Supplemental Leuconostoc mesenteroides strain NTM048 attenuates imiquimod-induced psoriasis in mice

C Ogawa1, R Inoue2, Y Yonejima3

  • 1Graduate School of Integrated Sciences for Life, Hiroshima University, Higashi-Hiroshima, Japan.

Abstract

Insights

Leuconostoc mesenteroides NTM048 reduced psoriasis symptoms in mice by lowering interleukin-17. This probiotic may improve psoriasis through gut microbiota modulation and increased deoxycholic acid levels.

Area of Science:

  • Microbiology
  • Immunology
  • Dermatology

Background:

  • Psoriasis is a chronic inflammatory skin condition linked to gut microbiota dysbiosis.
  • Investigating microbial interventions for psoriasis is a growing area of research.

Purpose of the Study:

  • To evaluate the therapeutic potential of Leuconostoc mesenteroides NTM048 in a mouse model of imiquimod-induced psoriasis.
  • To elucidate the mechanisms underlying the anti-psoriatic effects of NTM048.

Main Methods:

  • Mice received NTM048 orally for 21 days with topical imiquimod application.
  • Psoriatic symptoms, skin cytokine levels, plasma bile acids, and fecal microbiota were analyzed.
  • In vitro assays assessed the effect of deoxycholic acid on IL-17 production.

Main Results:

  • NTM048 treatment alleviated psoriatic symptoms like erythema and scaling.
  • Interleukin-17 (IL-17) levels in the skin were downregulated by NTM048.
  • Plasma deoxycholic acid (DCA) increased, and fecal microbiota composition shifted, with increased Akkermansia and decreased Staphylococcus/Streptococcus.
  • DCA treatment reduced IL-17 production in murine splenocytes.

Conclusions:

  • Leuconostoc mesenteroides NTM048 demonstrates a therapeutic effect on psoriasis in mice.
  • The mechanism involves IL-17 downregulation, potentially mediated by DCA produced by altered gut microbiota.
  • This highlights a potential skin-gut axis interaction in psoriasis management.

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