Epithelial inflammation response induced by Shigella flexneri depends on mucin gene expression.
The protective effects of different mucin gene profiles on gut protection were assessed by the evaluation of TNFalpha production by intestinal epithelial cells infected by Shigella flexneri. Three HT-29 cell lines were used: HT29-G(-) (enterocyte-like cells, secreting no mucins), HT29-FU (highly expressing MUC2 and MUC4) and HT29-MTX (highly expressing MUC3 and MUC5AC). These cells were infected either by an invasive (M90T) or the control isogenic (BS176) strains of S. flexneri, and TNFalpha mRNA production was quantified by competitive PCR. In the HT29-G(-) cells, M90T induced an increased production of TNFalpha mRNA compared to BS176, giving a TNFalpha ratio of 5.6 +/- 3.3. In contrast, similar levels of TNFalpha mRNA were detected in HT29-FU and HT29-MTX cells stimulated with either M90T or BS176, giving ratios of 1.4 +/- 1.3 and 1.0 +/- 0.1, respectively. The results suggest that mucin genes have abilities to protect epithelial cells against S. flexneri. Furthermore, the difference in the TNFalpha ratio between the HT29-FU and HT29-MTX cells suggests distinct protective effects for these two mucin-secreting epithelial cells.
D002478:Cells, Cultured; D004405:Dysentery, Bacillary / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D004848:Epithelium / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000235:genetics / Q000378:metabolism / Q000382:microbiology; D009077:Mucins / Q000235:genetics / Q000378:metabolism*; D012333:RNA, Messenger / Q000096:biosynthesis; D012763:Shigella flexneri / Q000378:metabolism / Q000502:physiology*; D014158:Transcription, Genetic; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis / Q000145:classification / Q000378:metabolism
D009077:Mucins; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha