PMID- 10329825
OWN - NLM
STAT- MEDLINE
DCOM- 19990608
LR  - 20190723
IS  - 0091-6749 (Print)
IS  - 0091-6749 (Linking)
VI  - 103
IP  - 5 Pt 1
DP  - 1999 May
TI  - Staphylococcal toxic shock syndrome toxin-1 inhibits monocyte apoptosis.
PG  - 895-900
AB  - BACKGROUND: Chronic atopic dermatitis (AD) lesions are associated with 
      colonization by exotoxin-producing Staphylococcus aureus. Evidence suggests that 
      cytokine production in AD, particularly of GM-CSF, prolongs survival of both 
      peripheral blood monocytes and dermal monocyte-macrophages, the predominate 
      inflammatory cell in lesions caused by chronic AD. OBJECTIVE: We sought to 
      determine whether the staphylococcal exotoxin, toxic shock syndrome toxin-1 
      (TSST-1), could stimulate prosurvival cytokine production in monocytes and 
      thereby inhibit apoptosis. METHODS: Cultures of peripheral blood monocytes from 
      normal donors and subjects with AD were incubated with various concentrations of 
      TSST-1, and the incidence of apoptosis was assessed by examining cytospin 
      preparations and the appearance of hypodiploid DNA in the flow cytometer. Culture 
      supernatants were analyzed for GM-CSF, IL-1beta, and TNF-alpha by ELISA. RESULTS: 
      TSST-1, in a concentration-dependent manner starting at 0.1 pg/mL, significantly 
      inhibited monocyte apoptosis and resulted in the production of the prosurvival 
      cytokines GM-CSF, IL-1beta, and TNF-alpha. In coculture conditions with 
      conditioned media from TSST-1-stimulated monocytes, with or without neutralizing 
      antibody to the various cytokines, the data show GM-CSF production was 
      responsible for the inhibition of apoptosis. CONCLUSIONS: The data strongly 
      suggest that staphylococcal exotoxins known to colonize skin lesions on patients 
      with chronic AD may induce the production of GM-CSF, resulting in inhibition of 
      monocyte-macrophage apoptosis, and thereby contribute to the chronicity of this 
      inflammatory disease.
FAU - Bratton, D L
AU  - Bratton DL
AD  - Division of Allergy-Immunology, Department of Pediatrics, and the Department of 
      Medicine, National Jewish Medical and Research Center, Denver, CO, USA.
FAU - May, K R
AU  - May KR
FAU - Kailey, J M
AU  - Kailey JM
FAU - Doherty, D E
AU  - Doherty DE
FAU - Leung, D Y
AU  - Leung DY
LA  - eng
GR  - AR41256/AR/NIAMS NIH HHS/United States
GR  - GM48211/GM/NIGMS NIH HHS/United States
GR  - HL34303/HL/NHLBI NIH HHS/United States
GR  - etc.
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Allergy Clin Immunol
JT  - The Journal of allergy and clinical immunology
JID - 1275002
RN  - 0 (Bacterial Toxins)
RN  - 0 (Enterotoxins)
RN  - 0 (Superantigens)
RN  - 0 (enterotoxin F, Staphylococcal)
RN  - 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor)
SB  - IM
MH  - Apoptosis/drug effects
MH  - *Bacterial Toxins
MH  - Dermatitis, Atopic/blood/pathology
MH  - Dose-Response Relationship, Drug
MH  - Enterotoxins/*pharmacology
MH  - Granulocyte-Macrophage Colony-Stimulating Factor/biosynthesis/blood
MH  - Humans
MH  - Monocytes/*cytology
MH  - Staphylococcus aureus/immunology
MH  - *Superantigens
EDAT- 1999/05/18 00:00
MHDA- 1999/05/18 00:01
CRDT- 1999/05/18 00:00
PHST- 1999/05/18 00:00 [pubmed]
PHST- 1999/05/18 00:01 [medline]
PHST- 1999/05/18 00:00 [entrez]
AID - S0091-6749(99)70435-5 [pii]
AID - 10.1016/s0091-6749(99)70435-5 [doi]
PST - ppublish
SO  - J Allergy Clin Immunol. 1999 May;103(5 Pt 1):895-900. doi: 
      10.1016/s0091-6749(99)70435-5.