Abstracts (complete list) - Wissenschaft Online

Arvind Batra, Markus M. Heimesaat, Stefan Bereswill, Jeannette Pietsch, Thorsten
Stroh, Rainer Glauben, Inka Fedke, Martin Zeitz, Britta Siegmund
TLR – expression in cells from adipose tissue – a contribution
to chronic inflammation?
Hypertrophy of mesenteric fat is a characteristic finding in Crohn’s disease. However,
the underlying mechanisms and the contribution to the disease itself are still unknown.
In addition to its endocrine role, adipose tissue is the producer of various proinflammatory
mediators like leptin, IL-6 and TNF-α. We recently demonstrated leptindependent
expression and function of Toll-like receptors (TLR) in murine preadipocytes
and adipocytes (Batra et al., Am J Pathol, in press). To transfer these findings to
humans TLR1 to -10 expression and function was analyzed in preadipocyte cell lines,
established from human mesenteric fat, by RT-PCR and TLR-specific stimulation with
subsequent evaluation of cytokine production. To further determine whether in vivo a
direct interaction of cells from adipose tissue and bacterial TLR-ligands can occur,
bacterial translocation was monitored in acute and chronic DSS-induced colitis in WT
and MyD88 +/- mice by analysis for the presence of life bacteria via culture.
In concordance with the murine system, in human preadipocyte cell lines TLR mRNA is
expressed and cells respond to TLR-specific stimulation as evaluated by IL-6 production.
In acute DSS-induced colitis no bacterial translocation was observed. In chronic DSSinduced
colitis bacterial translocation into various abdominal tissues including fat
occurred. Interestingly, bacterial translocation was more common in the MyD88 +/- mice
with alterations in TLR-signaling. Our data provide strong evidence that functional TLR
are expressed in preadipocytes and adipocytes across species. Suggesting that bacteria
translocating to the mesenteric fat during intestinal inflammations such as Crohn’s
disease can directly activate preadipocytes and adipocytes and thus might contribute to
the mesenteric hypertrophy observed.