ObjectiveTo examine the effects on mucosal selective transport of polymeric IgA (pIgA) and the ability of exogenous pIgA to provide protection despite altered mucosal transport. Summary Background DataParenteral 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. MethodsAfter 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.

Gastric injuries are equivalent to colon wounds in their contribution to IAA. Contamination from either organ without associated injury is minimally associated with IAA, but injury to both appears synergistic. The immunosuppressive effects of age and hemorrhage, in addition to significant associated injury, enhance the development of IAA.

Pancreatic injuries including those with indeterminate ductal status can be successfully managed with low morbidity and mortality using this simplified management protocol.