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Lactobacillus acidophilus suppresses colitis-associated activation of the IL-23/Th17 axis.

Chen L, Zou Y, Peng J, Lu F, Yin Y, Li F, Yang J - J Immunol Res (2015)

Bottom Line: The aim of this paper is to determine the modulatory effects of Lactobacillus acidophilus on the IL-23/Th17 immune axis in experimental colitis.DSS-induced mouse models of UC were to be saline, hormones, and different concentrations of Lactobacillus acidophilus intervention.And the results showed that administration of L. acidophilus suppressed Th17 cell-mediated secretion of proinflammatory cytokine IL-17 through downregulation of IL-23 and TGFβ1 expression and downstream phosphorylation of p-STAT3.

View Article: PubMed Central - PubMed

Affiliation: Department of Gastroenterology, Xiangya Hospital of Central South University, Changsha 410011, China.

ABSTRACT
The aim of this paper is to determine the modulatory effects of Lactobacillus acidophilus on the IL-23/Th17 immune axis in experimental colitis. DSS-induced mouse models of UC were to be saline, hormones, and different concentrations of Lactobacillus acidophilus intervention. The expression of interleukin- (IL-) 17, tumor necrosis factor α (TNFα), IL-23, transforming growth factor β1 (TGFβ1), signal transducer and activator of transcription 3 (STAT3), and phosphorylated (p)-STAT3 was examined by RT-PCR, Western blotting, and immunohistochemical analysis. And the results showed that administration of L. acidophilus suppressed Th17 cell-mediated secretion of proinflammatory cytokine IL-17 through downregulation of IL-23 and TGFβ1 expression and downstream phosphorylation of p-STAT3.

No MeSH data available.


Related in: MedlinePlus

Lactobacillus acidophilus treatment attenuated the phosphorylation level of STAT3 (p-STAT3) in colitis. The expression level of p-STAT3 was determined by both Western blotting (WB, (a)) and immunohistochemistry (IHC, (b)) in the colonic tissues of normal control mice group (normal) and DSS-induced model mice groups, including L. acidophilus-treated C4–C8 groups, prednisone acetate treated positive control (Pred), and nontreated (Non) and vehicle (Veh) treated control groups. Representative images of Western blotting and immunohistochemical staining showing subcellular localization of p-STAT3 in the colon of nontreated model control mice are shown on the left, and a bar graph representing mean ± SD (n = 8) values is shown on the right. A plotted trendline chart shows p-STAT3 expression in each group as determined by WB and IHC (c). aP < 0.05 versus Non, bP < 0.05 versus Veh, cP < 0.05 versus Pred, and dP < 0.05 versus normal.
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fig6: Lactobacillus acidophilus treatment attenuated the phosphorylation level of STAT3 (p-STAT3) in colitis. The expression level of p-STAT3 was determined by both Western blotting (WB, (a)) and immunohistochemistry (IHC, (b)) in the colonic tissues of normal control mice group (normal) and DSS-induced model mice groups, including L. acidophilus-treated C4–C8 groups, prednisone acetate treated positive control (Pred), and nontreated (Non) and vehicle (Veh) treated control groups. Representative images of Western blotting and immunohistochemical staining showing subcellular localization of p-STAT3 in the colon of nontreated model control mice are shown on the left, and a bar graph representing mean ± SD (n = 8) values is shown on the right. A plotted trendline chart shows p-STAT3 expression in each group as determined by WB and IHC (c). aP < 0.05 versus Non, bP < 0.05 versus Veh, cP < 0.05 versus Pred, and dP < 0.05 versus normal.

Mentions: STAT3 is an important transcription factor that mediates the establishment of Th17 cells in response to IL-23 and TGFβ1 [15, 16]. We therefore examined whether STAT3 expression is altered with diminished expression of IL-23 and TGFβ1 upon L. acidophilus treatment. We observed that STAT3 expression was upregulated in the colon of DSS-mediated colitis, which is consistent with previous reports [22, 23]. Although the decrease in the STAT3 mRNA level was relatively moderate in the L. acidophilus-treated groups (Figure 5(a)), an apparent decrease in STAT3 protein level was observed in contrast to the vehicle treated control group (Figure 5(b)). Among all the L. acidophilus-treated groups, inhibition of STAT3 protein expression was most obvious in C5 (Figure 5(c)). Because phospho- (p-) STAT3 is the functional form, it is important to understand whether the phosphorylation level of STAT3 is altered by L. acidophilus treatment. We observed that p-STAT3 was significantly (P < 0.05) lower in all groups (C4–C8) relative to the untreated or vehicle treated control groups by Western blotting analysis (Figure 6(a)). Moreover, immunohistochemical staining showed that p-STAT3 localized in the nuclei was predominantly expressed in the inflamed area in the DSS-induced untreated control group (Figure 6(b)). Importantly, L. acidophilus treatment caused a significant (P < 0.05) reduction in p-STAT3 signal, with a stronger effect in the C5 and C6 groups (Figures 6(b) and 6(c)). These findings suggest that administration of L. acidophilus improves colitis by restoring the homeostasis of p-STAT3-mediated cellular events, such as Th17 differentiation and IL-17 secretion.


