Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2020 Mar;21(3):1181-1191.
doi: 10.3892/mmr.2020.10925. Epub 2020 Jan 9.

Oral administration of Lactobacillus plantarum 06CC2 prevents experimental colitis in mice via an anti‑inflammatory response

Akihito Tanaka  1 , Shuji Kanmura  1 , Yuko Morinaga  1 , Katsuto Kawabata  1 , Shiho Arima  1 , Fumisato Sasaki  1 , Yuichirou Nasu  1 , Shiroh Tanoue  1 , Shinichi Hashimoto  1 , Masahiko Takeshita  2 , Shiro Takeda  3 , Akio Ido  1
Affiliations

Oral administration of Lactobacillus plantarum 06CC2 prevents experimental colitis in mice via an anti‑inflammatory response

Akihito Tanaka et al. Mol Med Rep. 2020 Mar.

Abstract

Dysbiosis of the enteric microbiota causes gastrointestinal diseases, including colitis. The present study investigated the beneficial effect of Lactobacillus plantarum 06CC2 in experimental colitis in mice. An experimental colitis model in C57BL6 mice was induced using dextran sulfate sodium. Mice were orally administered 06CC2 (06CC2 group) or PBS only (control group) by gavage. The disease activity index (DAI), histological grading, and colon tissue and colonic lamina propria mononuclear cells (LPMCs) were examined macroscopically and histopathologically, and the expression levels of inflammation‑associated cytokines (IL‑6, IL‑12, TNF‑α and IL‑10) in these samples were determined. Compared with the control group, the 06CC2 group exhibited a significantly lower DAI (1.5±0.8 vs. 0.2±0.3, respectively; P<0.05) and pathology score (6.3±1.5 vs. 3.8±1.3, respectively; P<0.05). IL‑10 expression in colonic LPMCs was higher in the 06CC2 group than in the control group, although there was no significant difference in IFN‑γ, IL‑6 or IL‑12 expression in colonic LPMCs between the two groups. In addition, 06CC2 stimulated the production of IL‑10 from CD11b‑positive cells and CD11c‑positive cells in the colon. The 06CC2 strain induced IL‑10 production in the colon and attenuated colon inflammation.

Keywords: colitis; inflammatory bowel disease; Lactobacillus; microbiota; interleukin‑10; Lactobacillus plantarum 06cc2.

