathogens.

Akisu, C, et al. Effect of human milk and colostrum on Entamoeba histolyica. World Journal of Gastroenterology 10(5):741-742 (2004). Colostrum was found to provide protection against Entamoeba histolyica, the cause of amoebiasis, a serious, chronic illness characterized by dysentery, gastrointestinal ulceration and abscess formation and intestinal blockage in infants particularly.

Julius, MH, et al. A colostral protein that induces the growth and differentiation of resting B lymphocytes. Journal of Immunology 140:1366-1371 (1988). Colostrinin has also been shown to induce the growth and differentiation of resting B lymphocytes. T and B lymphocytes are the two main types of lymphocytes involved in the immune response.

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Gastrointestinal Inflammation and Repair Group, Imperial College, London (2003). Unpublished research. In an in vitro experimental study, colostrum stimulated intestinal cell growth and reestablished a healthy epithelial layer following injury. In an in vivo experimental study, colostrum powder was also shown to reduce gastric injury.

Bitzan, MM, et al. Inhibition of Helicobacter pylori and Helicobacter mustelae binding to lipid receptors by bovine colostrum. Journal of Infectious Diseases 177:955-961 (1998). Bovine colostrum blocked binding of H. pylori (a major cause of chronic gastritis and ulcers in humans) and H. mustelae (a similar pathogen found in ferrets). This is apparently a function of the phosphatidylethanolamine found in colostrum and BIO-lipid.

Carver, JD, Barness, LA. Trophic factors for the gastrointestinal tract. Clinical Perinatology 23(2):265-285 (1996). Factors in colostrum which promote the development of the GI tract in newborn infants also help protect against such diseases as Crohn?s disease, colitis, necrotizing enterocolitis and diarrhea.

Bühler, C., et al. Small intestinal morphology in eight-day-old calves fed colostrum for different durations or only milk replacer and treated with long-R3-insulin-like growth factor I and growth hormone. Journal of Animal Science 76:758-765 (1998). The intestines of calves fed colostrum compared to those not fed colostrum revealed that those fed colostrum had significantly increased villus size and crypt depths. This translates into greater surface area and thus increased absorption of nutrients.

Bl?ttler, U, et al. Feeding colostrum, its composition and feeding duration variably modify proliferation and morphology of the intestine and digestive enzyme activities of neonatal calves. Journal of Nutrition 131(4):1256-1263 (2001). A similar study done on calves either receiving or not receiving colostrum. This study concentrated on the development and health of the gastrointestinal epithelium and found that the development and health of this epithelium was markedly superior in those receiving colostrum. Colostrum also influenced the production of lipase enzyme by the pancreas.

Pluske, JR, Morel, PCH. Increasing weaner pig productivity in New Zealand pig herds. Unpublished research (1999). Piglets fed a liquid supplement with colostrum powder had a marked increase in villi height in the lumen of the small intestine, indicating greater digestion and absorption of nutrients. There were also an increased number of immune cells in the villi, indicating enhanced immune competency.

Rooney, PJ, et al. A short review of the relationship between intestinal permeability and inflammatory joint disease. Clinical and Experimental Rheumatology 8:75-83 (1990). The connection between increased permeability of the intestines and inflammatory arthritis is examined. The gut is the likely source of the antigens which cause inflammatory arthritis.

Katz, KD, Hollander, D. Intestinal mucosal permeability and rheumatological diseases. Baillere?s Clinical Rheumatology 3(2):271-284 (1989). The inability of the intestinal lining to control the influx of antigens into the blood due to leaky gut or a dysfunctional immune system may represent the prime means by which the antigens which cause numerous diseases, including autoimmune diseases. Leaky gut has been linked to patients with ankylosing spondylitis, rheumatoid arthritis, Crohn?s disease, and celiac sprue (a genetic autoimmune disease characterized by damage to the small intestine due to eating wheat gluten).

Moller, W, et al. Use of bovine colostral milk as a preparation for the protection of the liver. US Patent #5,710,132 (1998). Whole bovine colostrum or an immunoglobulin preparation from colostrum are used to protect the liver from bacterial, viral or protozoan diseases, such as E. coli, rotavirus or cryptosporidia infection, as well as detoxify the liver by removing toxic protein metabolites such as ammonia. It can also be used to treat the effects of various liver diseases, such as liver inflammation, viral hepatitis, fibrosis of the liver, cirrhosis of the liver, fatty liver, and so forth. These effects include disturbances of the liver?s detoxification, excretory, conjugational and synthesizing functions, portal hypertension due to liver disease, and even coma due to liver failure. Supplementation can also be used to relieve stress on the liver due to liver insufficiency as a result of liver parenchyma damage or viral hepatitis, allowing the liver to heal and recover function.

