title: Modulation of the bovine trophoblastic innate immune response by Brucella abortus.
abstract: Brucellosis is still a widespread zoonotic disease. Very little is known about the interaction between Brucella abortus and trophoblastic cells, which is essential for better understanding the pathogenesis of the Brucella-induced placentitis and abortion, a key event for transmission of the disease. The goal of this study was to evaluate the profile of gene expression by bovine trophoblastic cells during infection with B. abortus. Explants of chorioallantoic membranes were inoculated with B. abortus strain 2308. Microarray analysis was performed at 4 h after infection, and expression of cytokines and chemokines by trophoblastic cells was assessed by real-time reverse transcription-PCR at 6 and 12 h after inoculation. In addition, cytokine and chemokine expression in placentomes from experimentally infected cows was evaluated. Expression of proinflammatory genes by trophoblastic cells was suppressed at 4 h after inoculation, whereas a significant upregulation of CXC chemokines, namely, CXCL6 (GCP-2) and CXCL8 (interleukin 8), was observed at 12 but not at 6 h after inoculation. Placentomes of experimentally infected cows had a similar profile of chemokine expression, with upregulation of CXCL6 and CXCL8. Our data indicate that B. abortus modulates the innate immune response by trophoblastic cells, suppressing the expression of proinflammatory mediators during the early stages of infection that is followed by a delayed and mild expression of proinflammatory chemokines, which is similar to the profile of chemokine expression in the placentomes of experimentally infected cows. This trophoblastic response is likely to contribute to the pathogenesis of B. abortus-induced placentitis.
authors.affiliation: Escola de Veterinária da UFMG, Depto. Clínica e Cirurgia Veterinária, Av. Antônio Carlos, 6627, 31270-901 Belo Horizonte, MG, Brazil.
authors.forename: Alcina V
authors.initials: AV
authors.lastname: Carvalho Neta
authors.forename: Ana P R
authors.initials: AP
authors.lastname: Stynen
authors.forename: Tatiane A
authors.initials: TA
authors.lastname: Paixão
authors.forename: Karina L
authors.initials: KL
authors.lastname: Miranda
authors.forename: Fabiana L
authors.initials: FL
authors.lastname: Silva
authors.forename: Christelle M
authors.initials: CM
authors.lastname: Roux
authors.forename: Renée M
authors.initials: RM
authors.lastname: Tsolis
authors.forename: Robin E
authors.initials: RE
authors.lastname: Everts
authors.forename: Harris A
authors.initials: HA
authors.lastname: Lewin
authors.forename: L Garry
authors.initials: LG
authors.lastname: Adams
authors.forename: Alex F
authors.initials: AF
authors.lastname: Carvalho
authors.forename: Andrey P
authors.initials: AP
authors.lastname: Lage
authors.forename: Renato L
authors.initials: RL
authors.lastname: Santos
mesh_terms: D000818:Animals; D002003:Brucella abortus / Q000276:immunology*; D002417:Cattle; D016207:Cytokines / Q000096:biosynthesis / Q000235:genetics; D015536:Down-Regulation; D005260:Female; D020869:Gene Expression Profiling; D054884:Host-Pathogen Interactions / Q000276:immunology*; D020411:Oligonucleotide Array Sequence Analysis; D010920:Placenta / Q000473:pathology; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013997:Time Factors; D014327:Trophoblasts / Q000276:immunology* / Q000378:metabolism / Q000382:microbiology*; D015854:Up-Regulation
chemical_list: D016207:Cytokines