Submitted to: Domestic Animal Endocrinology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 2/5/1999
Publication Date: N/A
Citation: Burvenich, C., Hoeben, D., Paape, M.J., Massart-Leen, A.M., Dosogne, H., Blum, J. 1999. Modulation of the Inflammatory Reaction and Neutrophil Defense of the Bovine Lactating Mammary Gland by Growth Hormone. Domestic Animal Endocrinology. 17(2):149-159.
Interpretive Summary: During the initial infection of the mammary gland by Gram-negative bacteria, the infecting bacteria come in a swift gush. Soon, millions of slender, rod-shaped bacteria fill the lumen of milk ducts and spread into the milk secreting alveoli of the mammary gland. They settle against the smooth folds of the epithelium, absorbing the abundant nutrients in the milk they are being bathed in and expel their own foul excretions or endotoxins. The epithelial cells release their defensive and messenger chemicals, signaling the body for help. Within minutes, scores of neutrophils, specialized first-line-of defense white blood cells, migrate from the bloodstream directly into the bacterial horde. The chemical messengers also stimulate the pituitary gland located at the base of the brain to release growth hormone into the circulation. The hormone finds its way into the battle zone of the mammary gland, activating the neutrophils and other immune cells, making them more efficient in killing the invading hoards of bacteria. After 24 hours, the balance of the struggle had already tipped away from the bacteria and normalcy is once again restored.
Technical Abstract: A great deal of research has been directed toward unraveling and defining the defense mechanisms of the udder. However, not too much is know about possible interactions between typical lacto- genic and galactopoietic hormones such as prolactin an growth hormone and the immunophysiology of the cow towards mastitis. Spontaneous release of growth hormone was observed after experi- mentall induced infection with Gram-negative bacteria. Further, administration of growth hormone to cows before experimental infection accelerated the normalization of the gland when compared to infected cows who received no growth hormone. Pretreatment with growth hormone also increased neutrophil oxidative burst activity, diapedesis and expression of adhesion molecules. Pretreatment also increased the number of circulating neutrophils. Results indicate a direct effect of growth hormone on neutrophil defense of the mammary gland.