Issue |
Vet. Res.
Volume 34, Number 5, September-October 2003
Mastitis of dairy ruminants
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Page(s) | 597 - 627 | |
DOI | https://doi.org/10.1051/vetres:2003024 | |
How to cite this article | Vet. Res. (2003) 597-627 |
DOI: 10.1051/vetres:2003024
The bovine neutrophil: Structure and function in blood and milk
Max J. Paapea, Douglas D. Bannermana, Xin Zhaob and Jai-Wei Leeba Immunology and Disease Resistance Laboratory, USDA-ARS, Beltsville, MD, 20705, USA
b Department of Animal Science, McGill University, Ste-Anne-de-Bellevue, Quebec, Canada
(Received 9 October 2002; accepted 24 April 2003)
Abstract
Migration of polymorphonuclear neutrophil leukocytes (PMN) into the mammary gland provide the first line of defense against
invading mastitis pathogens. Bacteria release potent toxins that activate white blood cells and epithelial cells in the mammary
gland to secrete cytokines that recruit PMN that function as phagocytes at the site of infection. While freshly migrated PMN
are
active phagocytes, continued exposure of PMN to inhibitory factors in milk such as fat globules and casein, leads to altered
PMN morphology and reduced phagocytosis. In the course of phagocytosing and destroying invading pathogens, PMN release chemicals
that not only kill the pathogens but that
also cause injury to the delicate lining of the mammary gland. This will result in permanent scarring and reduced numbers
of milk secretory cells. The life span of PMN is limited by the onset of apoptosis. To minimize damage to mammary tissue,
PMN undergo a specialized process of programmed cell death known as apoptosis. Macrophages quickly engulf and phagocytose
apoptotic PMN, thereby minimizing the release of PMN granular contents that are damaging to
tissue. The PMN possess an array of cell surface receptors that allow them to adhere and migrate through endothelium and to
recognize and phagocytose bacteria. One receptor found on phagocytes that is receiving considerable attention in the control
of infections by Gram-negative bacteria is CD14. Binding of lipopolysaccharide (LPS) to membrane bound CD14 causes release
of tumor necrosis factor-
and sepsis. Binding of LPS to soluble CD14 shed from CD14-bearing cells results in neutralization of LPS and rapid recruitment
of PMN to the site of infection. Recent advances in the fields of genomics and proteomics should greatly enhance our understanding
of the PMN role in controlling intramammary infections in ruminants. Further, manipulation of PMN, through either recombinant
proteins such as soluble CD14 that enhance PMN response or agents that mediate PMN apoptosis, may serve as novel therapeutics
for the treatment of mastitis.
Key words: neutrophil / chemotaxis / phagocytosis / oxidative burst / apoptosis / mastitis
Correspondence and reprints: Max J. Paape mpaape@anri.barc.usda.gov
© INRA, EDP Sciences 2003