Project description:We show here the transcriptional response in the liver of pigs infected or not with Ascaris suum, fed either a control pr a PAC-enriched diet
Project description:We show here the transcriptional response in the intestine of pigs infected or not with Ascaris suum, fed either a control pr a PAC-enriched diet
Project description:We show here the transcriptional response in the lung of pigs infected or not with Ascaris suum, fed either a control pr a PAC-enriched diet
Project description:Roundworm infections result in morbidity, causing significant health and economic concerns in humans and pigs, respectively. We investigated the humoral responses of A. suum infected pigs before and after transition from larval to adult stage and confirmed our previous report on the diagnostic value of human Ascaris-specific antibodies. We evaluated the systemic and mucosal humoral responses in Ascaris infected pigs at 14- and 35-days post-infection (dpi). Ascaris-specific antibodies against larval and adult worm antigens and adult excretory/secretory (ES) products in serum, broncho-alveolar lavage fluid and intestinal mucus were quantified by ELISA. IgA+ B cells in jejunal/ileal mesenteric lymph nodes (mLNs) were investigated using flow cytometry.
Project description:Ascariasis (roundworm) is the most prevalent parasitic nematode infection worldwide, impacting approximately 500 million people predominantly in low- and middle-income countries (LMICs). While people of all ages are infected with Ascaris, infection intensity (defined by worm burden) paradoxically peaks in pre-school and school aged children but then declines with age. The cause of age-dependent Ascaris worm intensity is not well understood but may be dependent on cellular changes in mucosal barrier sites. We have previously found that the gastric mucosa is a critical barrier site for Ascaris infection. Following oral ingestion of Ascaris eggs, larvae use AMCase secreted by gastric chief cells and acid secreted by gastric parietal cells to hatch. Once hatched, larvae translocate across the gastric mucosa to initiate the larval migratory cycle. However, inducing mucosal injury with administration of Tamoxifen induces mucosa cellular changes that impairs Ascaris hatching and reduces larval translocation across the gastric mucosa. In this study we established a repeated Ascaris suum challenge mouse model and evaluated if repeated Ascaris challenge also lead to cellular changes in the gastric mucosal barrier. We found that repeated Ascaris challenge caused cellular changes in the gastric mucosa which reduced worm intensity in the liver independent of the adaptive immune response. Thus, in endemic regions, where individuals experience recurrent infection throughout their lives, gastric cellular changes may be a key mechanism leading to the observed age-dependent Ascaris worm intensity changes from childhood to adulthood.
