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ARS Home » Research » Publications at this Location » Publication #124097
Title: APOPTOSIS OF CIRCULATING BOVINE NEUTROPHILS DURING MASTITIS

Author
item VAN OOSTVELDT, K - U GHENT BELGIUM
item TOMITA, G - USDA ARS BELTSVILLE MD
item PAAPE, MAX
item BURVENICH, C - U GHENT BELGIUM

Submitted to: International Dairy Federation Seminar
Publication Type: Proceedings
Publication Acceptance Date: 10/21/2001
Publication Date: N/A
Citation: N/A

Interpretive Summary: Neutrophils are important cells in the first line of defence against bacterial invasion of the bovine mammary gland. Before neutrophils can phagocytose bacteria, they must migrate from blood to the site of infection. Migration begins with the interaction between adhesion receptors on circulating neutrophils and the corresponding receptors on the blood vessels. This process is controlled by inflammatory mediators. After migration neutrophils phagocytose the invading bacteria and kill them through oxygen independent and oxygen dependent mechanisms. After migration and killing of bacteria, neutrophils die by apoptosis or necrosis. Apoptosis or programmed cell death is a physiological form of cell death that results in cell removal without inducing an inflammatory reaction. Apoptosis was found to be accelerated during Escherichia coli mastitis but not following mastitis induced with the endotoxin produced by E. coli.

Technical Abstract: Apoptosis of neutrophils regulates the clearance of neutrophils from the inflammatory site, and is an important aspect in controlling the inflammatory response of the bovine mammary gland. Neutrophils seldom undergo apoptotic cell death in the blood circulatory system. The percentage of apoptotic neutrophils in blood samples following a 3 h in vitro incubation taken from cows after Escherichia coli or endotoxin induced mastitis showed that E. coli challenge significantly increased the percentage of apoptotic neutrophils. Intramammary endotoxin challenge did not have any effect on neutrophil apoptosis. This finding suggests that short term intramammary exposure to endotoxin is not sufficient to induce apoptosis, and that long term exposure to E. coli was required. This observation together with altered neutrophil functions as related to E. coli or endotoxin challenge are discussed.