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2017 ; 7
(1
): 1206
Nephropedia Template TP
Sci Rep
2017[Apr]; 7
(1
): 1206
PMID28446778
show ga
Candida species are commensals but some develop biofilms in prosthetic materials
and host surfaces that may represent up to 30% of deaths related to infections,
particularly in immunosuppressed patients. Tumor necrosis factor (TNF) exhibits a
plethora of functions in host defense mechanisms whereas excessive release of TNF
in inflammation promotes tissue damage. Cytokines released in an inflammatory
milieu may influence the development of microorganisms either by promoting their
growth or displaying antimicrobial activity. In protozoa, TNF may affect growth
by coupling through a lectin-like domain, distinct from TNF receptors. TNF was
also shown to interact with bacteria via a mechanism that does not involve
classical TNF receptors. Using an in vitro C. albicans biofilm model, we show
that TNF dose-dependently prevents biofilm development that is blocked by
incubating TNF with N,N'-diacetylchitobiose, a major carbohydrate component of C.
albicans cell wall. This finding represents a relevant and hitherto unknown
mechanism that adds to the understanding of why TNF blockade is associated with
opportunistic C. albicans infections.
|Animals
[MESH]
|Anti-Infective Agents/*metabolism
[MESH]
|Biofilms/*drug effects/*growth & development
[MESH]