Inflammatory immune response of canine trophoblastic cells to infection with Brucella canis or to interaction with infected phagocytes.

FERNANDEZ, AG; HIELPOS, MS; FERRERO, MC; FOSSATI, CA; BALDI, PC

Buenos Aires

Congreso; LXIII Reunión Anual de la Sociedad Argentina de Inmunología, IV LASID Meeting, y II French-Argentinean Immunology Meeting; 2015

Sociedad Argentina de Inmunología y Sociedad Francesa de Inmunología

Abstract Text: Background: Brucella canis is an important cause of abortion in dogs, but the pathogenicmechanisms involved are unknown. We evaluated the ability of B. canis to infect canine trophoblasticcells and analyzed the inflammatory immune response triggered by infection or interaction with infectedphagocytes.Methods: trophoblastic cells were isolated from term placenta of healthy female dogs (obtained by Csection)and were characterized by their expression of cytokeratin 7. Neutrophils were isolated fromperipheral blood of healthy dogs. Trophoblasts were infected with B. canis for 48 h for intracellularcolony forming units (CFU) determination and measurement of LDH (lactate dehydrogenase) activity.Neutrophils were infected with B. canis for 24 h and conditioned media were used to stimulateuninfected trophoblasts. Proinflammatory cytokines were measured in all culture supernatants. Results: Isolated canine trophoblasts were positive for cytokeratin 7 staining. B. canis CFU countsinside trophoblasts increased significantly between 24 and 48 h post infection. LDH levels remainedsimilar between uninfected and infected cells. Both IL-8 and RANTES levels were significantly increasedin infected trophoblasts as compared to uninfected cells, whereas IL-6 remained undetectable.Trophoblasts also increased their secretion of IL-8 and RANTES upon stimulation with conditionedmedia from infected neutrophils.Conclusions: B. canis infects and replicates in canine trophoblasts without inducing cytotoxicity. Inresponse to B. canis infection or factors produced by infected neutrophils trophoblasts produceinflammatory mediators including IL-8 and RANTES (chemoattractants for neutrophils and severalleukocytic populations, respectively). The inflammatory response induced by these chemokines maycontribute to fetal miscarriage.