Abstract
IgA-coated Lactobacillus live in the mucous layer of the human or mammalian intestine in close proximity to epithelial cells. They act as potential probiotics for functional food development, but their physiological regulation has not yet been studied. We isolated IgA-targeted (Lactobacillus jensenii IgA21) and lumen lactic acid bacterial strains (Pediococcus acidilactici FS1) from the fecal microbiota of a healthy woman. C57BL/6 mice were fed a normal (CON) or high fat diet (HFD) for 6 weeks and then treated with IgA21 or FS1 for 4 weeks. HFD caused dyslipidemia, mucosal barrier damage, and intestinal microbiota abnormalities. Only IgA21 significantly inhibited dyslipidemia and gut barrier damage. This was related to significant up-regulation of mucin-2, PIgR mRNA expression, and colonic butyrate production (P < 0.05 vs. HFD). Unlike IgA21, FS1 caused a more pronounced gut dybiosis than did HFD, and, in particular, it induced a significant decrease in the Bacteroidales S24-7 group and an increase in Desulfovibrionaceae (P < 0.05 vs. CON). In conclusion, IgA-coated and non-coated lactic acid bacteria of gut have been demonstrated to differentially affect the intestinal barrier and serum lipids. This indicates that IgA-bound bacteria possess the potential to more easily interact with the host gut to regulate homeostasis.
Highlights
The availability of inexpensive, processed fatty foods promotes the spread of obesity worldwide, which is one of the greatest risk factors for the development of metabolic diseases (Ford et al, 2017)
Typical subgroup bacteria were cultured with Man Rogosa Sharpe (MRS) medium and gut microbiota medium (GMM) according to Venn diagrams comparing the operational taxonomic unit (OTU) memberships (Supplementary Figure S1a)
The MRS-enriched IgA-coated microbiota, was clearly different, and it was composed of Bifidobacterium, Escherichia, and Lactobacillus
Summary
The availability of inexpensive, processed fatty foods promotes the spread of obesity worldwide, which is one of the greatest risk factors for the development of metabolic diseases (Ford et al, 2017). Disruption of homeostasis in the gut microbiota is causally linked to the development of host metabolic diseases, including obesity (Rajani and Jia, 2018). Modest elevations in fasting serum endotoxins can be induced in lean mice that consume a high-fat diet (HFD) (Cani et al, 2007). This results in unfavorable alterations in the gut microbial composition, leading to increased intestinal permeability (Cani et al, 2009). The effect of Lactobacillus on HFD-induced obesity, is strain-dependent (Qiao et al, 2015), indicating that the interaction between bacteria and their hosts is very complex, highlighting the necessity to understand its mechanism of action to properly screen strains. There is a need to establish a targeted screening method for the protection of host mucosal barriers
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