Lactobacillus sakei K17, an inducer of IL-10 expression in antigen-presenting cells, attenuates TNBS-induced colitis in mice

Abstract

To understand the anti-colitic effects of probiotics that up-regulate interleukin (IL)-10 expression in dendritic cells (DCs) and macrophages, we isolated Lactobacillus sakei K17, which potently induced IL-10 expression in DCs and peritoneal macrophages in vitro, among the lactic acid bacteria strains collected from kimchi and investigated its anti-inflammatory effect in mice with 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis. Oral administration of K17 (2 × 10 CFU·mouse·day) in mice with TNBS-induced colitis suppressed colon shortening and myeloperoxidase activity, as well as infiltration of CD86cells into the colon. Treatment with K17 also increased TNBS-suppressed expression of tight junction proteins and IL-10, but inhibited activation of nuclear factor-kappaB (NF-κB) and mitogen-activated protein kinases and expression of tumor necrosis factor α and IL-17. Its effect was comparable with that of sulfasalazine (50 mg/kg), a positive commercial ant-colitic drug. Furthermore, treatment with K17 (1 × 10 CFU/mL) potently inhibited lipopolysaccharide (LPS)-stimulated NF-κB activation in DCs and peritoneal macrophages and restored tight junction protein expression in LPS-stimulated Caco-2 cells. These findings suggest that Lactobacillus sakei K17 may ameliorate colitis by up-regulating the expression of IL-10 and tight junction proteins and inhibiting NF-κB activation.

Lactobacillus rhamnosus HN001 and Lactobacillus acidophilus La-14 Attenuate Gardnerella vaginalis-Infected Bacterial Vaginosis in Mice

“…These results suggest that the anti-BV effect of orally administered L1, L2, or PM may be due to its regulatory effects on immune responses through the gastrointestinal tract rather than completion with or killing of GV in the vagina. These was supported by the reports that probiotics exhibited anti-inflammatory effects by inhibiting innate immune response, such as macrophage activation, by regulating NF-κB signaling, or by regulating adaptive immune response, such as Th cell differentiation [28,29]. In the present study, we found that these probiotics significantly inhibited NF-κB activation and TNF-α expression in LPS-stimulated macrophages, inhibited the differentiation of splenocytes into Th17 cells, and induced their differentiation into Tregs [28,30].…”

Hydrogen peroxide production by lactobacilli promotes epithelial restitution during colitis

“…Physiological benefits linked to lactobacilli in the intestine include strengthening of epithelial junction complexes, elevating the antioxidant status, decreasing pro-inflammatory cytokines, increasing anti-inflammatory cytokine release, and modulating regulatory T cells and macrophages [46] , [47] , [48] , [49] , [50] , [51] , [52] , [53] , but the underlying molecular mechanisms conveying these benefits in gut inflammation remain unknown. The host-protective role of lactobacilli was apparent in mice with Nox1–4 inactivation in the intestinal epithelium, which overcompensated the loss of epithelial ROS by significantly increasing the abundance of lactobacilli throughout the intestine.…”

The Immunomodulatory Properties of Extracellular Vesicles Derived from Probiotics: A Novel Approach for the Management of Gastrointestinal Diseases

“…In this context, the administration of Lactobacillus sakei , a bacterium isolated from the traditional seed mash used for brewing sake, showed the capacity to ameliorate colon shortening and MPO activity, as well as the infiltration of antigen presenting cells (APC) into the colon in the TNBS-induced colitis model. The treatment also increased TNBS-suppressed expression of tight junction proteins and IL-10 and inhibited NF-κB and MAPKs activation as well as the expression of TNF-α and IL-17 [110]. Likewise, the immunostimulatory effect of L. sakei was also demonstrated in vitro in IFN-γ-primed RAW 264.7 murine macrophages.…”