![]() ![]() ![]() The secreted products of goblet cells play an important role in innate immunity during intestinal infections. Goblet cells are a specific type of secretory cell that synthesizes and secretes various factors, trefoil peptides and mucins, which together form an intestinal mucus layer to protect intestinal epithelial cells. Goblet cells differentiate from pluripotent stem cells whose origin is the base of the intestinal crypt. The intestinal mucosal surface is covered by a hydrated gel formed by mucins, which create a barrier that prevents large particles (mostly bacteria) from directly contacting the epithelial cell layer. ![]() Tight junction proteins limit intestinal epithelial cell permeability and protect mucosal cells from being exposed to bacteria and toxic macromolecules. Tight junction proteins commonly include zonula occludens (ZO), occludin and the claudin family proteins. ![]() Tight junctions are multiprotein complexes composed of transmembrane proteins and peripheral membrane proteins. Epithelial cells and their tight junctions create a barrier between the external environment and the host. Impaired intestinal function caused by pathogens will lead to obstructed nutritional absorption, low immunity, and reduced growth performance of pigs, causing severe economic losses to the pig industry. The intestinal mucosal barrier plays an important role as the first barrier against pathogens in defending against harmful external factors and maintaining intestinal health. PRRSV infection reduces villus height in the cranial, medial, and caudal segments of the small intestine. PRRSV coinfection with pig epidemic diarrhoea virus (PEDV) not only impairs intestinal morphology but also decreases intestinal barrier integrity in growing pigs. The major clinical characteristics of PRRS include respiratory disorders and reproductive failure, usually accompanied by gastroenteritis-like symptoms, such as diarrhoea and haematochezia. Porcine reproductive and respiratory syndrome (PRRS) is a major immunosuppressive disease caused by porcine reproductive and respiratory syndrome virus (PRRSV) that threatens the pig industry worldwide. This study also provides a new hypothesis regarding the pathogenesis of PRRSV-induced diarrhoea. PRRSV infection impaired intestinal integrity by damaging physical and immune barriers in the intestine by inducing inflammation, which may be related to the regulation of the gut-lung axis. PRRSV infection aggravated the morphological depletion of tight junction proteins and increased IL-1β, IL-6, IL-8 and TNF-α expression by activating the NF-κB signalling pathway in the jejunum. PRRSV infection induced both lung and gut injury, markedly decreased villus height and the villus to crypt ratio in the small intestine, and obviously increased the number of goblet cells and the relative expression of MUC2 mRNA in the jejunum. PRRSV replicated in the lungs and small intestine, as demonstrated by absolute RT-qPCR quantification, and the PRRSV N protein was detected in the lung interstitium and jejunal mucosa. Observations of PRRSV replication and histology were conducted in the lungs and intestine, and goblet cell counts, relative MUC2 mRNA expression, and tight junction protein, proinflammatory cytokine, TLR4, MyD88, IκB and p-IκB expression were measured. An in vivo PRRSV-induced model was established in 30-day-old piglets by the intramuscular injection of 2 mL of 10 4 TCID 50/mL PRRSV for 15 days. The mechanism of intestinal barrier injury caused by PRRSV infection in piglets has yet to be investigated. Porcine reproductive and respiratory syndrome (PRRS) induces respiratory disease and reproductive failure accompanied by gastroenteritis-like symptoms. The Creative Commons Public Domain Dedication waiver ( ) applies to the data made available in this article, unless otherwise stated in a credit line to the data. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. ![]()
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