Route of nutrition influences generation of antibody-forming cells and initial defense to an active viral infection in the upper respiratory tract
Route of nutrition influences generation of antibody-forming cells and initial defense to an active viral infection in the upper respiratory tract
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DOI：
10.1097/00000658-200304000-00019
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发表时间：
2003-04-01
影响因子：
9
通讯作者：
Zarzaur, BL
中科院分区：
文献类型：
--
作者：
Johnson, CD;Kudsk, KA;Zarzaur, BL
目的评估缺乏肠道喂养是否会显著损害对急性病毒感染的特异性免疫反应的产生。背景资料但缺乏肠内刺激会造成粘膜免疫缺陷，其特征是呼吸道中IgA介导的防御功能丧失。使用测定法测定饮食操作后鼻道中免疫细胞的积累。病毒脱落和鼻腔伊加水平进行了测量，在其他组的mice.Results后确定的时间过程中的抗体形成细胞（AFC）通过ELISPOT与A/PR 8流感病毒的主动感染，一个显着的减少被发现在总AFC，IgA生产的AFC，和IgG生产的AFC在一个为期13天的实验过程中的病毒特异性呼吸道伊加水平的显着抑郁症。八天后，一个活跃的感染，七个全胃肠外营养喂养的动物继续有病毒脱落的鼻道相比，一个九个饲料喂养的小鼠和一个六只动物喂养一个复杂的肠内diet.Conclusions缺乏肠道刺激显着损害IgA介导的粘膜免疫的产生。
Objective To assess whether lack of enteral feeding significantly impairs generation of specific immune responses to an acute viral infection.Summary Background Data Parenteral feeding provides adequate nutrients to meet metabolic needs, but lack of enteral stimulation creates a defect in mucosal immunity characterized by loss of IgA-mediated defenses in the respiratory tract.The enzyme-linked immunospot (ELISPOT) assay was used to determine accumulation of immunologic cells in the nasal passages after diet manipulation. Viral shedding and nasal IgA levels were measured in additional groups of mice.Results After determining the time course of anti body-forming cells (AFCs) via ELISPOT to an active infection with the A/PR8 influenza virus, a significant reduction was found in total AFCs, IgA-producing AFCs, and IgG-producing AFCs over the course of a 13-day experiment with significant depression in viral-specific respiratory IgA levels. Eight days following an active infection, seven of nine total parenteral nutrition-fed animals continued to have viral shedding in the nasal passages compared to one of nine chow-fed mice and one of six animals fed a complex enteral diet.Conclusions Lack of enteral stimulation significantly impairs the generation of IgA-mediated mucosal immunity.