Role of Dectin-1 in the production of IL-10 and TNF-α by rat tracheal epithelial cells stimulated with heattreated Candida glabrata

Abstract:

ObjectiveTo investigate the effect of Dectin1 on the release of inflammatory factors interleukin10(IL10) and tumor necrosis factorα (TNFα) in rat tracheal epithelial cells (RTECs) stimulated with heattreated Candida glabrata(C. glabrata).MethodsRTECs cultivated in vitro were randomly divided into three groups, including control group(RTECs +sterile normal saline), fungal stimulation group(RTECs + heattreated C. glabrata), and inhibitor intervention group(RTECs + laminarin + heattreated C. glabrata), cells were harvested after incubation for 0, 2, 4, 6 hours respectively, cell survival rate was determined by MTT method, expression of Dectin1 was analyzed by Western Blot, expression of IL10 and TNFα were detected by enzymelinked immunosorbent assay (ELISA).ResultsHeattreated C. glabrata destroyed cell structure and reduced cell survival rate. At the beginning of the culture (0 h), cell survival rate, expressions of Dectin1, IL10 and TNFα among three groups were all not significantly different(all P>0.05). After incubation for 2, 4, 6 hours, expressions of Dectin1, IL10 and TNFα in fungal stimulation group and inhibitor intervention group were both significantly higher than control group; expressions of Dectin1, IL10,and TNFα in inhibitor intervention group was lower than fungal stimulation group(all P<0.05). The expressions of IL10 in inhibitor intervention group at 0 h and 2 h was not significantly different, expressions of Dectin1, IL10, and TNFα in fungal stimulation group and inhibitor intervention group at different incubation periods were significantly different(all P<0.05).ConclusionDectin1 is an important receptor for RTECs to recognize the heattreated C. glabrata, it induces the release of IL10 and TNFα, and mediate the occurrence of inflammation.