Mucus-Pathogen Interactions in the Gastrointestinal Tract of Farmed Animals

Abstract

Gastrointestinal infections cause significant challenges and economic losses in animal husbandry. As pathogens becoming resistant to antibiotics are a growing concern worldwide, alternative strategies to treat infections in farmed animals are necessary in order to decrease the risk to human health and increase animal health and productivity. Mucosal surfaces are the most common route used by pathogens to enter the body. The mucosal surface that lines the gastrointestinal tract is covered by a continuously secreted mucus layer that protects the epithelial surface. The mucus layer is the first barrier the pathogen must overcome for successful colonization, and is mainly composed of densely glycosylated proteins called mucins. The vast array of carbohydrate structures present on the mucins provide an important setting for host-pathogen interactions. This review summarizes the current knowledge on gastrointestinal mucins and their role during infections in farmed animals. We examine the interactions between mucins and animal pathogens, with a focus on how pathogenic bacteria can modify the mucin environment in the gut, and how this in turn affects pathogen adhesion and growth. Finally, we discuss analytical challenges and complexities of the mucus-based defense, as well as its potential to control infections in farmed animals.

Identification of Microbial Genetic Capacities and Potential Mechanisms Within the Rumen Microbiome Explaining Differences in Beef Cattle Feed Efficiency

“…To the best of our knowledge, this is one of the first times that Lawsonia known to be an obligate intracellular enteric pathogen in several animals including pig and horse (Vannucci and Gebhart, 2014) is reported in beef cattle. This genus seems to have developed a mechanism avoiding the host immune system by the production of sialic acid which is one of the main compounds constituting the mucus covering the intestine (Severi et al, 2007;Quintana-Hayashi et al, 2018). Similar mechanisms these genera may use to avoid the host immune system of the epithelia cells in the rumen.…”

Helicobacter suis infection alters glycosylation and decreases the pathogen growth inhibiting effect and binding avidity of gastric mucins

“…The main components of the mucus layer are the densely glycosylated mucin glycoproteins. 14,15 In the healthy human stomach, MUC5AC and MUC6 are the main secreted mucins, but during disease, MUC2 and MUC5B can also appear. 16,17 Proteomic analysis of mucins from healthy pigs identified predominantly MUC5AC, but MUC6 and MUC5B might also be members of the pig gastric mucin repertoire.…”

Do acute hepatopancreatic necrosis disease-causing PirAB VP toxins aggravate vibriosis?

“…These observations point in the direction of additive effects for strains that are virulent (wild type or strains in which quorum sensing gene deletions do not affect virulence), synergistic effects for strains with an attenuated (intermediate) virulence (MM30) and no affect for avirulent strains like the triple QS mutant. It is possible that the PirAB VP toxins, known to destroy epithelial cells in the Artemia gut [21,22,46,[65][66][67][68][69], facilitate the entry of MM30 strain, making epithelial cells a barrier to infection for MM30 cells. Additionally, the PirAB VP toxin supplementation also synergistically increases the in vivo virulence of V. alginolyticus AQ13-91 strain (wild type), an intermediate virulent strain.…”