Abstract
In murine abdominal sepsis by colon ascendens stent peritonitis (CASP), a strong increase in serum IgM and IgG antibodies was observed, which reached maximum values 14 days following sepsis induction. The specificity of this antibody response was studied in serum and at the single cell level using a broad panel of bacterial, sepsis-unrelated as well as self-antigens. Whereas an antibacterial IgM/IgG response was rarely observed, studies at the single-cell level revealed that IgM antibodies, in particular, were largely polyreactive. Interestingly, at least 16% of the IgM mAbs and 20% of the IgG mAbs derived from post-septic mice showed specificity for oxidation-specific epitopes (OSEs), which are known targets of the innate/adaptive immune response. This identifies those self-antigens as the main target of B cell responses in sepsis.
Highlights
Sepsis, by definition, is a life-threatening organ dysfunction caused by a dysregulated host response to infection [1, 2], which is associated with high morbidity and mortality [3, 4]
Enterococcus faecalis (E. faecalis) and Escherichia coli (E. coli), two microbial species of the intestinal flora, were regularly found in the blood of septic mice. Antibody binding to these bacteria as well as to Staphylococcus aureus (S. aureus), which is often observed in the murine intestine, was measured by ELISA
We investigated the binding of serum antibodies to two antigens the animals had never been exposed to, namely the classical TD protein antigen ovalbumin (OVA) and the hapten 2,4,6-trinitrophenyl (TNP) conjugated to bovine serum albumin (TNP-(14)-BSA)
Summary
By definition, is a life-threatening organ dysfunction caused by a dysregulated host response to infection [1, 2], which is associated with high morbidity and mortality [3, 4]. B cells have been ascribed a protective function in sepsis which encompasses antibody-dependent as well as -independent mechanisms [7, 8]. Mohr et al have shown that B cell priming with defined antigens is defective in sepsis [13]. We and other research groups have shown that sepsis induces high concentrations of serum IgM and IgG antibodies of unknown specificities [13, 14]. Since these may be responsible for the observed antibodymediated protection, we set out to examine their antigen specificities in a mouse model of abdominal sepsis
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