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Published online ahead of print on 30 September 2009 as doi:10.1099/vir.0.014613-0
J Gen Virol (2009), DOI 10.1099/vir.0.014613-0
© 2009 Society for General Microbiology

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Characterization of neutrophil extracellular traps in cats naturally-infected with the feline leukemia virus (FeLV).

Amanda Brito Wardini1, Anderson Baptista Guimarães-Costa2, Michelle Tanny Nascimento2, Natália Rocha Nadaes1, Maria das Graças Miranda Danelli1, Carlos Mazur1, Claudia F. Benjamim3, Elvira Maria Saraiva2 and Lucia Helena Pinto-da-Silva1,4

1 Unversidade Federal Rural do Rio de Janeiro;
2 Universidade Federal do Rio de Janeiro;
3 Universidade Federal do Rio de Janeiro

4 E-mail: lpinto_silva{at}yahoo.com

Feline leukemia virus (FeLV), a common, naturally-occurring gammaretrovirus in domestic cats, is associated with degenerative diseases of the hematopoietic system, immunodeficiency, and neoplasia. FeLV infection causes an important suppression of neutrophil functions, leading to opportunistic infections. Recently, a new microbicidal mechanism named NETosis was described in human, bovine, and fish neutrophils, as well as in chicken heterophils. The purpose of the present study was to characterize NETosis in feline neutrophils as well as evaluate neutrophil functions in naturally-infected, FeLV symptomatic and asymptomatic cats through the phagocytosis process, NET release, and MPO activity. Our results showed that feline neutrophils stimulated with protozoa parasites release structures constituted by DNA and histones, which were characterized as NETs by immunofluorescence. Quantification of NETs after neutrophils stimulation showed a significant increase in NET release by neutrophils from FeLV(-) and FeLV(+) asymptomatic cats as compared to FeLV(+) symptomatic ones. Moreover, released NETs and myeloperoxidase (MPO) activity in unstimulated neutrophils of FeLV(+) symptomatic cats are higher than those found in unstimulated neutrophils from FeLV(-) and FeLV(+) symptomatic cats. We report here for the first time NET release by feline neutrophils, along with the fact that NET induction may be modulated by a viral infection. Our results point to the observation that the NET mechanism appears to be over activated in FeLV(+) cats and that this feature could be considered a progression disease marker in feline leukemia viral infection.

Received 27 June 2009; accepted 24 September 2009.





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