Objective:
@EN Bacteroides fragilis is the most frequently isolated anaerobes in tissue of intraabdominal infection, particularly in intraabdominal sepsis or abscess. In acute experimental model with an intraabdominal infection, the response to B. fragilis
is
characterized by infiltration of neutrophils and monocytes. To understand the pathogenesis of B. fragilis infection, it is important to explore the mechanism for inflammatory signals such as chemokines induced by this bacteria. The goal of this
study
was to determine whether peritoneal monocytes or fibroblasts surrounding with intraabdominal abscess induced by B. fragilis could express chemokines such as monocyte chemotactic protein-1 (MCP-1) or macrophage inflammatory protein-1a (MIP-1a).
@ES Methods:
@EN 1) After C57BL/6 mice were intraperitoneally inoculated with abscess-inducing agents containing B. fragilis, RNA was extracted from the intraperitoneal tissues of the mice using Ottawa sand and the guanidinium thiocyanate-phenol-chloroform
method in
3 days later. 2) After C57BL/6 mouse peritoneal monocytes were infected with B. fragilis for 1, 4 and 9 hours, cellular RNA was extracted from the cells. 3) Fibroblasts isolated from intraabdominal abscess nodules induced by B. fragilis infection
were
growth in tissue culture for 3 to 4 weeks. After the fibroblasts were stimulated with IL-1α(0.1-10 ng/ml) or TNFα(0.1-10 ng/ml) for 24 hours, total cellular RNA was extracted. MCP-1 or MIP-1αmRNA expression was assessed using RTPCR. MCP-1 or
MIP-1α
proteins in cluture supernatants or tissue extracts were also measured by ELISA. @ES Results @EN 1) MCP-1 or MIP-1αmRNA was highly expressed in peritoneal tissue of C57BL/6 mice bearing with intraabdominal abscess induced by B. fragilis. 2)
Expression
of MCP-1 mRNA increased at 9 hours in mouse peritoneal monocytes infected with B. fragilis. MIP-1αmRNA was initially expressed and perisisted in the monocytes infected with B. fragilis for 9 hours. MCP-1 or MIP-1αproteins was also parallel to
the
expression of those chemokines. 3) The fibroblasts isolated from intraabdominal abscess nodules by B. fragilis infection constitutively expressed MCP-1, MIP-1α, production in the fibroblasts was significantly upregulated in response to
proinflammatory
cytokines produced in the monocytes, including IL-1αand TNFa, but MCP-1 production were not. The normal fibroblasts from uninfected mice didnot show significant production of MCP-1 or MIP-1a in response to IL-1a or TNFa.
@ES Conclusion:
@EN These results suggest that peritoneal monocytes and fibroblasts surrounding with abscesses induced by B. fragilis produce MCP-1 or MIP-1a. Furthermore, it could be extrapolated that those effects may play a role in the formation of
intraabdominal
abscess nodules.
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