ARS | Publication request: Severity variation of clinical E.coli mastitis in cows: where do we stand?

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: October 5, 2009
Publication Date: October 12, 2009
Citation: Burvenich, C., Peelman, L., De Spiegeleer, B., Stevens, M., Pezeshki, A., Detilleus, J.C., Capuco, A.V. 2009. Severity variation of clinical E.coli mastitis in cows: where do we stand? EADGENE conference on Genomics and Animal Health, Paris, France.Abstract.

Technical Abstract: Neutrophils are key effector cells that underpin both defence and severity of clinical coliform mastitis. Increased turnover and viability of neutrophils in the lumen of the bovine mammary gland facilitate the physiological response and acute inflammation that fuel this effective mammary defence mechanism in the lactating animal. During established and late lactation, a transient, dynamic, self-limiting inflammatory process accompanies this increased neutrophil activity. Local regulatory mechanisms adjust the magnitude of the inflammatory response such that the injurious condition is resolved. In contrast, neutrophil function of some periparturient cows (mainly multiparous) may be compromised. These neutrophils are unable to modulate the complex network of innate responses and homeostasis is lost. The inflammatory reaction overwhelms the host, leading to systemic inflammation and severe sepsis. Cytokines that were initially released to protect will now kill the host. Research in coliform mastitis focused primarily on neutrophil dysfunctions (diapedesis, phagocytosis, and bacterial killing). Cytokines provided a later focus. Recently, afferent TLR’s and downstream gene expression, as well as efferent NFk-B and cytokine gene expression have been subject of intense research. The dogma of Crick states that information is transferred unidirectionally from DNA to proteins. This concept is only partially compatible with the original concept of physiology of homeostasis, namely that functionality is attributable to a complex network of feedback mechanisms (e.g. local cross-talk, upstream and downstream regulation, epigenetics). There is evidence that inappropriate temporal and spatial expression of inflammatory genes and chemokinesis at the beginning of infection may contribute to the severity of coliform mastitis.