Lactobacillus acidophilus suppresses colitis-associated activation of the IL-23/Th17 axis.

Chen L, Zou Y, Peng J, Lu F, Yin Y, Li F, Yang J - J Immunol Res (2015)

Lactobacillus acidophilus treatment attenuated the phosphorylation level of STAT3 (p-STAT3) in colitis. The expression level of p-STAT3 was determined by both Western blotting (WB, (a)) and immunohistochemistry (IHC, (b)) in the colonic tissues of normal control mice group (normal) and DSS-induced model mice groups, including L. acidophilus-treated C4–C8 groups, prednisone acetate treated positive control (Pred), and nontreated (Non) and vehicle (Veh) treated control groups. Representative images of Western blotting and immunohistochemical staining showing subcellular localization of p-STAT3 in the colon of nontreated model control mice are shown on the left, and a bar graph representing mean ± SD (n = 8) values is shown on the right. A plotted trendline chart shows p-STAT3 expression in each group as determined by WB and IHC (c). aP < 0.05 versus Non, bP < 0.05 versus Veh, cP < 0.05 versus Pred, and dP < 0.05 versus normal.
© Copyright Policy - open-access
Related In: Results  -  Collection

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fig6: Lactobacillus acidophilus treatment attenuated the phosphorylation level of STAT3 (p-STAT3) in colitis. The expression level of p-STAT3 was determined by both Western blotting (WB, (a)) and immunohistochemistry (IHC, (b)) in the colonic tissues of normal control mice group (normal) and DSS-induced model mice groups, including L. acidophilus-treated C4–C8 groups, prednisone acetate treated positive control (Pred), and nontreated (Non) and vehicle (Veh) treated control groups. Representative images of Western blotting and immunohistochemical staining showing subcellular localization of p-STAT3 in the colon of nontreated model control mice are shown on the left, and a bar graph representing mean ± SD (n = 8) values is shown on the right. A plotted trendline chart shows p-STAT3 expression in each group as determined by WB and IHC (c). aP < 0.05 versus Non, bP < 0.05 versus Veh, cP < 0.05 versus Pred, and dP < 0.05 versus normal.
Mentions: STAT3 is an important transcription factor that mediates the establishment of Th17 cells in response to IL-23 and TGFβ1 [15, 16]. We therefore examined whether STAT3 expression is altered with diminished expression of IL-23 and TGFβ1 upon L. acidophilus treatment. We observed that STAT3 expression was upregulated in the colon of DSS-mediated colitis, which is consistent with previous reports [22, 23]. Although the decrease in the STAT3 mRNA level was relatively moderate in the L. acidophilus-treated groups (Figure 5(a)), an apparent decrease in STAT3 protein level was observed in contrast to the vehicle treated control group (Figure 5(b)). Among all the L. acidophilus-treated groups, inhibition of STAT3 protein expression was most obvious in C5 (Figure 5(c)). Because phospho- (p-) STAT3 is the functional form, it is important to understand whether the phosphorylation level of STAT3 is altered by L. acidophilus treatment. We observed that p-STAT3 was significantly (P < 0.05) lower in all groups (C4–C8) relative to the untreated or vehicle treated control groups by Western blotting analysis (Figure 6(a)). Moreover, immunohistochemical staining showed that p-STAT3 localized in the nuclei was predominantly expressed in the inflamed area in the DSS-induced untreated control group (Figure 6(b)). Importantly, L. acidophilus treatment caused a significant (P < 0.05) reduction in p-STAT3 signal, with a stronger effect in the C5 and C6 groups (Figures 6(b) and 6(c)). These findings suggest that administration of L. acidophilus improves colitis by restoring the homeostasis of p-STAT3-mediated cellular events, such as Th17 differentiation and IL-17 secretion.

Bottom Line: The aim of this paper is to determine the modulatory effects of Lactobacillus acidophilus on the IL-23/Th17 immune axis in experimental colitis.DSS-induced mouse models of UC were to be saline, hormones, and different concentrations of Lactobacillus acidophilus intervention.And the results showed that administration of L. acidophilus suppressed Th17 cell-mediated secretion of proinflammatory cytokine IL-17 through downregulation of IL-23 and TGFβ1 expression and downstream phosphorylation of p-STAT3.

View Article: PubMed Central - PubMed

Affiliation: Department of Gastroenterology, Xiangya Hospital of Central South University, Changsha 410011, China.

ABSTRACT
The aim of this paper is to determine the modulatory effects of Lactobacillus acidophilus on the IL-23/Th17 immune axis in experimental colitis. DSS-induced mouse models of UC were to be saline, hormones, and different concentrations of Lactobacillus acidophilus intervention. The expression of interleukin- (IL-) 17, tumor necrosis factor α (TNFα), IL-23, transforming growth factor β1 (TGFβ1), signal transducer and activator of transcription 3 (STAT3), and phosphorylated (p)-STAT3 was examined by RT-PCR, Western blotting, and immunohistochemical analysis. And the results showed that administration of L. acidophilus suppressed Th17 cell-mediated secretion of proinflammatory cytokine IL-17 through downregulation of IL-23 and TGFβ1 expression and downstream phosphorylation of p-STAT3.

No MeSH data available.


Related in: MedlinePlus