PROINFLAMMATORY PROPERTIES OF MOLLUSCUM BODIES

Citation
H. Takematsu et H. Tagami, PROINFLAMMATORY PROPERTIES OF MOLLUSCUM BODIES, Archives of dermatological research, 287(1), 1994, pp. 102-106
Citations number
27
Categorie Soggetti
Dermatology & Venereal Diseases
ISSN journal
03403696
Volume
287
Issue
1
Year of publication
1994
Pages
102 - 106
Database
ISI
SICI code
0340-3696(1994)287:1<102:PPOMB>2.0.ZU;2-8
Abstract
Molluscum contagiosum, a condition characterized by benign viral tumou rs, occasionally becomes inflamed and regresses spontaneously, an even t probably initiated by a host cell-mediated immune rejection against the lesion, but it inevitably involves the disruption of the epidermal tissue to expose the molluscum bodies to the tissue fluids of the der mis. It has been suggested that the molluscum bodies induce inflammati on by a mechanism similar to that involved in ruptured epidermal cysts or in acne. Despite the occasional development of inflammation in mol luscum contagiosum, the proinflammatory properties of molluscum bodies have never been studied in vitro. Thus, in the present study we sough t to determine whether molluscum bodies exert a proinflammatory effect by inducing neutrophil chemotaxis. When exposed to fresh serum in vit ro, water-insoluble components of molluscum bodies activated the alter native complement pathway to produce chemotactic C5a/C5a des Arg. We a lso found that an aqueous extract of molluscum bodies exerted potent c hemotactic activity for neutrophils. Remarkably high amounts of the im munoreactive proinflammatory cytokines IL-8 and GRO alpha were present in the extract even when compared with psoriatic scale extracts. Gel filtration HPLC of the extract demonstrated the presence of neutrophil chemotactic activity over a wide range of molecular mass. These data suggest that disruption of the epidermal wall of molluscum bodies indu ces acute inflammatory changes by activation of the alternative comple ment pathway on exposure to the tissue fluids, and that the molluscum bodies themselves release proinflammatory cytokines and other neutroph il chemotactic factors on decomposition.