@article{mexas_fogle_tompkins_tompkins_2008, title={CD4(+)CD25(+) regulatory T cells are infected and activated during acute FIV infection}, volume={126}, ISSN={["1873-2534"]}, DOI={10.1016/j.vetimm.2008.08.003}, abstractNote={HIV-induced AIDS may be mediated by the activation of immunosuppressive CD4+CD25+ T regulatory cells (Treg cells). Treg cells have been shown to regulate CD4+ and CD8+ immune responses to HIV and FIV antigens in vitro. We tested the hypothesis that Treg cells become infected and activated during the acute infection with FIV leading to the suppression of CD4+ T helper cell responses. Cats were experimentally infected with FIV-NCSU1 and blood and lymph node cells were collected at weekly intervals following inoculation. Real-time RT-PCR was used to determine plasma viremia and the relative expression of FIV, FoxP3, TGF-β, and GAPDH mRNA copies in CD4+CD25+ and CD4+CD25− T cell subsets. Flow cytometry was used to assess the absolute numbers of each cell type and the expression of surface TGF-β and intracellular FoxP3 in CD4+CD25+ and CD4+CD25− T cells at each time-point. Treg suppression of IL-2 production in CD4+ T helper cells was assessed by ELISPOT assays. Our results showed that peak viremia occurred at 2 weeks post infection and correlated with maximal infectivity in CD4+CD25+ T cell populations. FIV-gag-mRNA levels were higher in CD4+CD25+ T cells than CD4+CD25− T cells throughout the acute phase of infection. Induction of FoxP3 and TGF-β indicated activation of Treg cells during the acute stage infection, which was confirmed by Treg cell suppression of IL-2 production by CD4+ Th cells in an ELISPOT assay. Our findings support the hypothesis that early activation of Treg immunosuppressor function may limit an effective anti-FIV response, contributing to the establishment of chronic infection and the immunodeficiency caused by this virus.}, number={3-4}, journal={VETERINARY IMMUNOLOGY AND IMMUNOPATHOLOGY}, author={Mexas, Angela M. and Fogle, Jonathan E. and Tompkins, Wayne A. and Tompkins, Mary B.}, year={2008}, month={Dec}, pages={263–272} }
 @article{smithberg_fogle_mexas_reckling_lankford_tompkins_dean_2008, title={In vivo depletion of CD4(+)CD25(+) regulatory T cells in cats}, volume={329}, ISSN={["0022-1759"]}, DOI={10.1016/j.jim.2007.09.015}, abstractNote={To establish a characterized model of regulatory T cell (Treg) depletion in the cat we assessed the kinetics of depletion and rebound in peripheral and central lymphoid compartments after treatment with anti-CD25 antibody as determined by cell surface markers and FOXP3 mRNA expression. An 82% decrease in circulating CD4+CD25+ Tregs was observed by day 11 after treatment. CD4+CD25+ cells were also reduced in the thymus (69%), secondary lymphoid tissues (66%), and gut (67%). Although CD4+CD25+ cells rebound by day 35 post-treatment, FOXP3 levels remain depressed suggesting anti-CD25 antibody treatment has a sustainable diminutive effect on the Treg population. To determine whether CD25+ Treg depletion strategies also deplete activated CD25+ effector cells, cats were immunized with feline immunodeficiency virus (FIV) p24-GST recombinant protein, allowing them to develop a measurable memory response, prior to depletion with anti-CD25 antibody. Anti-FIV p24-GST effector cell activity in peripheral blood after depletion was sustained as determined by antigen-specific T cell proliferation and humoral responses against FIV p24-GST with an ELISA for antigen-specific feline IgG. Furthermore, development of an anti-mouse response in Treg-depleted cats was similar to control levels indicating the retained capacity to respond to a novel antigen. We conclude that despite alterations in CD25+ cell levels during depletion, the feline immune system remains functional. We demonstrate here a model for the study of disease pathogenesis in the context of reduced numbers of immunosuppressive CD4+CD25+ Tregs throughout the feline immune system.}, number={1-2}, journal={JOURNAL OF IMMUNOLOGICAL METHODS}, author={Smithberg, S. Rochelle and Fogle, Jonathan E. and Mexas, Angela M. and Reckling, Stacie K. and Lankford, Susan M. and Tompkins, Mary B. and Dean, Gregg A.}, year={2008}, month={Jan}, pages={81–91} }
