Microbial Ecology, Human Evolution, Immune System and Inflammation These include allergy, certain autoimmune diseases such as Celiac Disease (CeD), Inflammatory Bowel Disease (IBD), Irritable Bowel Syndrome (IBS), obesity and autism spectrum disorders (ASDs), which often tend to share similar environmental risk factors ( 1) and genetic risk alleles ( 2). The health status in our industrialized population is endangered by a plethora of ICD characterized by a widespread and latent low-grade inflammation. The inability of the body to eliminate an inflammation-inducing agent is the cause of a pro-inflammatory state that can spread all over the body. Chronic inflammation follows the failure of the immune system to shut down its reaction to a real or alleged attack. This is, in part, the cause of many inflammatory chronic diseases (ICDs) and poses a significant threat to human health and longevity. Chronic inflammation occurs at varying degrees with advanced age in all mammals, regardless of infection and progresses gradually. An excess of inflammation and the inability to stop this system can do more harm than good. We developed as a species because of our capacity to eliminate dangerous microbial species, but the survival tactics used by our immune system, that was necessary at a time when there were no antibiotics or drainage systems, turned against us. The hypothesis is that, if we think of inflammation from an evolutionary point of view, we are now the victims of our own success. On 23 February 2004, Time Magazine dedicated the cover to chronic inflammation with a provocative title: The Secret Killer. Furthermore, a decrease in gut dysbiosis and intestinal leakage after probiotic therapy may minimize the development of inflammatory biomarkers and blunt unnecessary activation of the immune system. In turn, probiotics improve the differentiation of T-cells against Th2 and development of Th2 cytokines such as IL-4 and IL-10. The present narrative review explores the interactions between gut microflora/probiotics and the immune system starting from the general perspective of a biological plausibility to get to the in vitro and in vivo demonstrations of a probiotic-based approach up to the possible uses for novel therapeutic strategies. When LPS binds endothelial cells to toll-like receptors (TLR 2, 4), dendritic cells and macrophage cells are activated, and inflammatory markers are increased. In addition to host gut functions (permeability and physiology), all these agents have profound implications for the gut microbiome composition. The use of probiotics could improve the gut microbial population, increase mucus-secretion, and prevent the destruction of tight junction proteins by decreasing the number of lipopolysaccharides (LPSs). Diet, age, BMI (body mass index), medications, and stress may confound the benefits of probiotic intake. Changes in gut microbiota can occur through modification in function, composition (dysbiosis), or microbiota–host interplays. Studies on animals and humans show that probiotics can have a pivotal effect on the modulation of immune and inflammatory mechanisms however, the precise mechanisms have not yet been well defined. This microbial community regulates some of the host’s metabolic and physiological functions and drives early-life immune system maturation, contributing to their homeostasis throughout life. A field of great interest is the association of either microbiota or probiotics with the immune system concerning clinical uses. On the other hand, to maintain host immune homeostasis, the intestinal microflora often exerts an immunoregulatory function that cannot be ignored. Therefore, the immune system has evolved to sustain the host–microbiota symbiotic relationship. On one side, in cases of opportunistic invasion, the abundant bacterial population inside intestinal tissues may face potential health problems such as inflammation and infections. Hosting millions of microorganisms, the digestive tract is the primary and most important part of bacterial colonization.
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