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. 2011 Mar 17;42(1):48.
doi: 10.1186/1297-9716-42-48.

The Vitamin D Receptor and Inducible Nitric Oxide Synthase Associated Pathways in Acquired Resistance to Cooperia Oncophora Infection in Cattle

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Free PMC article

The Vitamin D Receptor and Inducible Nitric Oxide Synthase Associated Pathways in Acquired Resistance to Cooperia Oncophora Infection in Cattle

Robert W Li et al. Vet Res. .
Free PMC article

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.

Figures

Figure 1
Figure 1
Selected pathways significantly impacted in the bovine small intestine during Cooperia oncophora infection at 14 dpi. The dashed line represents a significance level at P < 0.05. N = 4.
Figure 2
Figure 2
The expression profiles of NOS2 and COX2 in the bovine small intestine during Cooperia oncophora infection at 14 dpi. The expression value at the mRNA level was detected using quantitative RT-PCR. The expression value of the naïve control group was set as 1.0. The fold change (N = 4) were calculated using the 2-ΔΔCT method and normalized against the naïve control group (mean ± SD). NOS 2 = nitric oxide synthase 2, inducible; COX2 = PTGS2 (prostaglandin-endoperoxide synthase 2 (prostaglandin G/H synthase and cyclooxygenase)).
Figure 3
Figure 3
CDH26 expression in the bovine small intestine during Cooperia oncophora infection. The expression value at the mRNA level was detected using quantitative RT-PCR. The expression value of the naïve control group was set as 1.0. The fold change (N = 4) were calculated using the 2-ΔΔCT method and normalized against the naïve control group (mean ± SD). CDH26 = cadherin 26.
Figure 4
Figure 4
The expression of two genes in mucin biosynthesis in the bovine small intestine during Cooperia oncophora infection at 14 dpi. The expression value at the mRNA level was detected using quantitative RT-PCR. The expression value of the naïve control group was set as 1.0. The fold change (N = 4) were calculated using the 2-ΔΔCT method and normalized against the naïve control group (mean ± SD). MUC2 = mucin 2, oligomeric mucus/gel-forming; GCNT3 = glucosaminyl (N-acetyl) transferase 3, mucin type.
Figure 5
Figure 5
Western blot analysis of GCNT3 and SPP1 in the small intestine tissue (jejunum) during Cooperia oncophora infection at 14 dpi. The relative densities of the target bands were qualified using UN-SCAN-IT from Silk Scientific. GCNT3 = glucosaminyl (N-acetyl) transferase 3, mucin type. SPP1= secreted phosphoprotein 1 (osteopontin).

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