THE EFFECTS OF MALASSEZIA ON PRO-INFLAMMATORY CYTOKINE PRODUCTION BY HUMAN PERIPHERAL-BLOOD MONONUCLEAR-CELLS IN-VITRO

Citation
S. Kesavan et al., THE EFFECTS OF MALASSEZIA ON PRO-INFLAMMATORY CYTOKINE PRODUCTION BY HUMAN PERIPHERAL-BLOOD MONONUCLEAR-CELLS IN-VITRO, MEDICAL MYCOLOGY, 36(2), 1998, pp. 97-106
Citations number
34
Categorie Soggetti
Mycology,"Veterinary Sciences
Journal title
ISSN journal
13693786
Volume
36
Issue
2
Year of publication
1998
Pages
97 - 106
Database
ISI
SICI code
1369-3786(1998)36:2<97:TEOMOP>2.0.ZU;2-J
Abstract
Malassezia spp., the causative agents of pityriasis versicolor, are me mbers of the normal human cutaneous :microflora. Utilizing a combinati on of both enzyme-linked immunosorbent assay (ELISA) and bioassay, we have investigated the ability of both formalin-preserved and viable Ma lassezia (serovars A, B and C) to modulate proinflammatory cytokine (I L-6, IL-1 beta and TNF-alpha) release by human peripheral blood mononu clear cells (PBMNC) in vitro, over a 48-h co-incubation period. The re sults demonstrated that formalin-preserved Malassezia (serovars A, B a nd C) at mid-exponential phase were generally able to induce a pro-inf lammatory cytokine response at a yeast cell to PBMNC ratio of 1:1. In addition, the results consistently demonstrated that at a yeast cell t o PBMNC ratio of 20:1, formalin-preserved Malassezia, irrespective of serovar, growth phase or PBMNC donor, were capable of significantly (P <0.05) decreasing the release of both immunochemical IL-6 and IL-1 bet a plus bioactive IL-1 beta and TNF-alpha below that of unstimulated cu lture medium control values. This was apparent following 24- and 48-h co-incubation times, where maximal cytokine production was detected af ter 24 h. Similar results were obtained for the effect of viable Malas sezia on pro-inflammatory cytokine release by PBMNC. Our results sugge st that a possible inhibitory component, present perhaps within the ce ll wall of Malassezia, was responsible for this depressive effect on p ro-inflammatory cytokine production.