Abstract
Intramammary infusion of the antigen used to sensitize cows by the systemic route induces a local inflammation associated with neutrophil recruitment. We hypothesize that this form of delayed type hypersensitivity, which may occur naturally during infections or could be induced intentionally by vaccination, can impact the outcome of mammary gland infections. We immunized cows with ovalbumin to identify immunological correlates of antigen-specific mammary inflammation. Intraluminal injection of ovalbumin induced a mastitis characterized by a prompt tissue reaction (increase in teat wall thickness) and an intense influx of leukocytes into milk of 10 responder cows out of 14 immunized animals. The magnitude of the local inflammatory reaction, assessed through milk leukocytosis, correlated with antibody titers, skin thickness test, and production of IL-17A and IFN-γ in a whole-blood antigen stimulation assay (WBA). The production of these two cytokines significantly correlated with the magnitude of the milk leukocytosis following the ovalbumin intramammary challenge. The IL-17A and IFN-γ production in the WBA was dependent on the presence of CD4+ cells in blood samples. In vitro stimulation of peripheral blood lymphocytes with ovalbumin followed by stimulation with PMA/ionomycin allowed the identification by flow cytometry of CD4+ T cells producing either IL-17A, IFN-γ, or both cytokines. The results indicate that the antigen-specific WBA, and specifically IL-17A and IFN-γ production by circulating CD4+ cells, can be used as a predictor of mammary hypersensitivity to protein antigens. This prompts further studies aiming at determining how Th17 and/or Th1 lymphocytes modulate the immune response of the mammary gland to infection.
Highlights
Infection of the MG of dairy ruminants by pyogenic bacteria such as streptococci, staphylococci and coliforms is a common disease and a major economic problem for milk producers [1]
Little is known of the mechanism of this sensitization, but it has been shown that the mammary gland antigen-specific response can be transferred to naïve guinea pigs by adoptive transfer of lymphocytes but not by immune serum, leading the authors to conclude that the mASR was a local manifestation of a general state of lymphocyte-dependent hypersensitivity [10, 11]
This study was devised to investigate the hypothetical role of Th17 cells in the immune response of the mammary gland to infection by mastitis-causing bacteria
Summary
Infection of the MG of dairy ruminants by pyogenic bacteria such as streptococci, staphylococci and coliforms is a common disease and a major economic problem for milk producers [1]. The innate immune system is efficient at triggering an inflammatory response in the mammary gland [4, 5], hypersensitivity has long been suspected to contribute to the inflammatory response of the mammary gland to common mastitis-causing bacteria [6]. Little is known of the mechanism of this sensitization, but it has been shown that the mammary gland antigen-specific response (mASR) can be transferred to naïve guinea pigs by adoptive transfer of lymphocytes but not by immune serum, leading the authors to conclude that the mASR was a local manifestation of a general state of lymphocyte-dependent hypersensitivity [10, 11]
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