Abstract
ObjectiveInflammatory stimuli inducing epithelial-to-mesenchymal transition (EMT) can transdifferentiate mesenteric mesothelial cells into macrophages.MethodsSprague Dawley rat mesenteric mesothelial cells were used as a model. 1 ml Freund adjuvant was injected into the peritoneal cavity of rat and GM-CSF treatment was used to induce inflammation. IL-10 and IL-6 expression were studied by immunocytochemistry and Western blot analysis both in vivo and in vitro.ResultsControl mesothelial cell express anti-inflammatory IL-10, but no pro-inflammatory IL-6 expression could be detected in them. By the time of inflammation, IL-6 expression increased (reached the maximum level at the fifth day of inflammation), parallel to this the IL-10 entirely disappeared from these cells. In vitro GM-CSF treatment resulted in similar changes. As the mesothelial cells started to recover (at the eighth day of inflammation) IL-6 expression decreased and IL-10 level started to increase again.ConclusionThese data show that under inflammatory stimuli mesothelial cells—like macrophages—can produce pro-inflammatory cytokines.
Highlights
Monocytes and macrophages play important role in immune responses
Control mesothelial cell expresses anti-inflammatory IL-10 (Fig. 1g), but no pro-inflammatory IL-6 expression could be detected in them (Fig. 1a)
No IL-10 could be detected at the peak time of inflammation (Fig. 1i), but its level increased again after the eighth day of inflammation. (Fig. 1j)
Summary
Monocytes and macrophages play important role in immune responses. Under healthy conditions large number of these phagocytic cells reside in the peritoneal cavity as self-sustaining resident macrophages [1, 2]. During inflammation a heterogeneous population of phagocytes appear in the peritoneal cavity [3]. It seems likely that besides of activated tissue-resident, and infiltrating monocyte-derived macrophages, cells originating from non-hemopoietic sources should contribute to this subset of macrophages. That inflammation transdifferentiated mesenteric mesothelial cells into macrophages-like cells. During this transition mesothelial cells expressed ED1
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