Suppressive Effects of Oral Administration of Heat-Killed &lt;i&gt;Lactobacillus acidophilus&lt;/i&gt; on T Helper-17 Immune Responses in a Bovine β-Lactoglobulin-Sensitized Mice Model

Li, Aili; Meng, Xiang-Chen; Duan, Cuicui; Gui-cheng, Huo; Zheng, Quan-ling; Li, Dan

doi:10.1248/bpb.b12-00437

Cited by 22 publications

(20 citation statements)

References 36 publications

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“…In an allergy murine model, L. acidophilus attenuated IL-6 and IL-17 serum levels and downregulated the expression of IL-17A and retinoic acid-related orphan receptor gamma t in the spleen. 29 Recently, oral administration of L. acidophilus was found to inhibit the expression of IL-17, TNF-a, and IL-23, as well as STAT3 and phosphorylated STAT3 in colon tissue in a DSS-induced colitis model. 20 With respect to Treg cells, treatment with L. acidophilus augmented the expansion of Treg cells in intestinal intraepithelial and lamina propria lymphocytes in a 2,4,6-trinitrobenzene sulfonic acid-induced colitis model.…”

Section: Discussionmentioning

confidence: 99%

Lactobacillus acidophilus Improves Intestinal Inflammation in an Acute Colitis Mouse Model by Regulation of Th17 and Treg Cell Balance and Fibrosis Development

Park

Choi

Jhun

et al. 2018

Journal of Medicinal Food

124

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Disruption of the balance among the microbiota, epithelial cells, and resident immune cells in the intestine is involved in the pathogenesis of inflammatory bowel disease (IBD). Probiotics exert protective effects against IBD, and probiotic commensal Lactobacillus species are common inhabitants of the natural microbiota, especially in the gut. To investigate the effects of Lactobacillus acidophilus on the development of IBD, L. acidophilus was administered orally in mice with dextran sodium sulfate (DSS)-induced colitis. DSS-induced damage and the therapeutic effect of L. acidophilus were investigated. Treatment with L. acidophilus attenuated the severity of DSS-induced colitis. Specifically, it suppressed proinflammatory cytokines such as interleukin (IL)-6, tumor necrosis factor-α, IL-1β, and IL-17 in the colon tissues, which are produced by T helper (Th) 17 cells. Moreover, in vitro L. acidophilus treatment directly induced T regulatory (Treg) cells and the production of IL-10, whereas the production of IL-17 was suppressed in splenocytes. In addition, we found that L. acidophilus treatment decreased the levels of α-smooth muscle actin, a marker of activated myofibroblasts, and type I collagen compared with control mice. These results suggest that L. acidophilus may be a novel treatment for IBD by modulating the balance between Th17 and Treg cells, as well as fibrosis development.

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Section: Discussionmentioning

confidence: 99%

Lactobacillus acidophilus Improves Intestinal Inflammation in an Acute Colitis Mouse Model by Regulation of Th17 and Treg Cell Balance and Fibrosis Development

Park

Choi

Jhun

et al. 2018

Journal of Medicinal Food

124

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“…We have previously demonstrated that oral administration of L. acidophilus KLDS 1.0738 had protective effects on β‐Lg–induced hypersensitivity, characterized by inhibition of IgE production, regulation of the imbalance in Th cell subsets, and induction of oral tolerance . Recent reports in animal models and in clinical trials confirmed that the immunoinhibitory effects of probiotics were dependent on improving the gut microflora composition and SCFA metabolism .…”

Section: Discussionmentioning

confidence: 99%

Modulatory effect of Lactobacillus acidophilus KLDS 1.0738 on intestinal short‐chain fatty acids metabolism and GPR41/43 expression in β‐lactoglobulin–sensitized mice

