PMID- 8926044
OWN - NLM
STAT- MEDLINE
DCOM- 19961025
LR  - 20211203
IS  - 0360-3997 (Print)
IS  - 0360-3997 (Linking)
VI  - 20
IP  - 1
DP  - 1996 Feb
TI  - Candida albicans induces the release of inflammatory mediators from human 
      peripheral blood monocytes.
PG  - 107-22
AB  - Candida albicans (C. albicans) is a major nosocomial pathogen. We examined 
      arachidonic acid (AA) and cytokine production by monocytes stimulated with C. 
      albicans. [14C]-AA labeled monocytes released 8.9 +/- 2.3% of the incorporated AA 
      following stimulation with live C. albicans (C. albicans: monocyte of 16:1) (P = 
      0.0002). Prior studies indicate that soluble alpha-mannans and beta-glucans 
      antagonize mannose and beta-glucan receptors, respectively. Preincubation of 
      monocytes with alpha-mannan (100 micrograms/ml) caused 45.8 +/- 5.7% inhibition 
      of [14C]-AA release, whereas beta-glucan (100 micrograms/ml) yielded 43.7 +/- 
      6.0% inhibition (P < 0.05 for each compared to control). Additionally, monocytes 
      stimulated with C. albicans also released interleukin-1 beta (IL-1 beta), tumor 
      necrosis factor-alpha (TNF alpha), interleukin-6 (IL-6) and interleukin-8 (IL-8). 
      However, alpha-mannan or beta-glucan failed to inhibit IL-1 beta release. These 
      data indicate that C. albicans induces monocytes to release AA and inflammatory 
      cytokines. Furthermore, AA, but not cytokine liberation, is partially mediated by 
      alpha-mannan and beta-glucan components of the fungus.
FAU - Castro, M
AU  - Castro M
AD  - Division of Pulmonary and Critical Care, Mayo Clinic, Rochester, MN, USA.
FAU - Bjoraker, J A
AU  - Bjoraker JA
FAU - Rohrbach, M S
AU  - Rohrbach MS
FAU - Limper, A H
AU  - Limper AH
LA  - eng
GR  - AI 34336/AI/NIAID NIH HHS/United States
GR  - HL-28669/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Inflammation
JT  - Inflammation
JID - 7600105
RN  - 0 (Cytokines)
RN  - 0 (Glucans)
RN  - 0 (Interleukin-1)
RN  - 0 (Interleukin-6)
RN  - 0 (Interleukin-8)
RN  - 0 (Lectins, C-Type)
RN  - 0 (Mannans)
RN  - 0 (Mannose Receptor)
RN  - 0 (Mannose-Binding Lectins)
RN  - 0 (Oligosaccharides)
RN  - 0 (Receptors, Cell Surface)
RN  - 0 (Receptors, Immunologic)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (beta-glucan receptor)
RN  - 0 (laminariheptaose)
RN  - 27YG812J1I (Arachidonic Acid)
SB  - IM
MH  - Arachidonic Acid/*metabolism
MH  - Candida albicans/chemistry/*physiology
MH  - Cell Wall/chemistry
MH  - Cells, Cultured
MH  - Cytokines/biosynthesis/genetics/*metabolism
MH  - Gene Expression Regulation/drug effects
MH  - Glucans/*pharmacology
MH  - Humans
MH  - Interleukin-1/metabolism
MH  - Interleukin-6/metabolism
MH  - Interleukin-8/metabolism
MH  - *Lectins, C-Type
MH  - Mannans/*pharmacology
MH  - Mannose Receptor
MH  - *Mannose-Binding Lectins
MH  - Monocytes/drug effects/*metabolism
MH  - Oligosaccharides/pharmacology
MH  - Receptors, Cell Surface/drug effects/physiology
MH  - Receptors, Immunologic/drug effects/physiology
MH  - Tumor Necrosis Factor-alpha/metabolism
EDAT- 1996/02/01 00:00
MHDA- 1996/02/01 00:01
CRDT- 1996/02/01 00:00
PHST- 1996/02/01 00:00 [pubmed]
PHST- 1996/02/01 00:01 [medline]
PHST- 1996/02/01 00:00 [entrez]
AID - 10.1007/BF01487749 [doi]
PST - ppublish
SO  - Inflammation. 1996 Feb;20(1):107-22. doi: 10.1007/BF01487749.