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Protective effect of Lactobacillus reuteri DSM 17938 against experimental necrotizing enterocolitis is mediated by Toll-like receptor 2.

  • 2018-08-01
  • American Journal of Physiology-Gastrointestinal and Liver Physiology 315(2)
    • T. Hoang
    • Baokun He
    • Ting Wang
    • D. Tran
    • J. M. Rhoads
    • Yuying Liu

Abstract

Lactobacillus reuteri DSM 17938 (LR 17938) has been shown to reduce the incidence and severity of necrotizing enterocolitis (NEC). It is unclear if preventing NEC by LR 17938 is mediated by Toll-like receptor 2 (TLR2), which is known to mediate proinflammatory responses to bacterial cell wall components. NEC was induced in newborn TLR2-/- or wild-type (WT) mice by the combination of gavage-feeding cow milk-based formula and exposure to hypoxia and cold stress. Treatment groups were administered formula supplemented with LR 17938 or placebo (deMan-Rogosa-Sharpe media). We observed that LR 17938 significantly reduced the incidence of NEC and reduced the percentage of activated effector CD4+T cells, while increasing Foxp3+ regulatory T cells in the intestinal mucosa of WT mice with NEC, but not in TLR2-/- mice. Dendritic cell (DC) activation by LR 17938 was mediated by TLR2. The percentage of tolerogenic DC in the intestine of WT mice was increased by LR 17938 treatment during NEC, a finding not observed in TLR2-/- mice. Furthermore, gut levels of proinflammatory cytokines IL-1β and IFN-γ were decreased after treatment with LR 17938 in WT mice but not in TLR2-/- mice. In conclusion, the combined in vivo and in vitro findings suggest that TLR2 receptors are involved in DC recognition and DC-priming of T cells to protect against NEC after oral administration of LR 17938. Our studies further clarify a major mechanism of probiotic LR 17938 action in preventing NEC by showing that neonatal immune modulation of LR 17938 is mediated by a mechanism requiring TLR2. NEW & NOTEWORTHY Lactobacillus reuteri DSM 17938 (LR 17938) has been shown to protect against necrotizing enterocolitis (NEC) in neonates and in neonatal animal models. The role of Toll-like receptor 2 (TLR2) as a sensor for gram-positive probiotics, activating downstream anti-inflammatory responses is unclear. Our current studies examined TLR2 -/- mice subjected to experimental NEC and demonstrated that the anti-inflammatory effects of LR 17938 are mediated via a mechanism requiring TLR2.

Keywords: Inflammation; Toll-like receptor; intestinal mucosa; lactobacillus; necrotizing enterocolitis.

Research Insights

SupplementHealth OutcomeEffect TypeEffect Size
Lactobacillus reuteri DSM 17938Increased Regulatory T Cell CountBeneficial
Moderate
Lactobacillus reuteri DSM 17938Increased Tolerogenic Dendritic CellsBeneficial
Moderate
Lactobacillus reuteri DSM 17938Reduced Activated Effector CD4+ T Cells PercentageBeneficial
Moderate
Lactobacillus reuteri LRE02Increased Tolerogenic Dendritic CellsBeneficial
Moderate
Lactobacillus reuteri LRE02Reduced Occurrence of Necrotizing EnterocolitisBeneficial
Large
Lactobacillus reuteri LRE02Reduced Pro-Inflammatory CytokinesBeneficial
Moderate
Lactobacillus reuteri MAK02L14RIncreased Tolerogenic Dendritic CellsBeneficial
Moderate
Lactobacillus reuteri MAK02L14RReduced Pro-Inflammatory CytokinesBeneficial
Moderate
Lactobacillus reuteri OsfortisIncreased Regulatory T Cells in Intestinal MucosaBeneficial
Moderate
Lactobacillus reuteri OsfortisIncreased Tolerogenic Dendritic Cells in the IntestineBeneficial
Moderate
Lactobacillus reuteri OsfortisReduced Activated Effector CD4+ T Cells PercentageBeneficial
Moderate
Lactobacillus reuteri UALg-05Increased Regulatory T-CellsBeneficial
Moderate
Lactobacillus reuteri UALg-05Increased Tolerogenic Dendritic CellsBeneficial
Moderate
Lactobacillus reuteri UALg-05Reduced Pro-Inflammatory CytokinesBeneficial
Moderate
Lactobacillus reuteri UALg-05Reduced Risk of Necrotizing EnterocolitisBeneficial
Large
Lactobacillus reuteri UALre-16Increased Tolerogenic Dendritic CellsBeneficial
Moderate
Lactobacillus reuteri UALre-16Reduced Pro-inflammatory Cytokine LevelsBeneficial
Large
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