Cellular and humoral defence mechanisms in mares susceptible and resistant to persistent endometritis.
Both random and directional migration of blood neutrophils from 9 mares susceptible to persistent endometritis were significantly less (p less than 0.05) than neutrophils from 8 resistant mares. Serum from susceptible mares had significantly more (p less than 0.01) chemotactic activity than serum from resistant mares. Although phagocytosis of yeast blastospores by blood neutrophils from 4 resistant and 3 susceptible mares was similar, uterine neutrophils from susceptible mares were significantly worse (p less than 0.01) at phagocytosis than uterine neutrophils from resistant mares. Uterine washings from 17 susceptible mares were significantly better at opsonising yeast blastospores than washings from 14 resistant mares; however, washings from both groups had a similar ability to promote killing of S. zooepidemicus by neutrophils. When an immunologically non-specific endometritis was induced, washings from 3 susceptible mares were significantly worse at promoting bactericidal activity by 144 h than washings from 4 resistant mares (p less than 0.01). Haemolytic complement activity was significantly greater (p less than 0.001) in washings from 17 susceptible mares than from 14 resistant mares. Induction of acute endometritis resulted in high levels of haemolytic complement activity in 2 of 3 susceptible mares at 24 and 144 h, but only in small increases in 4 resistant mares. Thus, some abnormalities in neutrophil function were detected and a possible defect in promotion of neutrophil bactericidal activity by uterine secretions from susceptible mares but there was no evidence for any deficiency in haemolytic complement activity.
Watson
E D
ED
Department of Veterinary Medicine, University of Bristol, Langford, England.
Stokes
C R
CR
Bourne
F J
FJ
D000818:Animals; D002634:Chemotaxis, Leukocyte; D003165:Complement System Proteins / Q000378:metabolism; D004716:Endometritis / Q000209:etiology / Q000276:immunology / Q000662:veterinary*; D005260:Female; D006734:Horse Diseases / Q000209:etiology / Q000276:immunology*; D006736:Horses; D007111:Immunity, Cellular; D066298:In Vitro Techniques; D009504:Neutrophils / Q000276:immunology; D009895:Opsonin Proteins / Q000276:immunology; D010587:Phagocytosis; D012441:Saccharomyces cerevisiae / Q000276:immunology; D013291:Streptococcus / Q000276:immunology
D009895:Opsonin Proteins; D003165:Complement System Proteins