Inflammations of the bovine mammary gland (mastitis) in a milking herd caused by bacterial and fungal infections contribute to economic losses and remain a big challenge for veterinary medicine. Microorganisms have developed a number of strategies in order to evade the immune response of the host, which makes them significantly difficult to eliminate from the infected host. The intranuclear transcription factor NF-κB (nuclear factor κB) is one of the key elements that participate in inflammatory processes. Numerous studies have confirmed the activation of NF-κB by both gram-positive, mainly Staphylococcus aureus, and gram-negative bacteria, such as e.g. Escherichia coli. The activation of NF-κB is a result of the interaction of pathogen-associated molecular patterns (PAMP), such as LPS (lipopolysaccharides) and LTA (lipoteichoic acid), with particular cell surface receptors (TLRs, toll-like receptors). Staphylococcus aureus and Escherichia coli are responsible for chronic and acute forms of this disease, respectively. This article presents a review of the literature on different research methods: ex vivo (milk examination), in vitro (studies on cell cultures) and in vivo (mouse research models). Studies presented here showed different levels of NF-κB activation in inflammatory mechanisms linked to the activation of neutrophils (PMNs, polymorphonuclear cells) in which epithelial and endothelial cells of the mammary gland are also involved. Moreover, the use of transgenic mice for the detection of NF-κB activity in real time and the studies of apoptosis in the mammary gland are presented in this work. Additionally, the article discusses the influence of mastitis therapy on NF-κB activation. Results of the research on the biological role of NF-κB in described immune mechanisms that are linked to mastitis suggest their usefulness for developing efficient therapeutic strategies (prevention and efficient therapy).
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