Sequential changes in mucosal immunity after hemorrhagic shock.
Immunoinflammatory responses after shock and major trauma are characterized by an early hyperinflammatory response and later by compensatory anti-inflammatory host mediator production. This late phase is associated with depressed immune function that has been causally linked with post-traumatic infectious complications and late organ failure. Gut barrier failure is noted in this setting and may be an important source of nosocomial infections and organ failure. Secretory immunoglobulin A (sIgA) is the predominant immunoglobin at mucosal surfaces and is difficult to quantify in luminal secretions. Attempts to normalize sIgA concentrations may not be accurate and/or may not be applicable in vivo. A method using mucosal immunization with cholera toxin (ChT) to normalize gut sIgA levels was used to assess serial changes in sIgA after hemorrhagic shock (HS) in rodents. Total and anti-ChT sIgA levels were highly variable in both HS and sham animals. However, when normalized using the specific anti-ChT/total sIgA ratio, differences were clearly evident. This ratio was depressed between 3 and 10 days post-HS. The specific anti-ChT/total sIgA ratio is a reliable index of secretory antibody at gut luminal surfaces. Impaired mucosal immune function occurred in a time frame consistent with development of late nosocomial infections. This may be important mechanistically in the development of these infectious complications.