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1997 Abstract: 64 Endotoxemia in mice stimulates the production of complement C3 and serum amyloid A in mucosa of small and large intestine.

Abstracts
1997 Digestive Disease Week

Endotoxemia in mice stimulates the production of complement C3 and serum amyloid A in mucosa of small and large intestine.

O Wang, JJ Wang, JE Fischer, PO Hasselgren. Department of Surgery, University of Cincinnati, and Shriners Burns Institute, Cincinnati, OH.


Previous studies suggest that cultured intestinal epithelial cells express the acute phase proteins complement C3 and SAA. Mucosal production of acute phase proteins in vivo during endotoxemia is not known. We measured C3 and SAA protein and mRNA levels in mucosa of jejunum, ileum and colon during endotoxemia in mice. Methods: Endotoxemia was induced in male A/J mice by the s.c. injection of LPS (12.5 mg/kg). Control mice were injected with corresponding volumes of sterile saline. After 24 h, mucosa was harvested from the jejunum, ileum, and colon (left and right). Tissue levels of C3 and SAA were measured by ELISA and mRNA levels by Northern blot analysis. Results: Endotoxemia resulted in increased mucosal concentrations of C3 in all intestinal segments studied and of SAA in jejunum and ileum. The most pronounced increase in protein levels was seen in jejunum (Table). mRNAs for C3 and SAA were not constitutively expressed in small intestinal mucosa but were induced during endotoxemia. In mucosa of colon, mRNA for the acute phase proteins was expressed in control mice and was increased during endotoxemia (Figure [not available]).

                         C3         SAA
Jejunum:   Saline     17.0±1.5     1.3±0.1
           LPS        61.0±8.0*    5.1±1.0*
Ileum:     Saline     19.1±2.6     2.0±0.4
           LPS        30.2±3.6*    4.1±0.5*
Colon:     Saline     7.7±0.6      4.3±0.5
           LPS       21.4±2.2*     4.1±0.4

Results are means ± SEM with n >= 6 in each group. Results are given as ng/mg wet weight. *p < 0.01 vs saline (Figure [not available]).

Conclusions: Results suggest that mucosal production of certain acute phase proteins is increased during endotoxemia and that this response may be regulated at the transcriptional level. The results lend further support to the concept that the intestine is an important participant in the metabolic response to sepsis and endotoxemia.



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