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