Renegar K B, Kudsk K A, Dewitt R C, Wu Y, King B K
Department of Surgery, University of Tennessee--Memphis, Memphis, Tennessee, USA.
Ann Surg. 2001 Jan;233(1):134-8. doi: 10.1097/00000658-200101000-00019.
To examine the effects on mucosal selective transport of polymeric IgA (pIgA) and the ability of exogenous pIgA to provide protection despite altered mucosal transport.
Parenteral nutrition significantly impairs established antipseudomonal immunity and IgA-mediated antiviral immunity in association with gut-associated lymphoid tissue mass atrophy. Lack of enteral feeding also induces mucosal effects.
After immunization, nasotracheal levels of influenza-specific IgA were measured in cannulated mice randomized to chow feeding or parenteral nutrition. Nonimmune animals were randomized to chow or total parenteral nutrition, and after 5 days of diet were given a mixture of two antiinfluenza monoclonal antibodies, pIgA and IgG. Four hours after injection, nasal washes were collected and influenza-specific antibody levels were determined by enzyme-linked immunosorbent assay to calculate the selective transport index of IgA relative to IgG. In the final experiment, immunized animals were randomized to chow or parenteral feeding, and after 5 days, parenterally fed animals received either normal mouse serum or antiviral pIgA before viral challenge. Viral shedding was measured at 42 hours after challenge.
Parenteral nutrition significantly reduced virus-specific IgA in nasotracheal washes. Parenteral nutrition depressed the selective transport index, demonstrating impaired mucosal transport of pIgA. Parenterally fed animals given specific antiviral pIgA but not normal mouse serum eliminated virus from the airway and regained mucosal protection, demonstrating adequate residual transport for immunity if adequate pIgA is present.
Although both decreased IgA production due to gut-associated lymphoid tissue atrophy and impaired mucosal transport occur when enteral feeding is not provided, residual transport can provide antiviral protection if exogenous antiviral pIgA is available. Production, rather than transport, may be the most important factor in maintaining established respiratory tract IgA-mediated immunity.
研究对聚合免疫球蛋白A(pIgA)黏膜选择性转运的影响,以及尽管黏膜转运改变,外源性pIgA提供保护的能力。
肠外营养与肠道相关淋巴组织萎缩相关,会显著损害已建立的抗假单胞菌免疫和IgA介导的抗病毒免疫。缺乏肠内喂养也会引发黏膜效应。
免疫后,在随机分配至正常饮食喂养或肠外营养的插管小鼠中测量鼻气管中流感特异性IgA水平。将未免疫的动物随机分为正常饮食组或全肠外营养组,在饮食5天后给予两种抗流感单克隆抗体、pIgA和IgG的混合物。注射4小时后,收集鼻腔灌洗液,通过酶联免疫吸附测定法测定流感特异性抗体水平,以计算IgA相对于IgG的选择性转运指数。在最后一项实验中,将免疫动物随机分为正常饮食组或肠外喂养组,5天后,肠外喂养的动物在病毒攻击前接受正常小鼠血清或抗病毒pIgA。在攻击后42小时测量病毒排出量。
肠外营养显著降低了鼻气管灌洗液中病毒特异性IgA水平。肠外营养降低了选择性转运指数,表明pIgA的黏膜转运受损。接受特异性抗病毒pIgA而非正常小鼠血清的肠外喂养动物从气道中清除了病毒并恢复了黏膜保护,表明如果存在足够的pIgA,有足够的残余转运用于免疫。
尽管在不提供肠内喂养时,由于肠道相关淋巴组织萎缩导致的IgA产生减少和黏膜转运受损均会发生,但如果有外源性抗病毒pIgA,残余转运可提供抗病毒保护。产生而非转运可能是维持已建立的呼吸道IgA介导免疫的最重要因素。