Home >> Parasite Immunology, Volume 30, Number 8

Free Content Toxocara canis larval excretory/secretory proteins impair eosinophil-dependent resistance of mice to Nippostrongylus brasiliensis

Authors: GIACOMIN, P. R.1; CAVA, M.1; TUMES, D. J.1; GAULD, A. D.1; IDDAWELA, D. R.; MCCOLL, S. R.1; PARSONS, J. C.2; GORDON, D. L.3; DENT, L. A.1

Source: Parasite Immunology, Volume 30, Number 8, August 2008 , pp. 435-445(11)

Publisher: Wiley-Blackwell

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Abstract:

SUMMARY

Survival of parasitic helminths within a host requires immune evasion and excretory/secretory (ES) proteins may contribute to this process. Eosinophils are important effector cells in immunity of mice to the nematode Nippostrongylus brasiliensis and eosinophilic interleukin-5 transgenic (IL-5 Tg) mice are highly resistant to the earliest stages of primary infections. In contrast, Toxocara canis is largely resistant to eosinophils, with viable larvae encysted in tissues often surrounded by these and other leucocytes. The aim of this study was to investigate whether T. canis ES (TES) proteins inhibit eosinophil-dependent resistance to N. brasiliensis. Mouse serum pre-treated with TES had reduced capacity to mediate the adherence of leucocytes to N. brasiliensis infective-stage larvae (L3) and this correlated with reduced complement C3 deposition on the parasite. TES did not inhibit eosinophil survival or eotaxin-dependent eosinophil migration in vitro. Cellular inflammation and eosinophil degranulation in the skin in response to injection of L3 was also not impaired by TES. However, when TES was included with L3 in an inoculum given to IL-5 Tg mice, a greatly increased number of parasites migrated to the lung. This suggests that the early eosinophil-dependent resistance in these mice was suppressed, by mechanisms yet to be determined.

Keywords: eosinophil; excretory/secretory protein; immune evasion; Nippostrongylus brasiliensis; Toxocara canis

Document Type: Research article

DOI: http://dx.doi.org/10.1111/j.1365-3024.2008.01040.x

Affiliations: 1: School of Molecular and Biomedical Science, University of Adelaide, Adelaide, South Australia, Australia, 2: Department of Primary Industries, Attwood, Victoria, Australia, 3: Department of Microbiology and Infectious Diseases, Flinders Medical Centre, Bedford Park, South Australia, Australia

Publication date: 2008-08-01

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