Immunoinflammatory responses after shock and major trauma are characterized
by an early hyperinflammatory response and later by compensatory anti-infl
ammatory host mediator production. This late phase is associated with depre
ssed immune function that has been causally linked with post-traumatic infe
ctious complications and late organ failure. Gut barrier failure is noted i
n this setting and may be an important source of nosocomial infections and
organ failure. Secretory immunoglobulin A (sIgA) is the predominant immunog
lobin at mucosal surfaces and is difficult to quantify in luminal secretion
s. Attempts to normalize sIgA concentrations may not be accurate and/or may
not be applicable in vivo. A method using mucosal immunization with choler
a toxin (ChT) to normalize gut sIgA levels was used to assess serial change
s 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 norm
alized using the specific anti-ChT/total sIgA ratio, differences were clear
ly evident. This ratio was depressed between 3 and 10 days post-HS. The spe
cific anti-ChT/total sIgA ratio is a reliable index of secretory antibody a
t 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 complic
ations.