PMID- 8381770
OWN - NLM
STAT- MEDLINE
DCOM- 19930318
LR  - 20210526
IS  - 0019-9567 (Print)
IS  - 1098-5522 (Electronic)
IS  - 0019-9567 (Linking)
VI  - 61
IP  - 3
DP  - 1993 Mar
TI  - Staphylococcus aureus toxic shock syndrome toxin 1 and Streptococcus pyogenes 
      erythrogenic toxin A modulate inflammatory mediator release from human 
      neutrophils.
PG  - 1055-61
AB  - We studied the influence of staphylococcal toxic shock syndrome toxin 1 and 
      streptococcal erythrogenic (pyrogenic) toxin A (ETA) on intact and 
      digitonin-permeabilized human polymorphonuclear granulocytes (PMNs). As was shown 
      by reversed-phase high-performance liquid chromatography analysis, toxic shock 
      syndrome toxin 1 or ETA alone, in the absence of any additional stimulus, did not 
      induce the generation of the chemoattractant leukotriene B4 (LTB4) from PMNs in a 
      wide range of concentrations. In addition, pretreatment of intact PMNs with 
      either toxin potentiated formyl-methionyl-leucyl-phenylalanine (fMLP)- and washed 
      Staphylococcus aureus cell-induced generation of LTB4 in a time- and 
      dose-dependent manner. This increase included LTB4 as well as its inactive 
      omega-oxidated compounds. Further studies revealed evidence that toxin exposure 
      was accompanied by enhanced cellular receptor expression for fMLP as well as for 
      LTB4. The intrinsic GTPase activity of membrane fractions was modulated by both 
      toxins. Short-term incubation with ETA increased the GTPase activity of PMNs up 
      to 141%. Inhibitory effects were obtained when GTP-binding protein functions were 
      stimulated with sodium fluoride (NaF). In addition, specific binding of Gpp(NH)p 
      to GTP-binding protein was inhibited by both toxins during the first 10 min of 
      incubation and was restored at later times of incubation. Our data therefore 
      suggest that both toxins significantly affect the signal transduction pathways of 
      human PMNs, which results in immunomodulatory functions.
FAU - Hensler, T
AU  - Hensler T
AD  - Medizinische Mikrobiologie und Immunologie, AG Infektabwehrmechanismen, 
      Ruhr-Universitat Bochum, Germany.
FAU - Koller, M
AU  - Koller M
FAU - Geoffroy, C
AU  - Geoffroy C
FAU - Alouf, J E
AU  - Alouf JE
FAU - Konig, W
AU  - Konig W
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Infect Immun
JT  - Infection and immunity
JID - 0246127
RN  - 0 (Bacterial Proteins)
RN  - 0 (Bacterial Toxins)
RN  - 0 (Enterotoxins)
RN  - 0 (Exotoxins)
RN  - 0 (Membrane Proteins)
RN  - 0 (Receptors, Formyl Peptide)
RN  - 0 (Receptors, Immunologic)
RN  - 0 (SpeA protein, Streptococcus pyogenes)
RN  - 0 (Superantigens)
RN  - 0 (enterotoxin F, Staphylococcal)
RN  - 0 (erythrogenic toxin)
RN  - 1HGW4DR56D (Leukotriene B4)
RN  - 37H9VM9WZL (Calcimycin)
RN  - 59880-97-6 (N-Formylmethionine Leucyl-Phenylalanine)
RN  - 8ZYQ1474W7 (Sodium Fluoride)
RN  - EC 3.6.1.- (GTP-Binding Proteins)
SB  - IM
MH  - *Bacterial Proteins
MH  - *Bacterial Toxins
MH  - Calcimycin/pharmacology
MH  - Enterotoxins/*immunology
MH  - Exotoxins/*immunology
MH  - GTP-Binding Proteins/metabolism
MH  - Humans
MH  - In Vitro Techniques
MH  - Leukotriene B4/metabolism
MH  - *Membrane Proteins
MH  - N-Formylmethionine Leucyl-Phenylalanine/pharmacology
MH  - Neutrophils/*immunology
MH  - Receptors, Formyl Peptide
MH  - Receptors, Immunologic/metabolism
MH  - Sodium Fluoride/pharmacology
MH  - Staphylococcus aureus/*immunology
MH  - Streptococcus pyogenes/*immunology
MH  - *Superantigens
PMC - PMC302838
EDAT- 1993/03/01 00:00
MHDA- 1993/03/01 00:01
PMCR- 1993/03/01
CRDT- 1993/03/01 00:00
PHST- 1993/03/01 00:00 [pubmed]
PHST- 1993/03/01 00:01 [medline]
PHST- 1993/03/01 00:00 [entrez]
PHST- 1993/03/01 00:00 [pmc-release]
AID - 10.1128/iai.61.3.1055-1061.1993 [doi]
PST - ppublish
SO  - Infect Immun. 1993 Mar;61(3):1055-61. doi: 10.1128/iai.61.3.1055-1061.1993.