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Cell mediated immune response in goats after experimental challenge with the virulent Brucella melitensis strain 16M and the reduced virulence strain Rev. 1
- Higgins, Jennifer L., Bowen, Richard A., Gonzalez-Juarrero, Mercedes
- Veterinary immunology and immunopathology 2018 v.202 pp. 74-84
- Brucella melitensis, CD4-positive T-lymphocytes, animal models, brucellosis, flow cytometry, goats, granulocytes, hosts, humans, immune response, inflammation, interferon-gamma, mitogens, monocytes, pathogens, pregnancy, vaccines, virulence
- Brucella melitensis is the etiologic agent of brucellosis in small ruminants and a common cause of disease in humans. While the protective immune response against this pathogen has been well studied in the mouse model, little is known of the immune response triggered by B. melitensis infection in natural hosts. The objective of the present study was to evaluate the caprine immune response over the course of infection with virulent B. melitensis strain 16 M and reduced virulence vaccine strain Rev. 1. Pregnant goats were infected at 11–14 weeks of gestation with 8 × 106 or 8 × 107 CFU of B. melitensis. Changes in granulocyte, monocyte, and mononuclear cell numbers were monitored by flow cytometry. Proliferative and functional responses of CD4+ T cells and WC1+ γδ T cells were also studied. B. melitensis 16 M infection triggered a pro-inflammatory response characterized by increased numbers of granulocytes, monocytes, and lymphocytes. The relative lymphocytosis was comprised of increases in CD4+ but not WC1+ T cell types in most animals. Little proliferative response was observed in Rev. 1-infected goats. Analysis of lymphocyte function suggested a degree of potential CD4+ T cell anergy, with low levels of CD25 expression and unresponsiveness to mitogen stimulation noted post-infection. The components of the protective response elicited by the Rev. 1 vaccine strain remain undefined. The study suggests a potential WC1+ γδ T cell mediated response, with high percentages of γδ T cells found to produce IFN-γ at various time points over the course of Brucella infection.