Abstract
Cooperia oncophora is an economically important gastrointestinal nematode in ruminants. Acquired resistance to Cooperia oncophora infection in cattle develops rapidly as a result of prior infections. Naïve cattle, when given a primary infection of high-dose infective L3 larvae, develop a strong immunity to subsequent reinfection. Compared to primary infection, reinfection resulted in a marked reduction in worm establishment. In order to understand molecular mechanisms underlying the development of acquired resistance, we characterized the transcriptomic responses of the bovine small intestine to a primary infection and reinfection. A total of 23 pathways were significantly impacted during infection. The vitamin D receptor activation was strongly induced only during reinfection, suggesting that this pathway may play an important role in the development of acquired resistance via its potential roles in immune regulation and intestinal mucosal integrity maintenance. The expression of inducible nitric oxide synthase (NOS2) was strongly induced during reinfection but not during primary infection. As a result, several canonical pathways associated with NOS2 were impacted. The genes involved in eicosanoid synthesis, including prostaglandin synthase 2 (PTGS2 or COX2), remained largely unchanged during infection. The rapid development of acquired resistance may help explain the lack of relative pathogenicity by Cooperia oncophora infection in cattle. Our findings facilitate the understanding of molecular mechanisms underlying the development of acquired resistance, which could have an important implication in vaccine design.
Highlights
Cooperia oncophora is one of the most economically important gastrointestinal nematodes in ruminants that result in production inefficiency
While uncharacterized genetic makeup of experiment animals and a small sample size used in challenge studies are a major concern, a significant reduction in worm burden and a higher percentage of immature larvae recovered in reinfected animals (15.2% vs. 9.4% in primarily infected animals, P < 0.1) suggested these animals had acquired protective immunity to infection
It has long been recognized that genetics plays an important role in the host’s ability to resist gastrointestinal nematode infections in ruminants, even though the heritability of the resistance trait is relatively low to moderate in most cases
Summary
Cooperia oncophora is one of the most economically important gastrointestinal nematodes in ruminants that result in production inefficiency. Pathophysiological changes induced by infection are typically restricted to the site of infection, mainly in the duodenum and jejunum. C. oncophora infection in cattle elicits a Th2-like immune response, characterized by up-regulation of IL-4 and the involvement of both eosinophils and mucosal IgA [4,5,6,7]. C. oncophora-specific serum and mucosal IgG1 and IgA are strongly induced upon experimental challenge in cattle [8]. PIGR, a gene responsible for trans-epithelial transport of polymeric immunoglobulins, such as IgA dimers and IgM pentamers, into mucosal and glandular secretions, is strongly up-regulated in the heifers resistant to parasitic nematodes after experimental parasite challenge [7]. The peak in antibody titres is preceded by a significant increase in B and MHCII+ cells in the draining lymph nodes, suggesting that B cells may play an important role in development of acquired immunity against the parasite [8]
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