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Infect. Immun., 04 1995, 1223-1228, Vol 63, No. 4
CE Walters, E Ingham, EA Eady, JH Cove, JN Kearney and WJ Cunliffe
The ability of a range of skin commensal microorganisms to modulate
interleukin-1 (IL-1) release by cultured human keratinocytes and peripheral
blood mononuclear cells (PBMCs) was investigated by a combination of
enzyme-linked immunosorbent assays and bioassays. Three fractions
(formaldehyde-treated whole cells, culture supernatants, and cellular
fractions) were prepared from Propionibacterium acnes, Propionibacterium
granulosum, Staphylococcus epidermidis, Staphylococcus capitis,
Staphylococcus hominis, and Malassezia furfur serovar B. The levels of
immunochemical IL-1 alpha released by cultured keratinocytes during
coincubations with these microbial fractions ranged from 0 to 136 pg/ml and
were maximal after 72 h. No microbial fraction consistently upregulated
immunochemical IL-1 alpha release by freshly isolated keratinocytes from
two donors and a transformed cell line, all of which produced the cytokine
constitutively to various extents. Bioassays revealed that most of the IL-1
released was biologically inactive. In contrast, whole cells of
formaldehyde-treated P. granulosum and S. epidermidis significantly
stimulated release of IL- 1 beta by PBMCs from three donors compared with
the negative control (culture medium). Release was maximal at 24 h.
Coincubation with intact cells of the yeast M. furfur significantly
decreased levels of IL-1 beta below the values for the negative control by
PBMCs from all three donors. There was good correlation between bioassay
data and immunoassay data for IL-1 beta, and the depressive effect of M.
furfur cells on cytokine production by all three cultures of PBMCs was
mirrored in the levels of bioactive cytokine. This reduction in IL-1 beta
release by PBMCs by M. furfur may provide an explanation why dermatoses
thought to be caused by this yeast are essentially noninflammatory or only
mildly inflammatory.
Copyright © 1995, American Society for Microbiology
In vitro modulation of keratinocyte-derived interleukin-1 alpha (IL-1 alpha) and peripheral blood mononuclear cell-derived IL-1 beta release in response to cutaneous commensal microorganisms
Department of Microbiology, University of Leeds, United Kingdom.
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