 @article{mexas_hess_hawkins_martin_2006, title={Pulmonary lesions in cats with diabetes mellitus}, volume={20}, ISSN={["1939-1676"]}, DOI={10.1892/0891-6640(2006)20[47:PLICWD]2.0.CO;2}, abstractNote={Diabetes mellitus (DM) is a common endocrinopathy of cats and humans. Although few studies have examined the effects of DM on the pulmonary system, changes in pulmonary function and immunology in humans with type I and II diabetes, and pulmonary lesions in a murine diabetic model have been documented. Our objective was to determine whether pulmonary lesions occurred in cats with DM. Medical records and necropsy evaluations of 42 cats with DM were compared with those of 45 age-matched, nondiabetic cats for the presence of clinical evidence of respiratory disease and pulmonary histopathological findings at the time of necropsy. No statistical difference was noted in the presence of clinical evidence of respiratory disease between cats with diabetes and control cats. Nevertheless, there was a significant association between the presence of abnormal pulmonary histopathology and DM (P= .018, odds ratio = 3 inclusive of all cats; P= .005, odds ratio = 5 when non-DM cats with overt clinical evidence of respiratory disease were excluded). Pulmonary abnormalities detected by histopathological examination in cats with diabetes included congestion and edema, histiocytosis, pneumonia, smooth muscle hypertrophy, fibrosis, mineralization, neoplasia, and type II pneumocyte hyperplasia. The observed association between DM and pulmonary lesions in cats, independent of clinical evidence of respiratory disease, emphasizes the need for careful assessment of the respiratory tract in sick cats with diabetes.}, number={1}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Mexas, AM and Hess, RS and Hawkins, EC and Martin, LD}, year={2006}, pages={47–51} }
 @article{breitschwerdt_debroy_mexas_brown_remick_2005, title={Isolation of necrotoxigenic Escherichia coli from a dog with hemorrhagic pneumonia}, volume={226}, ISSN={0003-1488}, url={http://dx.doi.org/10.2460/javma.2005.226.2016}, DOI={10.2460/javma.2005.226.2016}, abstractNote={A 7-month-old sexually intact male Cocker Spaniel was admitted to the North Carolina State University Veterinary Teaching Hospital for evaluation of lethargy, panting, and excessive salivation that had become progressively severe during a 5-hour period. Despite intensive medical care, the dog died within the first 24 hours of hospitalization, and death was attributed to acute, severe, necrotizing pneumonia. Lung tissue collected at necropsy by use of swabs was cultured and yielded an isolate of Escherichia coli; because of the rapid progression of illness in an otherwise healthy dog, the isolate underwent virulence typing and was determined to be a necrotoxigenic E. coli. Necrotoxigenic E. coli produce a toxin called cytotoxic necrotizing factor and are known to be involved in extraintestinal infections, including urinary tract infection, in humans and animals. Virulence typing of E. coli isolates from dogs with peracute pneumonia is recommended to further characterize the epidemiologic characteristics and public health importance of necrotoxigenic E. coli.}, number={12}, journal={Journal of the American Veterinary Medical Association}, publisher={American Veterinary Medical Association (AVMA)}, author={Breitschwerdt, Edward B. and DebRoy, Chitrita and Mexas, Angela M. and Brown, Talmage T. and Remick, Amera K.}, year={2005}, month={Jun}, pages={2016–2019} }
 @article{mexas_hancock_breitschwerdt_2002, title={Bartonella henselae and Bartonella elizabethae as Potential Canine Pathogens}, volume={40}, ISSN={0095-1137}, url={http://dx.doi.org/10.1128/jcm.40.12.4670-4674.2002}, DOI={10.1128/JCM.40.12.4670-4674.2002}, abstractNote={ABSTRACT}, number={12}, journal={Journal of Clinical Microbiology}, publisher={American Society for Microbiology}, author={Mexas, A. M. and Hancock, S. I. and Breitschwerdt, E. B.}, year={2002}, month={Dec}, pages={4670–4674} }