Salmonella Typhimurium and Multidirectional Communication in the Gut

Abstract

The mammalian digestive tract is home to trillions of microbes, including bacteria, archaea, protozoa, fungi, and viruses. In monogastric mammals the stomach and small intestine harbor diverse bacterial populations but are typically less populated than the colon. The gut bacterial community (microbiota hereafter) varies widely among different host species and individuals within a species. It is influenced by season of the year, age of the host, stress and disease. Ideally, the host and microbiota benefit each other. The host provides nutrients to the microbiota and the microbiota assists the host with digestion and nutrient metabolism. The resident microbiota competes with pathogens for space and nutrients and, through this competition, protects the host in a phenomenon called colonization resistance. The microbiota participates in development of the host immune system, particularly regulation of autoimmunity and mucosal immune response. The microbiota also shapes gut–brain communication and host responses to stress; and, indeed, the microbiota is a newly recognized endocrine organ within mammalian hosts. Salmonella enterica serovar Typhimurium (S. Typhimurium hereafter) is a food-borne pathogen which adapts to and alters the gastrointestinal (GI) environment. In the GI tract, S. Typhimurium competes with the microbiota for nutrients and overcomes colonization resistance to establish infection. To do this, S. Typhimurium uses multiple defense mechanisms to resist environmental stressors, like the acidic pH of the stomach, and virulence mechanisms which allow it to invade the intestinal epithelium and disseminate throughout the host. To coordinate gene expression and disrupt signaling within the microbiota and between host and microbiota, S. Typhimurium employs its own chemical signaling and may regulate host hormone metabolism. This review will discuss the multidirectional interaction between S. Typhimurium, host and microbiota as well as mechanisms that allow S. Typhimurium to succeed in the gut.

Pathogenicity island excision during an infection by Salmonella enterica serovar Enteritidis is required for crossing the intestinal epithelial barrier in mice to cause systemic infection

“…Notably, the main mechanism used by Salmonella to adapt to environmental conditions during the initial passage through the host gut are encoded in the core genome, which acts independent of the genes acquired by HGT, including the virulence genes encoded in SPIs. These regulatory systems encoded within these SPIs comprise, among others, the activation of ATR systems [41][42][43], systems related to survival under limitation of nutrient step [44,45], tolerance to hyperosmolarity and anaerobic environments [46][47][48], as well as quorum sensing [49]. Although initially these systems are responsible for the adaptation to the adverse intestinal environment of the host, some of them (such as the two-component systems PhoPQ and PmrAB, or the OmpR protein) are also responsible for the activation of genes encoded within the pathogenicity islands and other HGT elements, to ensure the passage through the intestinal barrier [50][51][52].…”

Loving the poison: the methylcitrate cycle and bacterial pathogenesis

“…Moving to a whole-animal infection model (pigs), supplementation of the diet with a mixture of organic acids including propionate resulted in decreased Salmonella recovery from the mesenteric lymph nodes [64]. Thus, simple dietary supplementation with SCFAs, especially propionate, may be a promising intervention strategy for decreasing Salmonella infection in farm animals [65]. Interestingly, it has also been suggested that the production of propionate by intestinal microflora may be a protective mechanism to control the host response to commensals.…”

Peer Review #2 of "Organic acids and 2,4-Di-tert-butylphenol: major compounds of Weissella confusa WM36 cell-free supernatant against growth, survival and virulence of Salmonella Typhi (v0.2)"

“…In addition, the QseB regulator of the host's normal flora is also recognized for epinephrine, norepinephrine and neurotransmitter. This system induces the SPI-2 gene expression to support Salmonella survival in macrophage, as well as facilitates the expression of gene encoded on SPI-1 and SPI-3 (Bearson & Bearson, 2008;Gart et al, 2016;Morei, Weinshenker & Sperandio, 2010) In this present work, the sdiA and luxS only, were chosen for the QS genes by interfering with the expression of these genes with CFCS. They have clear known signaling pathways, and are associated with the critical induction of SPI genes.…”