title: Downregulation of human polymorphonuclear cell activities exerted by microorganisms belonging to the alpha-2 subgroup of Proteobacteria (Afipia felis and Rochalimaea henselae).
abstract: Intracellular pathogens have evolved effective mechanisms in order to survive in an intracellular environment, thus avoiding destruction by phagocytic cells. In this regard, a correlation between resistance to phagocytic killing and expression of pathogenic potency has been established. In this report, we have studied the interaction between human polymorphonuclear cells (PMN) and two gram-negative microorganisms, Afipia felis and Rochalimaea henselae, which belong to the alpha-2 subgroup of the class Proteobacteria. A. falis has been previously proposed as the causative agent of Cat Scratch Disease (CSD), but several recent lines of evidence attribute a major role to R. henselae. Of note, CSD is a syndrome characterized by a chronic lymphoadenopathy, involving macrophages and endothelial cells with a progression towards a granulomatous process and/or angiogenesis. Since members of the alpha-2 subgroup of Proteobacteria have the property to survive intracellularly, we have evaluated the effects exerted by A. felis and R. henselae on human PMN in terms of chemotaxis locomotion, degranulation and oxidative metabolism. Results will show an impairment of PMN activities as a consequence of the challenge with both microrganisms. In particular, inhibition of PMN oxidative function occurred either as result of a direct exposure to both A. felis and R. henselae or when PMN were primed by bacteria for the N-formyl-methionyl-leucyl-phenylalanine enhancement of the oxidative burst. These findings may account for the ability of A. felis and R. henselae to survive within PMN as expression of a further mechanism of pathogenic potency, influencing also the nature and the evolution of inflammatory response in the lesion sites.
authors.affiliation: Institutes of Medical Microbiology, General Pathology, University of Bari, Italy.
authors.forename: D
authors.initials: D
authors.lastname: Fumarola
authors.forename: S
authors.initials: S
authors.lastname: Pece
authors.forename: R
authors.initials: R
authors.lastname: Fumarulo
authors.forename: R
authors.initials: R
authors.lastname: Petruzzelli
authors.forename: B
authors.initials: B
authors.lastname: Greco
authors.forename: G
authors.initials: G
authors.lastname: Giuliani
authors.forename: A B
authors.initials: AB
authors.lastname: Maffione
authors.forename: E
authors.initials: E
authors.lastname: Jirillo
mesh_terms: D018416:Bartonella henselae / Q000276:immunology*; D002372:Cat-Scratch Disease / Q000382:microbiology; D015550:Cell Degranulation / Q000502:physiology; D002634:Chemotaxis, Leukocyte / Q000502:physiology; D015536:Down-Regulation / Q000276:immunology; D006090:Gram-Negative Bacteria / Q000276:immunology*; D006801:Humans; D066298:In Vitro Techniques; D008163:Luminescent Measurements; D009504:Neutrophils / Q000276:immunology / Q000382:microbiology*; D017382:Reactive Oxygen Species / Q000378:metabolism; D015054:Zymosan / Q000494:pharmacology
chemical_list: D017382:Reactive Oxygen Species; D015054:Zymosan