Cytoskeleton remodeling and alterations in smooth muscle contractility in the bovine jejunum during nematode infection

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Abstract

Gastrointestinal nematodes of the genus Cooperia are arguably the most important parasites of cattle. The bovine jejunal transcriptome was characterized in response to Cooperia oncophora infection using RNA-seq technology. Approximately 71% of the 25,670 bovine genes were detected in the jejunal transcriptome. However, 16,552 genes were expressed in all samples tested, probably representing the core component of the transcriptome. Twenty of the most abundant genes accounted for 12.7% of the sequences from the transcriptome. A 164-h infection seemingly induced a minor change in the transcriptome (162 genes). Additionally, a total of 162,412 splice junctions were identified. Among them, 1,164 appeared unique to 1 of the 2 groups: 868 splice junctions were observed only in infected animals, while 278 were only present in all 4 control animals. Biological functions associated with muscle contraction were predominant Gene Ontology terms enriched in the genes differentially expressed by infection. The primary function of two of the four regulatory networks impacted was related to skeletal and muscular systems. A total of 34 pathways were significantly impacted by infection. Several pathways were directly related to host immune responses, such as acute phase response, leukocyte extravasation, and antigen presentation, consistent with previous findings. Calcium signaling and actin cytoskeleton signaling were among the pathways most significantly impacted by infection in the bovine jejunum. Together, these data suggest that smooth muscle hypercontractility may be initiated as a result of a primary C. oncophora infection, which may represent a mechanism for host responses in the jejunum during nematode infection. © 2011 Springer-Verlag (outside the USA).

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Li, R. W., & Schroeder, S. G. (2012). Cytoskeleton remodeling and alterations in smooth muscle contractility in the bovine jejunum during nematode infection. Functional and Integrative Genomics, 12(1), 35–44. https://doi.org/10.1007/s10142-011-0259-7

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