title: Interactions between professional phagocytes and Brucella spp.
abstract: Induced pathogenicity in animals and humans differs considerably. This review is devoted to the relations between Brucella spp. and professional phagocytes, particularly macrophages and macrophagic cell lines in vitro. Although numerous studies have been reported, the type of ingestion by macrophages, the receptor involved, and the molecular mechanisms, are poorly understood. The ability of most Brucella species to actively inhibit their ingestion by neutrophils or macrophages has been proposed as an explanation for the poor rate of in vitro phagocytosis and in vivo alteration of the phagocytic cells. Oxidative burst plays a significant role in the antibacterial processes of phagocytic cells. The effects of whole or fractioned B. abortus on the ability of neutrophils to induce an oxidative burst in response to stimulation with opsonized zymosan particles were examined. Besides oxygen-based killing, the phagocytic cells have developed other types of defence, including hydrolytic enzymes and reactive halides. Inside the cell, the bacteria encounter new environmental conditions. Their survival is conditioned by an adaptation to this new situation. Pathogens that have acquired the ability to multiply within macrophages should synthesize products specifically interacting with the host cell defence system. Survival of intracellular pathogens is closely linked to the mechanisms of evasion from cellular defences. Brucellae stay in membrane bound vacuoles called phagosomes, but the exact nature and the maturation pathway of this compartment have not yet been understood. Macrophages play a central role in the evolution of brucellosis; this first interaction between the pathogens and the cell will determine the course of the disease. There are natural differences between brucellae species regarding macrophage response to the bacteria.
authors.affiliation: INSERM U-431, Université Montpellier II, France. liautard@crit.univ-montp2.fr
authors.forename: J P
authors.initials: JP
authors.lastname: Liautard
authors.forename: A
authors.initials: A
authors.lastname: Gross
authors.forename: J
authors.initials: J
authors.lastname: Dornand
authors.forename: S
authors.initials: S
authors.lastname: Köhler
mesh_terms: D000818:Animals; D002002:Brucella / Q000502:physiology*; D002006:Brucellosis / Q000276:immunology* / Q000382:microbiology; D002417:Cattle; D002460:Cell Line; D016207:Cytokines / Q000502:physiology; D003594:Cytoplasmic Granules / Q000201:enzymology / Q000378:metabolism; D006801:Humans; D007113:Immunity, Innate; D008264:Macrophages / Q000382:microbiology / Q000502:physiology; D051379:Mice; D009504:Neutrophils / Q000201:enzymology / Q000382:microbiology / Q000502:physiology; D009195:Peroxidase / Q000502:physiology; D010586:Phagocytes / Q000201:enzymology / Q000382:microbiology / Q000502:physiology*; D010587:Phagocytosis; D016897:Respiratory Burst; D013045:Species Specificity; D014617:Vacuoles / Q000382:microbiology
chemical_list: D016207:Cytokines; D009195:Peroxidase