Lactobacillus rhamnosus HDB1258 modulates gut microbiota-mediated immune response in mice with or without lipopolysaccharide-induced systemic inflammation

Abstract

Background Gut microbiota closely communicate in the immune system to maintain a balanced immune homeostasis in the gastrointestinal tract of the host. Oral administration of probiotics modulates gut microbiota composition. In the present study, we isolated Lactobacillus rhamnosus HDB1258, which induced tumor necrosis factor (TNF)-α and interleukin (IL)-10 expression in macrophages, from the feces of breastfeeding infants and examined how HDB1258 could regulate the homeostatic immune response in mice with or without lipopolysaccharide (LPS)-induced systemic inflammation. Results Oral administration of HDB1258 significantly increased splenic NK cell cytotoxicity, peritoneal macrophage phagocytosis, splenic and colonic TNF-α expression, TNF-α to IL-10 expression ratio, and fecal IgA level in control mice, while Th1 and Treg cell differentiation was not affected in the spleen. However, HDB1258 treatment significantly suppressed peritoneal macrophage phagocytosis and blood prostaglandin E2 level in mice with LPS-induced systemic inflammation. Its treatment increased LPS-suppressed ratios of Treg to Th1 cell population, Foxp3 to T-bet expression, and IL-10 to TNF-α expression. Oral administration of HDB1258 significantly decreased LPS-induced colon shortening, myeloperoxidase activity and NF-κB+/CD11c+ cell population in the colon, while the ratio of IL-10 to TNF-α expression increased. Moreover, HDB1258 treatment shifted gut microbiota composition in mice with and without LPS-induced systemic inflammation: it increased the Cyanobacteria and PAC000664_g (belonging to Bacteroidetes) populations and reduced Deferribacteres and EU622763_s group (belonging to Bacteroidetes) populations. In particular, PAC001066_g and PAC001072_s populations were negatively correlated with the ratio of IL-10 to TNF-α expression in the colon, while the PAC001070_s group population was positively correlated. Conclusions Oral administered HDB1258 may enhance the immune response by activating innate immunity including to macrophage phagocytosis and NK cell cytotoxicity in the healthy host and suppress systemic inflammation in the host with inflammation by the modulation of gut microbiota and IL-10 to TNF-α expression ratio in immune cells.

Lactobacillus rhamnosus and Bifidobacterium longum alleviate colitis and cognitive impairment in mice by regulating IFN-γ to IL-10 and TNF-α to IL-10 expression ratios

“…Macrophages (1 × 10 6 cell/well) were incubated with Candida albicans (1 × 10 4 CFU/well) in the 24-well microplates with RPMI 1640 medium for 24 h. Cultured supernatant (0.2 mL) was cultured in SDA plates for 24 h at 30°C 43 . The phagocytic activity (%) was indicated as [1-(the number of Candida albicans colonies grown in SDA per the number of Candida albicans initially incubated with macrophages)] × 100.…”

“…NK cells were isolated from splenocytes prepared from the spleen of mice using a NK cell isolation kit and suspended in RFA, as described previously 43 . NK cell cytotoxicity was assayed by measuring the cytotoxicity against YAC-1 cells labeled with a Vybrant CFDA SE Cell Tracer kit according to the manufacturer’s protocol.…”

Gut Dysbiosis during COVID-19 and Potential Effect of Probiotics

“…Fecal levels of IL-8 and IL-23 and intestinal specific IgA responses were vastly associated with severe COVID-19 disease, which indicated the co-existence of systemic and local intestine inflammation in critically ill patients [ 38 ]. One of the commercial probiotics, Lactobacillus rhamnosus HDB1258, might be effective in treating COVID-19 by modulating both microbiota-mediated immunity in gut and systemic inflammation induced by lipopolysaccharide [ 39 ]. Accordingly, concomitant targeting on local and systemic inflammatory responses by probiotics is reasonably believed to be valuable to counteract COVID-19-related gut and systemic inflammation.…”

2′‐Fucosyllactose promotes Lactobacillus rhamnosus KLDS 8001 to repair LPS‐induced damage in Caco‐2 cells

“…As reported by Han et al., oral administration of L . rhamnosus HDB1258 alleviated LPS‐induced reduction in myeloperoxidase activity and weak expression of NF‐κB signaling in rats (Han et al., 2021). He et al discovered that 2′‐FL could diminish LPS‐induced inflammation by inhibiting Toll‐like receptor 4 expression by lowering CD14 transcription and translation (He et al., 2016).…”