کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2461422 1555027 2015 7 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Local pulmonary immune responses in domestic cats naturally infected with Cytauxzoon felis
موضوعات مرتبط
علوم زیستی و بیوفناوری علوم کشاورزی و بیولوژیک علوم دامی و جانورشناسی
پیش نمایش صفحه اول مقاله
Local pulmonary immune responses in domestic cats naturally infected with Cytauxzoon felis
چکیده انگلیسی

Cytauxzoonosis is a hemoprotozoal disease of cats and wild felids in the South and Southeastern United States caused by Cytauxzoon felis. Although the causative agent has been recognized since the seventies, no study has examined the local immune response in affected organs, such as the lung, and compared them to the lungs of uninfected domestic cats. Previous studies have suggested that the histopathologic findings in the lungs of C. felis-infected cats are caused by the release of pro-inflammatory mediators, such as cytokines and increased production of inducible nitric oxide synthase (iNOS), by the infected macrophages. Our laboratory had previously found an upregulation of the adhesion molecule CD18, which can stimulate the release of these pro-inflammatory mediators. The objective of this study was to characterize local pulmonary immune responses in cats naturally infected with C. felis. Immunohistochemistry was performed to detect tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6, iNOS, and major histocompatibility complex (MHC) II in 19 lungs from affected cats that died between 2005 and 2013. Results showed increased expression of all of these molecules when compared to lungs from uninfected, healthy cats. Furthermore, MHC II is expressed in the endothelium of C. felis naturally infected cats. These results support that there is a marked, local, pro-inflammatory immune response that can contribute to the pathogenesis of cytauxzoonosis in the lungs.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Veterinary Immunology and Immunopathology - Volume 163, Issues 1–2, 15 January 2015, Pages 1–7
نویسندگان
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