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. 2022 Jan-Dec;14(1):2145843.
doi: 10.1080/19490976.2022.2145843.

Lactobacillus johnsonii alleviates colitis by TLR1/2-STAT3 mediated CD206+ macrophagesIL-10 activation

Ding-Jia-Cheng Jia  1   2 , Qi-Wen Wang  2   3 , Ying-Ying Hu  2   3 , Jia-Min He  2   3 , Qi-Wei Ge  1   2 , Ya-Dong Qi  2   3 , Lu-Yi Chen  2   4 , Ying Zhang  2   3 , Li-Na Fan  1   2 , Yi-Feng Lin  1   2 , Yong Sun  1   2 , Yao Jiang  1   2 , Lan Wang  2   3 , Yan-Fei Fang  2   3 , Hui-Qin He  3 , Xiong-E Pi  5 , Wei Liu  5 , Shu-Jie Chen  2   3   6 , Liang-Jing Wang  1   2   6
Affiliations

Lactobacillus johnsonii alleviates colitis by TLR1/2-STAT3 mediated CD206+ macrophagesIL-10 activation

Ding-Jia-Cheng Jia et al. Gut Microbes. 2022 Jan-Dec.

Abstract

Imbalance of gut microbiota homeostasis is related to the occurrence of ulcerative colitis (UC), and probiotics are thought to modulate immune microenvironment and repair barrier function. Here, in order to reveal the interaction between UC and gut microbiota, we screened a new probiotic strain by 16S rRNA sequencing from Dextran Sulfate Sodium (DSS)-induced colitis mice, and explored the mechanism and clinical relevance. Lactobacillus johnsonii (L. johnsonii), as a potential anti-inflammatory bacterium was decreased colonization in colitis mice. Gavage L. johnsonii could alleviate colitis by specifically increasing the proportion of intestinal macrophages and the secretion of Il-10 with macrophages depleted model and in Il10-/- mice. We identified this subset of immune cells activated by L. johnsonii as CD206+ macrophagesIL-10. Mechanistically, L. johnsonii supplementation enhanced the mobilization of CD206+ macrophagesIL-10 through the activation of STAT3 in vivo and in vitro. In addition, we revealed that TLR1/2 was essential for the activation of STAT3 and the recognition of L. johnsonii by macrophages. Clinically, there was positive correlation between the abundance of L. johnsonii and the expression level of MRC1, IL10 and TLR1/2 in UC tissues. L. johnsonii could activate native macrophages into CD206+ macrophages and release IL-10 through TLR1/2-STAT3 pathway to relieve experimental colitis. L. johnsonii may serve as an immunomodulator and anti-inflammatory therapeutic target for UC.

Keywords: IL-10; Lactobacillus johnsonii; Macrophages; STAT3; Ulcerative colitis.

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Conflict of interest statement

No potential conflict of interest was reported by the author(s).

Figures

Figure 1.
Figure 1.
L. johnsonii relieved DSS-induced colitis and maintained intestinal mucosal barrier.
Figure 2.
Figure 2.
Macrophages immune response was involved in the anti-inflammatory effect by L. johnsonii in colitis.
Figure 3.
Figure 3.
L. johnsonii promoted CD206+ macrophagesIL-10 activation in vivo and in vitro.
Figure 4.
Figure 4.
STAT3 signaling was essential for L. johnsonii activated CD206+macrophagesIL-10.
Figure 5.
Figure 5.
TLR1/2 participated in the recognition of L. johnsonii by CD206+macrophagesIL-10.
Figure 6.
Figure 6.
The abundance of L. johnsonii was positively correlated with MRC1, IL10 and TLR1/2 in UC patients.
Figure 7.
Figure 7.
The schematic diagram of L. johnsonii relieving colitis.
See this image and copyright information in PMC

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