In 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 O 2 ؊ production was evaluated. We investigated the priming effect by incubating PMN with purified pituitary cGH at various concentrations (10 to 800 g/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-m-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 O 2 ؊ 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.Polymorphonuclear neutrophil granulocytes (PMN) play an important role in organisms' first line of defense against invading agents (25,42). Upon activation in the bloodstream, the PMN become more adhesive, allowing receptor-mediated margination and adhesion to the vasculature (26, 40-42, 44, 51, 58). Then, adherent PMN undergo shape change and crawl on the surface of the endothelial cells, followed by transendothelial migration into the extracellular compartment (5, 40-42, 44, 51). Subsequently, PMN migrate along a chemotactic gradient toward the offending stimulus to finally kill the invading agent by phagocytosis or release of granule contents and reactive oxygen metabolites (2,25,42,56).Growth hormone (GH) has been identified as a factor involved in the regulation of PMN function by priming (17-19, 28, 37-39, 43, 52, 54), whereby the response of PMN to an activating stimulus is potentiated (7). Except for one report (37), previous work shows that GH primes human (18,19,28,39,43,52), porcine (18,19), and bovine (18) PMN in vitro for an enhanced respiratory burst and a reduced chemotactic migration of human PMN (17, 52, 54), which has been suggested to be due to GH-induced hyperadhesiveness (52). These findings correlate with observations for human acromegalic patients, in whom the respiratory burst is increased (38) and the chemotactic response is decreased (16). In contrast to the findings for ...