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Title: EFFECT OF LIPOPOLYSACCHARIDE AND TUMOR NECROSIS FACTOR -A ON CELL DEATH OF BOVINE POLYMORPHONUCLEAR LEUKOCYTES AND THE RESPIRATORY BURST ACTIVITY, PHAGOCYTOSIS CAPACITY AND CD18 EXPRESSION OF ANNEXIN-V-POSITIVE LEUKOCYTES

Author
item OOSTVELDT, K - GHENT UNIV BELGIUM
item Paape, Max
item BURVENICH, C - GHENT UNIV BELGIUM

Submitted to: Domestic Animal Endocrinology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 4/2/2002
Publication Date: 11/1/2002
Citation: OOSTVELDT, K.V., PAAPE, M.J., BURVENICH, C. EFFECT OF LIPOPOLYSACCHARIDE AND TUMOR NECROSIS FACTOR -A ON CELL DEATH OF BOVINE POLYMORPHONUCLEAR LEUKOCYTES AND THE RESPIRATORY BURST ACTIVITY, PHAGOCYTOSIS CAPACITY AND CD18 EXPRESSION OF ANNEXIN-V-POSITIVE LEUKOCYTES. DOMESTIC ANIMAL ENDOCRINOLOGY. 2002.

Interpretive Summary: Neutrophils are phagocytic cells that engulf and destroy invading pathogens. They represent the first line of defense against infection. Infection results when the neutrophils defensive capabilities are compromised. Researchers in the Immunology and Disease Resistance have reported that during infection by Gram- negative bacteria such as Escherichia coli, the capability of neutrophils to engulf and destroy E. coli are reduced. Escherichia coli secrete lipopolysaccharide (LPS) which causes the secretion of tumor necrosis factor (TNF). The researchers were able to show that both LPS and TNF contribute to the reduced ability of neutrophils to engulf and destroy E. coli by inducing neutrophil apoptosis or programmed cell death. Failure by neutrophils to contain the infection results in rapid multiplication of the bacteria and the onset of clinical symptoms and possible death. Monoclonal antibodies to LPS or TNF did not prevent the adverse effect that they had on neutrophils. In order to prevent the destruction of neutrophils, the scientists are developing novel recombinant proteins to neutralize the deadly effects that bacterial toxins have on neutrophils.

Technical Abstract: Polymorphonuclear leukocytes (PMN) play an important role in defense of the mammary gland against infections caused by Escherichia coli. During mastitis, PMN are confronted with various inflammatory mediators that are expected to modulate their cellular functions. During severe coliform mastitis, peaks in the concentrations of lipopolysaccharide (LPS) and TNF-alpha are detected in plasma. In this study, bovine PMN apoptosis was induced with LPS and TNF-alpha in whole blood after a 6 h incubation at 37C. The apoptosis inducing effect of LPS on PMN could not be negated following incubation of co-cultures with either anti-bovine TNF-alpha or anti-human CD14 monoclonal antibodies. In a second study, apoptotic PMN were shown to have the same level of expression of CD18 as normal PMN. However, phagocytosis and respiratory burst activity after stimulation with PMA or E. coli were reduced compared to normal PMN. The functional impairment in phagocytosis and oxidative burst could be important in defense of the mammary gland against invading pathogens.