A Cell Proliferation and Inflammatory Signature is Induced byLawsonia intracellularisInfection in Swine
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Abstract
Lawsonia intracellularis causes porcine proliferative enteropathy. This is an enteric disease characterized by thickening of the wall of the ileum that leads to decreased growth and diarrhea of animals. In this study, we investigated the host response to L. intracellularis infection by performing transcriptomic and pathway analysis of intestinal tissue in groups of infected and non-infected animals at 14, 21 and 28 days post challenge. At the peak of infection, when animals developed most severe lesions, infected animals expressed higher levels of several genes involved in cellular proliferation and inflammation including matrix metalloproteinase-7 ( MMP7 ), transglutaminase-2 ( TGM2 ) and Oncostatin M ( OSM ). Histomorphology also revealed general features of intestinal inflammation. This study identified important pathways associated with the host response in developing and resolving lesions due to L. intracellularis infection. Importance Lawsonia intracellularis is among the most important enteric pathogens of swine and it can also infect other mammalian species. Much is still unknown regarding its pathogenesis and the host response, especially at the site of infection. In this study we uncovered several novel genes and pathways associated with infection. These differentially expressed genes, in addition to histological changes in infected tissue, revealed striking similarities between L. intracellularis infection and cellular proliferation mechanisms described in some cancers and inflammatory diseases of the gastrointestinal tract. This research sheds important light into the pathogenesis of L. intracellularis and the host response associated with the lesions caused by infection.
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