<i>Lactobacillus acidophilus</i>Suppresses Colitis-Associated Activation of the IL-23/Th17 Axis

Chen, Lin Lin; Zou, Yiyou; Peng, Jie; Lu, Fanggen; Yin, Yani; Li, Fujun; Yang, Junwen

doi:10.1155/2015/909514

Cited by 100 publications

(86 citation statements)

References 34 publications

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“…Additionally, the study showed that IL‐17‐driven inflammatory reaction led to bacterial clearance . None of the examined LAB strains induced this cytokine in our experimental system confirming that commensal LAB strains are rather poor IL‐17 inducers . Enhancement of Th1 response by Lr (low Treg population, low level of IL‐10, and high concentrations of IL‐12p70 and IFN‐γ) may promote the elimination of potentially pathogenic bacteria, such as Hp .…”

Section: Discussionsupporting

confidence: 55%

“…48 None of the examined LAB strains induced this cytokine in our experimental system confirming that commensal LAB strains are rather poor IL-17 inducers. 63,64 Enhancement of Th1 response by Lr (low Treg population, low level of IL-10, and high concentrations of IL-12p70 and IFN-γ) may promote the elimination of potentially pathogenic bacteria, such as Hp. 55 This is important because Hp counts in the individuals with symptomatic inflammation were shown to be higher than in the asymptomatic carriers.…”

Section: Discussionmentioning

confidence: 99%

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Selected commensal bacteria change profiles of Helicobacter pylori‐induced T cells via dendritic cell modulation

et al. 2019

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Background The mechanisms of downregulation of protective immunity against Helicobacter pylori (Hp) infection strongly depend on dendritic cell (DC)‐induced T‐lymphocyte differentiation pattern. Lactic acid bacteria (LAB) strains can modulate Hp‐induced immunoresponse by changes in DC activation profiles. Here, we want to find out if the LAB‐pulsed DCs will change Hp‐induced T‐cell responsiveness patterns. Materials and Methods The naive peripheral CD4+ T cells were co‐cultured with Hp CagA + pulsed monocyte‐derived DCs (DC/CD4+ T cell) in the presence/absence of the feces‐derived probiotics: antagonistic or non‐antagonistic to Hp (Lactobacillus rhamnosus 900, Lr, Lactobacillus paracasei 915, Lp, respectively), as assessed by the agar slab method. The regulatory T‐cell (Treg) population was assessed by flow cytometry, and IFN‐γ, IL‐12p70, IL‐10, and IL‐17A levels were evaluated by ELISA method. Results The Hp‐pulsed DC/CD4+ T‐cell co‐cultures were characterized by high IL‐10, decreased IL‐12p70 and IFN‐γ levels, and elevated Treg population. In contrast, Lr‐pulsed DC/CD4+ T‐cell co‐cultures expressed low IL‐10, high IL‐12p70 and IFN‐γ levels and declined Treg population; this responsiveness pattern was not changed by Hp. The responsiveness pattern of the Lp/Hp‐pulsed DC/CD4+ T‐cell co‐cultures did not differ from those pulsed with Hp alone. Conclusion In contrast to Lp, Lr probiotic strain overcomes Hp‐mediated immune profile in the DC/T‐cell co‐cultures toward Th1 pattern and limited generation of Tregs in vitro. Lr may therefore be used as a component of anti‐Hp treatment.

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Section: Discussionsupporting

confidence: 55%

Section: Discussionmentioning

confidence: 99%

Selected commensal bacteria change profiles of Helicobacter pylori‐induced T cells via dendritic cell modulation

et al. 2019

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“…Numerous probiotics have been found to downregulate IL-17 production and alleviate colitis, including B. breve (317), B. longum (318), L. acidophilus (319), B. longum subsp. infantis (304), and Streptococcus thermophilus ST28 (320).…”

Section: Protective Mechanisms Of Probiotics Against Ulcerative Colitismentioning

confidence: 99%

Gleaning Insights from Fecal Microbiota Transplantation and Probiotic Studies for the Rational Design of Combination Microbial Therapies

et al. 2017

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SUMMARY Beneficial microorganisms hold promise for the treatment of numerous gastrointestinal diseases. The transfer of whole microbiota via fecal transplantation has already been shown to ameliorate the severity of diseases such as Clostridium difficile infection, inflammatory bowel disease, and others. However, the exact mechanisms of fecal microbiota transplant efficacy and the particular strains conferring this benefit are still unclear. Rationally designed combinations of microbial preparations may enable more efficient and effective treatment approaches tailored to particular diseases. Here we use an infectious disease, C. difficile infection, and an inflammatory disorder, the inflammatory bowel disease ulcerative colitis, as examples to facilitate the discussion of how microbial therapy might be rationally designed for specific gastrointestinal diseases. Fecal microbiota transplantation has already shown some efficacy in the treatment of both these disorders; detailed comparisons of studies evaluating commensal and probiotic organisms in the context of these disparate gastrointestinal diseases may shed light on potential protective mechanisms and elucidate how future microbial therapies can be tailored to particular diseases.

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“…[3][4][5] Evidence for the role of the gut microbiome in psoriasis has been suggested by Zakostelska et al, 6 who have shown that exposure of mice to antibiotics inhibited psoriasis induction. The mice were characterized by an increase in fecal Lactobacilles, which suppress the interleukin-23-T-helper 17 axis, 7 implicated in psoriatic disease pathogenesis. 8 Others have shown that neonatal treatment of mice with vancomycin and polymyxin led to dysregulation of the gut and skin microbiota in adulthood, as manifested by exacerbated imiquimod-induced psoriasis.…”

Section: Introductionmentioning

confidence: 99%

Psoriatic patients have a distinct structural and functional fecal microbiota compared with controls

Shapiro

Cohen

Shalev

et al. 2019

The Journal of Dermatology

124

149

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Alterations in the gut microbiome have been implicated in the pathogenesis of several immune‐mediated inflammatory diseases such as psoriatic arthritis. This work aimed to characterize the gut microbial signature of patients with active psoriasis as compared with age‐, body mass index‐ and comorbidity‐matched non‐psoriatic controls and to correlate them with differential expression of metabolic pathways. Fecal samples were processed and 16S rRNA was sequenced. PICRUSt was used to perform an analysis of metabolic pathways. Of the 46 participants, 52% (n = 24) suffered from psoriasis. There was a significant difference in β‐diversity between the two groups. Psoriatic patients had a significant increase in the Firmicutes and Actinobacteria phyla as compared with matched controls. At the genus level, psoriatic patients had a unique bacterial composition. At the species level, the psoriatic patients showed significant increases in the relative proportions of (false discovery rate, <0.05) in Ruminoccocus gnavus, Dorea formicigenerans and Collinsella aerofaciens, while Prevotella copri and Parabacteroides distasonis were significantly decreased as compared with controls. PICRUSt analysis revealed increases in metabolic pathways related to lipopolysaccharide function in the psoriatic cohort. These data demonstrate unique fecal microbial and metabolic signatures in psoriatic patients.

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Lactobacillus acidophilusSuppresses Colitis-Associated Activation of the IL-23/Th17 Axis

Cited by 100 publications

References 34 publications

Selected commensal bacteria change profiles of Helicobacter pylori‐induced T cells via dendritic cell modulation

Selected commensal bacteria change profiles of Helicobacter pylori‐induced T cells via dendritic cell modulation

Gleaning Insights from Fecal Microbiota Transplantation and Probiotic Studies for the Rational Design of Combination Microbial Therapies

Psoriatic patients have a distinct structural and functional fecal microbiota compared with controls

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