IL-4 enhances IEC-6 intestinal epithelial cell proliferation yet has no effect on IL-6 secretion.
Intestinal epithelial cells (IEC) form an important line of defence at the intestinal mucosa by providing a barrier to lumenal contents and also by their ability to secrete various inflammatory cytokines. Recently, several T cell-derived cytokines have been shown to regulate specific IEC functions. In this study, the effect of IL-4 on IEC proliferation and secretion of the inflammatory cytokine IL-6 was investigated using the non-transformed rat IEC-6 intestinal epithelial cell line. Recombinant rat (rr)IL-4 was found to enhance IEC-6 cell proliferation over 4 days of culture, and this enhancement was dose-dependent. Further studies using specific antibodies confirmed that IL-4 induced the effect and that the effect was not mediated by autocrine-produced transforming growth factor-alpha. However, IL-4 did not induce IL-6 secretion by the IEC-6 cells, nor did it alter IL-1 beta-induced IL-6 secretion. These results indicate that T cells may be capable of regulating IEC proliferation via the secretion of IL-4 without altering the capacity of the IEC to function in the inflammatory response by secreting IL-6.
McGee
D W
DW
Department of Biological Sciences, Binghamton University (SUNY) 13902-6000, USA.
Vitkus
S J
SJ
D000818:Animals; D002455:Cell Division / Q000187:drug effects; D002460:Cell Line; D004847:Epithelial Cells; D004848:Epithelium / Q000187:drug effects; D015847:Interleukin-4 / Q000494:pharmacology*; D015850:Interleukin-6 / Q000378:metabolism*; D007422:Intestines / Q000166:cytology / Q000187:drug effects* / Q000276:immunology; D051381:Rats; D011994:Recombinant Proteins / Q000494:pharmacology
D015850:Interleukin-6; D011994:Recombinant Proteins; D015847:Interleukin-4