Wang

Zhang

et al. 2019

Microbiology and Immunology

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We investigated the correlation between the beneficial effect of Lactobacillus acidophilus on gut microbiota composition, metabolic activities, and reducing cow's milk protein allergy. Mice sensitized with β‐lactoglobulin (β‐Lg) were treated with different doses of L. acidophilus KLDS 1.0738 for 4 weeks, starting 1 week before allergen induction. The results showed that intake of L. acidophilus significantly suppressed the hypersensitivity responses, together with increased fecal microbiota diversity and short‐chain fatty acids (SCFAs) concentration (including propionate, butyrate, isobutyrate, and isovalerate) when compared with the allergic group. Moreover, treatment with L. acidophilus induced the expression of SCFAs receptors, G‐protein–coupled receptors 41 (GPR41) and 43 (GPR43), in the spleen and colon of the allergic mice. Further analysis revealed that the GPR41 and GPR43 messenger RNA expression both positively correlated with the serum concentrations of transforming growth factor‐β and IFN‐γ (p < .05), but negatively with the serum concentrations of IL‐17, IL‐4, and IL‐6 in the L. acidophilus–treated group compared with the allergic group (p < .05). These results suggested that L. acidophilus protected against the development of allergic inflammation by improving the intestinal flora, as well as upregulating SCFAs and their receptors GPR41/43.

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“…Recent studies indicated that application of lactobacilli could attenuate airway hyperreactivity by induction of Tregs in a mouse model of asthma (Jan et al 2012;Karimi et al 2009). We also showed Lactobacillus acidophilus strain KLDS 1.0738 had the ability to suppress the β-lg allergic symptoms and Th17 cytokine production (Li et al 2013). Moreover, some studies focused on the effect of probiotics on activating the cytokine-mediated STAT pathways to regulate the immune responses.…”

Section: Introductionmentioning

confidence: 83%

“…Subsequently, we observed that oral administration of L. acidophilus KLDS 1.0738 suppressed β-lg-induced inflammatory, including alleviating eosinophil inflammatory influx and the severe histologic features in the colons and lungs of the sensitized mice. It was previously shown that L. acidophilus treatment could increase the Treg-related cytokines and transcription factor production (IL-10, TGF-β1, Foxp3) but suppress the Th17-type levels (IL-17A, RORγt) (Li et al 2013). In this study, addition of L. acidophilus to β-lg-immunized mice could significantly upregulate the number of Treg cells and downregulate the number of Th17 cells compared with the allergy group (P < 0.05).…”

Section: Discussionmentioning

confidence: 99%

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Lactobacillus acidophilus regulates STAT3 and STAT5 signaling in bovine β-lg-sensitized mice model

Zhang

Sun

et al. 2016

Dairy Sci. & Technol.

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Our previous study has shown that oral supplementation with Lactobacillus acidophilus KLDS 1.0738 could inhibit β-lactoglobulin (β-lg) allergy. In this study, we investigated the effect of L. acidophilus on the balance between T helper type 17 (Th17) cells and regulatory T cells (Treg) in allergic mouse model and explored the participation of related signal transducers and activator of transcription (STAT) in this process. Bovine β-lg-sensitized mice received strains KLDS 1.0738 for 3 weeks. After the allergen challenge, the percentages of Treg and Th17 cells, cytokine and STAT mRNA expression, and pSTAT protein levels were detected by flow cytometry, quantitative RT-PCR, and western blot, respectively. The results showed that stimulation with β-lg increased the levels of IL-6, pSTAT3, and Th17 cells, but decreased the levels of IL-2, pSTAT5, and Treg cells compared to the controls (P < 0.05). However, oral administration of L. acidophilus KLDS 1.0738 suppressed β-lg-induced inflammatory and improved the Treg/Th17 imbalance. In addition, L. acidophilus-treated group presented decrease in pSTAT3 activation, SOCS3, and IL-6 level, but increase in STAT5a/b, CD25, and IL-2 mRNA expression. These findings suggest that L. acidophilus could regulate IL-6/STAT3 and IL-2/STAT5 pathway, which may be responsible for the Treg/Th17 imbalance in β-lg-sensitized mice.

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Suppressive Effects of Oral Administration of Heat-Killed <i>Lactobacillus acidophilus</i> on T Helper-17 Immune Responses in a Bovine β-Lactoglobulin-Sensitized Mice Model

Cited by 22 publications

References 36 publications

Lactobacillus acidophilus Improves Intestinal Inflammation in an Acute Colitis Mouse Model by Regulation of Th17 and Treg Cell Balance and Fibrosis Development

Lactobacillus acidophilus Improves Intestinal Inflammation in an Acute Colitis Mouse Model by Regulation of Th17 and Treg Cell Balance and Fibrosis Development

Modulatory effect of Lactobacillus acidophilus KLDS 1.0738 on intestinal short‐chain fatty acids metabolism and GPR41/43 expression in β‐lactoglobulin–sensitized mice

Lactobacillus acidophilus regulates STAT3 and STAT5 signaling in bovine β-lg-sensitized mice model

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