Impairment of mucosal immunity by parenteral nutrition: Depressed nasotracheal influenza-specific secretory IgA levels and transport in parenterally fed mice

Citation
Kb. Renegar et al., Impairment of mucosal immunity by parenteral nutrition: Depressed nasotracheal influenza-specific secretory IgA levels and transport in parenterally fed mice, ANN SURG, 233(1), 2001, pp. 134-138
Citations number
25
Categorie Soggetti
Surgery,"Medical Research Diagnosis & Treatment
Journal title
ANNALS OF SURGERY
ISSN journal
00034932 → ACNP
Volume
233
Issue
1
Year of publication
2001
Pages
134 - 138
Database
ISI
SICI code
0003-4932(200101)233:1<134:IOMIBP>2.0.ZU;2-V
Abstract
Objective To examine the effects on mucosal selective transport of polymeric IgA (plg A) and the ability of exogenous plgA to provide protection despite altered mucosal transport. Summary Background Data Parenteral nutrition significantly impairs established antipseudomonal immu nity and IgA-mediated antiviral immunity in association with gut-associated lymphoid tissue mass atrophy. Lack of enteral feeding also induces mucosal effects. Methods After immunization, nasotracheal levels of influenza-specific IgA were meas ured in cannulated mice randomized to chow feeding or parenteral nutrition, Nonimmune animals were randomized to chow or total parenteral nutrition, a nd after 5 days of diet were given a mixture of two antiinfluenza monoclona l antibodies, plgA and IgG. Four hours after injection, nasal washes were c ollected and influenza-specific antibody levels were determined by enzyme-l inked immunosorbent assay to calculate the selective transport index of IgA relative to IgG. In the final experiment, immunized animals were randomize d to chow or parenteral feeding, and after 5 days, parenterally fed animals received either normal mouse serum or antiviral plgA before viral challeng e. Viral shedding was measured at 42 hours after challenge. Results Parenteral nutrition significantly reduced virus-specific IgA in nasotrache al washes. Parenteral nutrition depressed the selective transport index, de monstrating impaired mucosal transport of plgA. Parenterally fed animals gi ven specific antiviral plgA but not normal mouse serum eliminated virus fro m the airway and regained mucosal protection, demonstrating adequate residu al transport for immunity if adequate plgA is present. Conclusion Although both decreased IgA production due to gut-associated lymphoid tissu e atrophy and impaired mucosal transport occur when enteral feeding is not provided, residual transport can provide antiviral protection if exogenous antiviral plgA is available. Production, rather than transport, may be the most important factor in maintaining established respiratory tract IgA-medi ated immunity.