Identification of Inflammatory and Regulatory Cytokines IL-1α-, IL-4-, IL-6-, IL-12-, IL-13-, IL-17A-, TNF-α-, and IFN-γ-Producing Cells in the Milk of Dairy Cows with Subclinical and Clinical Mastitis

In naturally occurring bovine mastitis, effects of infection depend on the host inflammatory response, including the effects of secreted cytokines. Knowledge about the inflammatory and regulatory cytokines in milk cells of free-stall barn dairy cows and in naturally occurring mastitis is lacking as most studies focus on induced mastitis. Hereby, the aim of the study was to determine inflammatory and regulatory cytokines in the milk of dairy cows with subclinical and clinical mastitis. The following examinations of milk samples were performed: differential counting of somatic cells (SCC), bacteriological examination, and immunocytochemical analysis. Mean SCC increased in subclinical and clinical mastitis cases. The number of pathogenic mastitis-causing bacteria on plates increased in subclinical mastitis cases but decreased in clinical mastitis. The inflammatory and regulatory markers in the milk cells of healthy cows showed the highest mean cell numbers (%). In mastitis cases, immunoreactivity was more pronounced for IL-4, IL-6, IL-12, IL-13, IL-17A, TNF-alpha, and IFN-gamma. Data about subclinical and clinical mastitis demonstrate inflammatory responses to intramammary infection driven by IL-1 alpha, IL-4, and IL-17A. Moreover, the host defense response in mastitis is characterized by continuation or resolution of initial inflammation. IL-12 and INF-gamma immunoreactivity was recognized to differ mastitis cases from the relative health status.

Automated summary

This study aimed to investigate the inflammatory and regulatory cytokines in the milk of dairy cows with subclinical and clinical mastitis. The results showed that IL-1 alpha, IL-4, and IL-17A drive the inflammatory responses in mastitis cases. Furthermore, the host defense response in mastitis is characterized by the continuation or resolution of the initial inflammation.