Abstract
lntracellular 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 α2 subgroup of the class Proteobacteria. A. felis 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 α2 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.
| Original language | English |
|---|---|
| Pages (from-to) | 449-461 |
| Number of pages | 13 |
| Journal | Immunopharmacology and Immunotoxicology |
| Volume | 16 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - 1994 |
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ASJC Scopus subject areas
- Immunology
- Immunology and Allergy
- Pharmacology
- Toxicology
- Health, Toxicology and Mutagenesis
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Downregulation of human polymorphonuclear cell activities exerted by microorganisms belonging to the α2 subgroup of proteobacteria (afipia fs and rochallmaea henselae). / Fumarola, D.; Pece, S.; Fumarulo, R.; Petruzzelli, R.; Greco, B.; Giuliani, G.; Maffione, A. B.; Jirillo, E.
In: Immunopharmacology and Immunotoxicology, Vol. 16, No. 3, 1994, p. 449-461.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Downregulation of human polymorphonuclear cell activities exerted by microorganisms belonging to the α2 subgroup of proteobacteria (afipia fs and rochallmaea henselae)
AU - Fumarola, D.
AU - Pece, S.
AU - Fumarulo, R.
AU - Petruzzelli, R.
AU - Greco, B.
AU - Giuliani, G.
AU - Maffione, A. B.
AU - Jirillo, E.
PY - 1994
Y1 - 1994
N2 - lntracellular 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 α2 subgroup of the class Proteobacteria. A. felis 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 α2 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.
AB - lntracellular 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 α2 subgroup of the class Proteobacteria. A. felis 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 α2 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.
UR - http://www.scopus.com/inward/record.url?scp=0027981892&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0027981892&partnerID=8YFLogxK
U2 - 10.3109/08923979409007104
DO - 10.3109/08923979409007104
M3 - Article
C2 - 7528238
AN - SCOPUS:0027981892
VL - 16
SP - 449
EP - 461
JO - Immunopharmacology and Immunotoxicology
JF - Immunopharmacology and Immunotoxicology
SN - 0892-3973
IS - 3
ER -