Fibroblasts can produce IL-8 in response to infection, contributing to chemotaxis in inflammation.
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May broaden IL-8 sources to fibroblasts in animal viral models; challenges monocyte-centric consensus and leaves open human translation.
So far, the role of fibroblasts in inflammatory processes has been underestimated. We have previously shown that stimulation of fibroblasts with viruses or bacteria results in a simultaneous production of several cytokines, including interferon-beta, interleukin (IL) 6 and colony-stimulating factors. We here report that virally infected fibroblasts produce also a chemotactic factor for granulocytes. The activity is inducible not only by measles virus but also by IL 1 beta and the double-stranded RNA poly(rI).poly(rC). This factor, when purified to homogeneity, occurs as a 6-7-kDa protein doublet upon sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The pure protein is serologically related to a fully characterized granulocyte chemotactic peptide (GCP) from monocytes, designated IL8. Furthermore, the chemotactic factor from fibroblasts has an NH2-terminal sequence identical to that of GCP/IL8, small differences in NH2-terminal processing being observed. Finally, in addition to diploid fibroblasts, the osteosarcoma MG-63 cell line is also a producer of GCP/IL8. It can thus be concluded that GCP/IL8 can be produced by several cell types in response to infection and that fibroblasts can contribute to chemotaxis in inflammation.
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Damme et al. (1989) studied this question.
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