PubMed Disclaimer

Figures

Figure 1.
Figure 1.
LPMCs isolated from entire mouse colons were co-cultured with 06CC2 (0, 1, 10 and 100 µg/ml). The gene expression levels of IL-12α, TNF-α, TGF-β and IL-10 were significantly and dose-dependently higher in LPMCs exposed to 06CC2; IL-10 gene expression was particularly high compared with the other genes. IL-12α, IL-4 and IL-23α were analyzed using Tukey's test. TNF-α, TGF-β and IL-10 were analyzed using Dunnet T3 test. *P<0.05 vs. 0 µg/ml. IL, interleukin; LPMCs, lamina propria mononuclear cells; TGF-β, transforming growth factor β; TNF-α, tumor necrosis factor α.
Figure 2.
Figure 2.
IL-10 expression in CD11c-positive and CD11b-positive cells in colonic lamina propria mononuclear cells under co-culture with 06CC2. Top panel, CD11c; lower panel, CD11b. Data were analyzed using Tukey's test. *P<0.05 and **P<0.01 vs. 0 µg/ml. IL-10, interleukin 10.
Figure 3.
Figure 3.
TLR2, TLR3 and TLR4 expression in CD11c-positive cells in colonic lamina propria mononuclear cells under co-culture with 06CC2. Data were analyzed using Mann-Whitney's U test. *P<0.05. TLR, toll-like receptor.
Figure 4.
Figure 4.
Inflammatory and anti-inflammatory cytokine gene expression in the large intestine. The expression of IL-10 was significantly increased in 06CC2-treated mice compared with control. IL-6 and IL-10 were analyzed by Tukey's test. TNF-α and IL-12α were analyzed by Dunnet T3 test. *P<0.05. IL, interleukin; TNF-α, tumor necrosis factor α.
Figure 5.
Figure 5.
Effects of oral administration of LP 06CC2 in mice with DSS-induced colitis. (A) In a mouse experimental colitis model, 06CC2 was administered by oral gavage prior to the induction of DSS-colitis. (B) Final body weight relative to Day 0 (%). (C) DAI scores. (D) Colon lengths (mm). (E) Histopathology of the distal large intestine and the pathological score. Magnification, ×200. (F) Cytokine gene expression in colonic lamina propria mononuclear cells. Data were analyzed by (B and D) Tukey's test, (C) Dunnett T3 test and (E and F) Games-Howell test. *P<0.05 and **P<0.01, as indicated. DAI, disease activity index; DSS, dextran sulfate sodium; IL, interleukin; TNF-α, tumor necrosis factor α.
Figure 6.
Figure 6.
Effect of anti-IL-10 neutralizing antibody on LP 06CC2-treated colitis model mice. Mice were allocated into six groups: Group A is a control; Group B received only anti-IL-10 neutralizing antibody without DSS or 06CC2; Group C received DSS and PBS gavage; Group D received DSS and 06CC2 gavage but no intraperitoneal injection; Group E received DSS, 06CC2 gavage, and control IgG intraperitoneal injection; and Group F received DSS, 06CC2 gavage, and intraperitoneal injection of anti-IL-10 neutralizing antibody. (A) Experimental design. (B) Alterations in body weight. (C) Histopathology of the distal large intestine and the pathological score. Magnification, ×200. *P<0.01. DSS, dextran sulfate sodium; IL-10, interleukin 10.
Figure 7.
Figure 7.
Bacterial counts of Lactobacillus, Bifidobacterium, Bacteroides-Prevotella and Clostridium in feces of 06CC2-treated colitis model mice. Bifidobacterium, Bacteroides-Prevotella and Clostridium data were analyzed by Tukey's test. Lactobacillus data were analyzed by Dunnet T3 test. *P<0.05, **P<0.01 and ***P<0.001, as indicated. DSS, dextran sulfate sodium.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Khor B, Gardet A, Xavier RJ. Genetics and pathogenesis of inflammatory bowel disease. Nature. 2011;474:307–317. doi: 10.1038/nature10209. - DOI - PMC - PubMed
    1. Garrett WS, Lord GM, Punit S, Lugo-Villarino G, Mazmanian SK, Ito S, Glickman JN, Glimcher LH. Communicable ulcerative colitis induced by T-bet deficiency in the innate immune system. Cell. 2007;131:33–45. doi: 10.1016/j.cell.2007.08.017. - DOI - PMC - PubMed
    1. Elinav E, Strowig T, Kau AL, Henao-Mejia J, Thaiss CA, Booth CJ, Peaper DR, Bertin J, Eisenbarth SC, Gordon JI, Flavell RA. NLRP6 inflammasome regulates colonic microbial ecology and risk for colitis. Cell. 2011;145:745–757. doi: 10.1016/j.cell.2011.04.022. - DOI - PMC - PubMed
    1. Atarashi K, Tanoue T, Oshima K, Suda W, Nagano Y, Nishikawa H, Fukuda S, Saito T, Narushima S, Hase K, et al. Treg induction by a rationally selected mixture of clostridia strains from the human microbiota. Nature. 2013;500:232–236. doi: 10.1038/nature12331. - DOI - PubMed
    1. Atarashi K, Tanoue T, Shima T, Imaoka A, Kuwahara T, Momose Y, Cheng G, Yamasaki S, Saito T, Ohba Y, et al. Induction of colonic regulatory T cells by indigenous Clostridium species. Science. 2011;331:337–341. doi: 10.1126/science.1198469. - DOI - PMC - PubMed

MeSH terms