Cross-Talk Between the Intestinal Epithelium and Salmonella Typhimurium

Abstract

Salmonella enterica serovars are invasive gram-negative bacteria, causing a wide range of diseases from gastroenteritis to typhoid fever, representing a public health threat around the world. Salmonella gains access to the intestinal lumen after oral ingestion of contaminated food or water. The crucial initial step to establish infection is the interaction with the intestinal epithelium. Human-adapted serovars such as S. Typhi or S. Paratyphi disseminate to systemic organs and induce life-threatening disease known as typhoid fever, whereas broad-host serovars such as S. Typhimurium usually are limited to the intestine and responsible for gastroenteritis in humans. To overcome intestinal epithelial barrier, Salmonella developed mechanisms to induce cellular invasion, intracellular replication and to face host defence mechanisms. Depending on the serovar and the respective host organism, disease symptoms differ and are linked to the ability of the bacteria to manipulate the epithelial barrier for its own profit and cross the intestinal epithelium.This review will focus on S. Typhimurium (STm). To better understand STm pathogenesis, it is crucial to characterize the crosstalk between STm and the intestinal epithelium and decipher the mechanisms and epithelial cell types involved. Thus, the purpose of this review is to summarize our current knowledge on the molecular dialogue between STm and the various cell types constituting the intestinal epithelium with a focus on the mechanisms developed by STm to cross the intestinal epithelium and access to subepithelial or systemic sites and survive host defense mechanisms.

Research Note: Xylooligosaccharide directly attenuates Salmonella Typhimurium colonization and its induction of impairments in intestinal barrier and growth performance of broilers

“…Salmonella colonization of the intestine contributes to its invasion and damage to host intestinal mucosa that separates internal organs from intestinal lumen ( Menard et al, 2022 ). As an essential constituent of intestinal mucosal barriers, intraepithelial tight junctions are comprised of diversified proteins that sustain intestinal integrity against paracellular penetration and enteric pathogen invasion ( Menard et al, 2022 ). To date, few study was available regarding the protective effect of XOS on intestinal barrier in animals.…”

“…These results corresponded to the observed mitigating effects of XOS addition on ileal colonization of S. Typhimurium and its translocation to extra-intestinal organs (liver and spleen) of broilers. Because the loss of intestinal integrity resulting from S. Typhimurium challenge is associated with intestinal inflammation ( Menard et al, 2022 ), intestinal inflammatory cytokine expression profile was then determined in this study. The results showed that supplementing XOS to challenged broilers did not ( P > 0.05) reverse the upregulations ( P < 0.05) of ileal IL-1 β and IL-8 ( Figure 1 F), but elevated ( P < 0.05) ileal TNF- α expression that remained unchanged following challenge.…”

“…Strikingly, this study uncovered some differences in the results of intestinal inflammation and intestinal integrity between in vitro and in vivo experiments. These implied a complexity of the interplay between S. Typhimurium invasion and intestinal gene responses of hosts ( Menard et al, 2022 ), which might depend on the time-points postinfection and gut microbial actions.…”

Astragalus polysaccharide: implication for intestinal barrier, anti-inflammation, and animal production

“…Enterocytes account for >80% of epithelial cells are specialized to absorb and export luminal nutrients ( 48 ). Goblet cells secrete mucins to protect mucous membranes, enteroendocrine cells secrete peptide hormones and Paneth cells produce a number of antimicrobial peptides ( 49 , 50 ). Additionally, intercellular junctional complexes including tight junctions (TJ), adherens junctions, gap junctions, and desmosomes provide contact or tightly bound between neighboring cells and play a critical role in the regulation of paracellular permeability and epithelial barrier integrity ( 42 , 51 ).…”

Plant-Derived Phenolic Acids Limit the Pathogenesis of Salmonella Typhimurium and Protect Intestinal Epithelial Cells during Their Interactions

“…The capability to adhere to and later invade multiple cell types within the gastrointestinal (GI) tract of a human host, especially intestinal epithelial cells, is an important virulence factor of ST that creates further challenges for effective treatments [ 20 ]. These virulence factors serve as a survival mechanism that allows the bacteria to avoid natural shedding by the host, as well as neutralization by the immune system, while also allowing the pathogen to proliferate intracellularly and potentially spread systemically if it reaches deeper layers of tissues [ 21 ].…”