K. Taira, R. Yazawa, A. Watanabe, Y. Ishikawa, M. Okamoto, A. Takahashi and F. Asai
Diabetes mellitus is one of the most common endocrine disorders and its continuous global increase is due to factors as population growth, urbanization, aging, and increasing prevalence of obesity and physical inactivity. The effect of pinworm infection on the development of hyperglycemia was examined in WBN/K-Lepf (fa/fa) rats, a new model of the obese type 2 diabetes mellitus (T2DM) with pancreatitis. The rats were orally administered Syphacia muris eggs (infected group) and distilled water (control group). Hyperglycemia onset in the infected group was significantly delayed compared to the control group. Neither body weight nor intake of food and water were affected by S. muris infection. This study demonstrated that S. muris infection delayed the onset of T2DM in fa/fa rats and suggested that elucidation of the underlying mechanism and relevant pathways in the helminth-mediated protection may lead to the development of a new strategy to prevent diabetes mellitus.
Syphacia muris is a ubiquitous nematode parasite and common contaminant of laboratory rats. A lthough S. muris infection is considered symptomless, it has some effects on the host’s immunity and therefore can interfere with experimental settings and interrupt final results. However, the molecular mechanisms involved in the alteration within the host’s immunity remain unclear because of the absence of information about mRNA expressed in this parasite. In this study we performed the transcriptome profiling of S. muris by next-generation sequencing. After de novo assembly and annotation, 14,821 contigs were found to have a sequence homology with any nematode sequence. Gene ontology analysis showed that the majority of the expressed genes are involved in cellular process, binding, and catalytic activity. Although the rate of expressed genes involved in the immune system was low, we found candidate genes that might be involved in the alteration within the host’s immunity by regulating the host’s innate immune response.