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Peer-reviewed veterinary case report

Characterization of the Priming Effect by Pituitary Canine Growth Hormone on Canine Polymorphonuclear Neutrophil Granulocyte Function

Journal:
Clinical Diagnostic Laboratory Immunology
Year:
2000
Authors:
Petersen, Thomas K. et al.
Affiliation:
<!--label omitted: 1-->Department of Clinical Studies, Central Laboratory, The Royal Veterinary and Agricultural University, Copenhagen, Denmark,1 and
Species:
dog

Abstract

ABSTRACTIn this report, we demonstrate that canine growth hormone (cGH) is capable of priming canine polymorphonuclear neutrophil granulocytes (PMN) in a manner resembling that of human PMN. The cGH influences important functions that are involved in the process of recruitment of PMN, i.e., shape change, chemotaxis, CD11b/CD18 expression, adhesion, and subsequent transendothelial migration. Also, intracellular O2−production was evaluated. We investigated the priming effect by incubating PMN with purified pituitary cGH at various concentrations (10 to 800 μg/liter). The capacity for shape change was significantly (P< 0.05) enhanced, whereas the chemotactic response under agarose was significantly (P< 0.05) reduced. The chemotactic migration in Boyden chambers (10-μm-thick polycarbonate filter; lower surface count technique) was significantly (P< 0.05) enhanced, presumably due to cGH-induced hyperadhesiveness to the lower surface of the filters. The adhesion in albumin-coated microtiter plates and adherence to canine pulmonary fibroblasts were significantly (P< 0.05) increased, and the increased adhesion resulted in a significant (P< 0.01) increase in transendothelial migration using canine jugular vein endothelial cells. The increase in adhesion was associated with a significant increase in CD11b/CD18 expression. Furthermore, intracellular O2−production was significantly enhanced in response to both phorbol myristate acetate (P< 0.01) and opsonized zymosan (P< 0.05). In the absence of a PMN-stimulating agent, cGH did not influence the effector functions investigated except for an increased expression of CD11b/CD18.

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Original publication: https://doi.org/10.1128/cdli.7.2.226-232.2000