Clostridium butyricum alleviates intestinal low-grade inflammation in TNBS-induced irritable bowel syndrome in mice by regulating functional status of lamina propria dendritic cells

Figure 4 Effects of Clostridium butyricum on the quantity and functional status of the lamina propria dendritic cells. A: Flow cytometry of CD11c+ LPDCs expression; B: Flow cytometry of CD11C+CD80+ LPDCs expression; C: Flow cytometry of CD11c+Tim3+ LPDCs expression; D: Flow scatter plot of all test indicators; E: Tim-3 mRNA levels measured by real-time PCR; F: Tim3 protein expression measured by Western blot analysis. The results showed that the expression of CD11c+, CD11C+CD80+, and CD11c+Tim3+ LPDCs in the intestinal inflammatory state of IBS was significantly higher than in that in the normal control group, and the costimulatory molecule CD80 representing DC in the activated mature state was also significantly increased (P < 0.01). However, the above indicators were significantly decreased after C. butyricum intervention. Our experimental results suggest that the LPDCs participate in and promote the intestinal inflammatory immune response of IBS and C. butyricum suppresses intestinal inflammation by reducing the number, function, and immunoregulatory molecule Tim3 of LPDCs in IBS mice. ^aP < 0.05, ^bP < 0.05, ^cP < 0.05 vs control group, IBS + normal saline group, and IBS group, respectively. IBS: Irritable bowel syndrome; LPDCs: Lamina propria dendritic cells.