Gluckman, PD, Mellor, DJ. Use of growth factor IGF-I and/or IGF-II. US Patent #5,710,127 (1998). Use of IGF-I or IGF-II to prevent or treat pancreatic disorders and insufficiency. It can promote growth of the pancreas in diseases such as cystic fibrosis or partial/total pancreatectomy where pancreatic tissue is lost.

Vaarla, O. The gut immune system and type 1 diabetes. Annals of the New York Academy of Science 958:39-46 (2002). There is increasing evidence that the gut immune system is important in the development of type 1 (autoimmune) diabetes. One of the causes of type diabetes in children may be too early introduction of cow?s milk to the diet in infants, which causes an autoimmune response to insulin.

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Edde, L, et al. Lactoferrin protects neonatal rats from gut-related systemic infection. American Journal of Physiology: Gastrointestinal Liver Physiology 281:G1140-G1150 (2001). Lactoferrin protected neonatal rats from E. coli infection in the intestines. Lactoferrin plus lysozyme was bactericidal against the E. coli.

Qiu, J, et al. Human milk lactoferrin inactivates two putative colonization factors expressed by Haemophilus influenzae. Proceedings of the National Academy of Sciences USA 95:12641-12646 (1998). Lactoferrin prevents colonization of Haemophilus influenzae, the primary cause of otitis media and other respiratory infections in children, by inactivating two colonization factors expressed by the bacteria.

Hasegawa, K, et al. Inhibition with lactoferrin of in vitro infection with human herpes virus. Japanese Journal of Medical Science and Biology 47:73-85 (1994). Both human and bovine lactoferrin inhibit infection with human herpes simplex virus and human cytomegalovirus in cell cultures.

van der Strate, BW, et al. Antiviral activities of lactoferrin. Antiviral Research 52(3):225-239 (2001). Lactoferrin is effective against both DNA and RNA viruses, including rotavirus, respiratory syncytial virus, herpes virus and HIV, both by blocking cellular receptors and by directly binding to the viruses.

Andersson, Y, et al. Lactoferrin is responsible for the fungistatic effect of human milk. Early Human Development 59:95-105 (2000). Lactoferrin, through its iron-binding ability, is very effective against fungal infections with Candida and other fungi.

Samaranayake, YH, et al. Antifungal effects of lysozyme and lactoferrin against genetically similar, sequential Candida albicans isolates from a human immunodeficiency virus-infected Southern Chinese cohort. Journal of Clinical Microbiology 39(9):3296-3302 (2001). Lactoferrin plus lysozyme is very effective in killing nearly all oral strains of Candida, which is of particular importance to AIDS sufferers who are often unable to fight off Candida overgrowths, such as thrush.

Gahr, M, et al. Influence of lactoferrin on the function of human polymorphonuclear leukocytes and monocytes. Journal of Leukocyte Biology 49(5):427-433 (1991). White blood cells (polymorphonuclear leucocytes) exposed to lactoferrin from bovine colostrum exhibit increased motility and produce more superoxide (a powerful antioxidant).

Tsuda, H, et al. Prevention of colon carcinogenesis and carcinoma metastasis by orally administered bovine lactoferrin in animals. BioFactors 12:83-88 (2000). In an experimental animal study, supplementation with bovine lactoferrin showed significant protection from development of cancerous tumors in the colon as well as protection against lung metastasis. Administration of the lactoferrin was accompanied by marked increases in cytotoxic white blood cells in the blood.

Masuda, C, et al. Chemopreventive effects of bovine lactoferrin on N-butyl-N-(4-hydroxybutyl)nitrosamine-induced rat bladder carcinogenesis. Japanese Journal of Cancer Research 91:582-588 (2000). Bovine lactoferrin also prevented the development of bladder cancer in another experimental animal system.

Tanaka, T, et al. Chemopreventive effect of bovine lactoferrin on 4-nitroquinoline 1-oxide-induced tongue carcinogenesis in male F344 rats. Japanese Journal of Cancer Research 91(1):25-33 (2000). The same effect of lactoferrin was found in an experimental tongue cancer system.

