The mammalian gastrointestinal tract harbors trillions of commensal microorganisms, collectively known as the microbiota. The microbiota is a critical source of environmental stimuli and, thus, has a tremendous impact on the health of the host. The microbes within the microbiota regulate homeostasis within the gut, and any alteration in their composition can lead to disorders that include inflammatory bowel disease, allergy, autoimmune disease, diabetes, mental disorders, and cancer. Hence, restoration of the gut flora following changes or imbalance is imperative for the host. The low-molecular-weight compounds and nutrients such as short-chain fatty acids, polyamines, polyphenols, and vitamins produced by microbial metabolism of nondigestible food components in the gut actively participate in various epigenomic mechanisms that reprogram the genome by altering the transcriptional machinery of a cell in response to environmental stimuli. These epigenetic modifications are caused by a set of highly dynamic enzymes, notably histone acetylases, deacetylases, DNA methylases, and demethylases, that are influenced by microbial metabolites and other environmental cues. Recent studies have shown that host expression of histone acetylases and histone deacetylases is important for regulating communication between the intestinal microbiota and the host cells. Histone acetylases and deacetylases influence the molecular expression of genes that affect not only physiological functions but also behavioral shifts that occur via neuroepigenetic modifications of genes. The underlying molecular mechanisms, however, have yet to be fully elucidated and thus provide a new area of research. The present review provides insights into the current understanding of the microbiota and its association with mammalian epigenomics as well as the interaction of pathogens and probiotics with host epigenetic machinery.

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It is reasonable to conclude that consumption of A1 "like" variants of β-casein induced inflammatory response in gut by activating Th2 pathway as compared to A2A2 variants. The present study thus supports the purported deleterious impacts of consumption of A1 "like" variants of β-casein and suggests possible aggravation of inflammatory response for etiology of various health disorders.

SummaryThe mechanism by which probiotic lactobacilli affect the immune system is strain specific. As the immune system is a multicompartmental system, each strain has its way to interact with it and induce a visible and quantifiable effect. This review summarizes the interplay existing between the host immune system and probiotic lactobacilli, that is, with emphasis on lactobacilli as a prototype probiotic genus. Several aspects including the bacterial-host crosstalk with the mucosal and systemic immune system are presented, as well as short sections on the competing effect towards pathogenic bacteria and their uses as delivery vehicle for antigens.

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Imbalance in Th1/Th2 immune pathways and cellular antioxidant systems with progressive aging are among the leading causes of increased risk of morbidity and mortality in elderly. Although probiotics have been considered to boost immune system, there is a lack of comprehensive analysis of probiotic effects on aging physiology. The present study aimed at determining anti-immunosenescence potential of milk fermented with probiotic Lactobacillus rhamnosus (LR) in 16 months old mice by concurrent analysis of immunosenescence markers associated with Th1/Th2 profile of splenocytes, inflamm-aging in plasma, neutrophil functions and antibody response in intestine along with analysis of antioxidant enzymes in liver and red blood cells (RBCs) after feeding trials of 1 and 2 months, respectively. An enteropathogenic Escherichia coli (ATCC 14948)-based infection model in aging mice was also designed to validate protective attributes of LR. Splenocytes registered increased IFN-γ and decreased IL-4 and IL-10 production in LR-fed animals. Neutrophil respiratory burst enzymes and phagocytosis increased significantly while no aggravation in plasma levels of MCP-1 and TNF-α was observed. Further, owing to increased Th1 response, antibodies registered a decrease in IgG1/IgG2a ratio and IgE levels in LR groups. No significant variations were observed in secretory IgA and IgA + cells in the intestine. Antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase) in LR-fed groups recorded increased activities which were more pronounced in the liver than in RBCs. LR supplementation significantly reduced E. coli translocation to organs (intestine, liver, spleen, peritoneal fluid) by enhancing E. coli-specific antibodies (IgA and IgG1) and inflammatory proteins. In conclusion, LR supplementation alleviated immunosenescence-associated Th1/Th2 imbalance, improved antioxidant capacity, and enhanced resistance of aged mice to E. coli infection thereby signifying its potential in augmenting healthy aging.

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