المؤلفون: Wilson, D L, Rathinam, V A K, Qi, W, Wick, L M, Landgraf, Jeff, Bell, J A, Plovanich-Jones, A, Parrish, J, Finley, R L, Mansfield, L S, Linz, J E

المصدر: Wilson, D L; Rathinam, V A K; Qi, W; Wick, L M; Landgraf, Jeff; Bell, J A; Plovanich-Jones, A; Parrish, J; Finley, R L; Mansfield, L S; Linz, J E (2010). Genetic diversity in Campylobacter jejuni is associated with differential colonization of broiler chickens and C57BL/6J IL10-deficient mice. Microbiology, 156(7):2046-2057.

مصطلحات موضوعية: Functional Genomics Center Zurich, Systems Biology / Functional Genomics, 570 Life sciences, biology, 610 Medicine & health

الوصف: Previous studies have demonstrated that Campylobacter jejuni, the leading causative agent of bacterial food-borne disease in the USA, exhibits high-frequency genetic variation that is associated with changes in cell-surface antigens and ability to colonize chickens. To expand our understanding of the role of genetic diversity in the disease process, we analysed the ability of three C. jejuni human disease isolates (strains 11168, 33292 and 81-176) and genetically marked derivatives to colonize Ross 308 broilers and C57BL/6J IL10-deficient mice. C. jejuni colonized broilers at much higher efficiency (all three strains, 23 of 24 broilers) than mice (11168 only, 8 of 24 mice). C. jejuni 11168 genetically marked strains colonized mice at very low efficiency (2 of 42 mice); however, C. jejuni reisolated from mice colonized both mice and broilers at high efficiency, suggesting that this pathogen can adapt genetically in the mouse. We compared the genome composition in the three wild-type C. jejuni strains and derivatives by microarray DNA/DNA hybridization analysis; the data demonstrated a high degree of genetic diversity in three gene clusters associated with synthesis and modification of the cell-surface structures capsule, flagella and lipo-oligosaccharide. Finally, we analysed the frequency of mutation in homopolymeric tracts associated with the contingency genes wlaN (GC tract) and flgR (AT tracts) in culture and after passage through broilers and mice. C. jejuni adapted genetically in culture at high frequency and the degree of genetic diversity was increased by passage through broilers but was nearly eliminated in the gastrointestinal tract of mice. The data suggest that the broiler gastrointestinal tract provides an environment which promotes outgrowth and genetic variation in C. jejuni; the enhancement of genetic diversity at this location may contribute to its importance as a human disease reservoir.

وصف الملف: application/pdf

العلاقة: https://www.zora.uzh.ch/id/eprint/35678/9/mic.0.035717-0v1.pdfTest; info:pmid/20360176; urn:issn:1350-0872

الإتاحة: https://doi.org/10.5167/uzh-3567810.1099/mic.0.035717-0Test
https://www.zora.uzh.ch/id/eprint/35678Test/
https://www.zora.uzh.ch/id/eprint/35678/9/mic.0.035717-0v1.pdfTest

المؤلفون: Mansfield, L. S., Bell, J. A., Wilson, D. L., Murphy, A. J., Elsheikha, H. M., Rathinam, V. A. K., Fierro, B. R., Linz, J. E., Young, V. B.

المصدر: Infection and Immunity ; volume 75, issue 3, page 1099-1115 ; ISSN 0019-9567 1098-5522

الوصف: Campylobacter jejuni is a globally distributed cause of human food-borne enteritis and has been linked to chronic joint and neurological diseases. We hypothesized that C. jejuni 11168 colonizes the gastrointestinal tract of both C57BL/6 mice and congenic C57BL/6 interleukin-10-deficient (IL-10 −/− ) mice and that C57BL/6 IL-10 −/− mice experience C. jejuni 11168-mediated clinical signs and pathology. Individually housed mice were challenged orally with C. jejuni 11168, and the course of infection was monitored by clinical examination, bacterial culture, C. jejuni -specific PCR, gross pathology, histopathology, immunohistochemistry, and anti- C. jejuni -specific serology. Ceca of C. jejuni 11168-infected mice were colonized at high rates: ceca of 50/50 wild-type mice and 168/170 IL-10 −/− mice were colonized. In a range from 2 to 35 days after infection with C. jejuni 11168, C57BL/6 IL-10 −/− mice developed severe typhlocolitis best evaluated at the ileocecocolic junction. Rates of colonization and enteritis did not differ between male and female mice. A dose-response experiment showed that as little as 10 6 CFU produced significant disease and pathological lesions similar to responses seen in humans. Immunohistochemical staining demonstrated C. jejuni antigens within gastrointestinal tissues of infected mice. Significant anti- C. jejuni plasma immunoglobulin levels developed by day 28 after infection in both wild-type and IL-10-deficient animals; antibodies were predominantly T-helper-cell 1 (Th1)-associated subtypes. These results indicate that the colonization of the mouse gastrointestinal tract by C. jejuni 11168 is necessary but not sufficient for the development of enteritis and that C57BL/6 IL-10 −/− mice can serve as models for the study of C. jejuni enteritis in humans.

الإتاحة: https://doi.org/10.1128/iai.00833-06Test

المؤلفون: Mansfield, L. S., Bell, J. A., Wilson, D. L., Murphy, A. J., Elsheikha, H. M., Rathinam, V. A. K., Fierro, B. R., Linz, J. E., Young, V. B.

المصدر: Infection and Immunity; March 2007, Vol. 75 Issue: 3 p1099-1115, 17p

مستخلص: ABSTRACTCampylobacter jejuniis a globally distributed cause of human food-borne enteritis and has been linked to chronic joint and neurological diseases. We hypothesized that C. jejuni11168 colonizes the gastrointestinal tract of both C57BL/6 mice and congenic C57BL/6 interleukin-10-deficient (IL-10−/−) mice and that C57BL/6 IL-10−/−mice experience C. jejuni11168-mediated clinical signs and pathology. Individually housed mice were challenged orally with C. jejuni11168, and the course of infection was monitored by clinical examination, bacterial culture, C. jejuni-specific PCR, gross pathology, histopathology, immunohistochemistry, and anti-C. jejuni-specific serology. Ceca of C. jejuni11168-infected mice were colonized at high rates: ceca of 50/50 wild-type mice and 168/170 IL-10−/−mice were colonized. In a range from 2 to 35 days after infection with C. jejuni11168, C57BL/6 IL-10−/−mice developed severe typhlocolitis best evaluated at the ileocecocolic junction. Rates of colonization and enteritis did not differ between male and female mice. A dose-response experiment showed that as little as 106CFU produced significant disease and pathological lesions similar to responses seen in humans. Immunohistochemical staining demonstrated C. jejuniantigens within gastrointestinal tissues of infected mice. Significant anti-C. jejuniplasma immunoglobulin levels developed by day 28 after infection in both wild-type and IL-10-deficient animals; antibodies were predominantly T-helper-cell 1 (Th1)-associated subtypes. These results indicate that the colonization of the mouse gastrointestinal tract by C. jejuni11168 is necessary but not sufficient for the development of enteritis and that C57BL/6 IL-10−/−mice can serve as models for the study of C. jejunienteritis in humans.

المؤلفون: Wilson, D L, Rathinam, V A K, Qi, W, Wick, L M, Landgraf, Jeff, Bell, J A, Plovanich-Jones, A, Parrish, J, Finley, R L, Mansfield, L S, Linz, J E

مصطلحات موضوعية: 2. Zero hunger

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_________::1440079ed81d33edc7cb06d962c57f87Test