Ushida, Y, et al. Possible chemopreventive effects of bovine lactoferrin on esophagus and lung carcinogenesis in the rat. Japanese Journal of Cancer Research 90:262-267 (1999). Lactoferrin was also found to protect the esophagus and the lung from experimental cancer induction.

Iigo, M, et al. Inhibitory effects of bovine lactoferrin on colon carcinoma 26 lung metastasis in mice. Clinical and Experimental Metastasis 17(1):35-40 (1999). Lactoferrin increased levels of cytotoxic white blood cells and inhibited metastasis to the lung in experimentally induced colon cancer in mice.

Kuhara, T, et al. Orally administered lactoferrin exerts an antimetastatic effect and enhances production of IL-18 in the intestinal epithelium. Nutrition and Cancer 38(2):192-199 (2000). A similar study on the protective effects of lactoferrin supplementation on protecting from lung metastasis in experimentally induced colon cancer. In addition to the increase in cytotoxic cells seen in other studies, there was also an increase in IL-18 production in the intestinal epithelium, suggesting it plays a role in mediating the inhibition of the cancers.

Tsuda, H, et al. Milk and dairy products in cancer prevention: focus on bovine lactoferrin. Mutation Research 462(2-3):227-233 (2000). In addition to the protection provided by lactoferrin against the development of cancers, conjugated linoleic acid (CLA) also plays an inhibitory role on cancer development.

Tsuda, H, et al. Cancer prevention by bovine lactoferrin and underlying mechanisms--a review of experimental and clinical studies. Biochemistry and Cell Biology 80(1):131-136 (2002). Lactoferrin supplementation in experimental animal models of colon cancer show that it also suppresses phase I enzymes, such as cytochrome P450 1A2, by cancer cells, while enhancing the activity of phase II enzymes, such as glutathione S-transferase, both of which act to inhibit the development of these cancers. Lactoferrin also boosts local and systemic immunity, particularly the activity of cytotoxic lymphocytes and natural killer cells in the intestinal mucosa and peripheral blood, which in turn stimulates the production of IL-18 and caspase-1 in intestinal epithelial cells and possibly the appearance of interferon-gamma (INF-?) positive cells. Bovine lactoferrin was also found to have anti-hepatitis C activity. Chronic hepatitis due to infection with hepatitis C virus is a major causative factor in the development of hepatocellular carcinoma.

Fujita, K, et al. Down-regulation of 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx)-induced CYP1A2 expression is associated with bovine lactoferrin inhibition of MeIQx-induced liver and colon carcinogenesis in rats. Japanese Journal of Cancer Research 93(6):616-625 (2002). The mechanism of action of bovine lactoferrin on down regulating the expression of carcinogenic agents is explored.

Iigo, M, et al. Orally administered bovine lactoferrin induces caspase-1 and interleukin-18 in the mouse intestinal mucosa: a possible explanation for inhibition of carcinogenesis and metastasis. Cytokine 25(1):36-44 (2004). Oral lactoferrin administration increased the production of IL-18 by intestinal epithelial cells followed by increases in caspase-1 and INF-?, which potentiate the activity of cytotoxic lymphocytes and natural killer cells in attacking cancer cells.

Andersson, Y, et al. Lactoferrin is responsible for the fungistatic effect of human milk. Early Human Development 59(2):95-102 (2001). Lactoferrin inhibits the growth of Candida albicans through its ability to sequester iron.

Kimber, I, et al. Lactoferrin: influences on Langerhans cells, epidermal cytokines, and cutaneous inflammation. Biochemistry and Cell Biology 80(1):103-107 (2002). Apart from its modulation anti-inflammatory cytokines, lactoferrin also expresses an anti-inflammatory effect through controlling the migration of epidermal Langerhans cells. Lactoferrin inhibited the migration of these cells when the skin was exposed to an irritant, thus decreasing the inflammatory response.

Ward, PP, et al. Lactoferrin and host defense. Biochemistry and Cell Biology 80(1):95-102 (2002). Lactoferrin is a prominent component of the first line of defense against infection and inflammation. It accomplishes its activity through a variety of methods, most notably iron sequestration and its effect on down-regulating TNF-a, which controls the inflammatory cascade.

Griffiths, CE, et al. Exogenous topical lactoferrin inhibits allergen-induced Langerhans cell migration and cutaneous inflammation in humans. British Journal of Dermatology 144(4):715-725 (2001). Lactoferrin influences inflammation inhibiting Langerhans cell migration, normally controlled by TNF-a and IL-1?, which are inhibited by lactoferrin.

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