PMID- 20465563
OWN - NLM
STAT- MEDLINE
DCOM- 20100816
LR  - 20211020
IS  - 1365-2567 (Electronic)
IS  - 0019-2805 (Print)
IS  - 0019-2805 (Linking)
VI  - 130
IP  - 4
DP  - 2010 Aug
TI  - Staphylococcal enterotoxin A induction of pro-inflammatory cytokines and 
      lethality in mice is primarily dependent on MyD88.
PG  - 516-26
LID - 10.1111/j.1365-2567.2010.03249.x [doi]
AB  - Staphylococcal enterotoxin (SE) -induced toxic shock is triggered by inflammatory 
      cytokine signal amplification after SE binding to major histocompatibility 
      complex class II molecules on antigen-presenting cells and T-cell receptors. 
      Identifying host cellular elements contributing to this pro-inflammatory signal 
      amplification is critical for developing a strategy for therapeutic intervention. 
      Myeloid differentiation primary-response protein 88 (MyD88) is an intracellular 
      signalling adaptor protein primarily known for mediating pro-inflammatory 
      cytokine responses. We investigated the role of MyD88 in staphylococcal 
      enterotoxin A (SEA) -treated cell cultures and mouse models of toxic shock. Our 
      results demonstrated that elevated levels of tumour necrosis factor-alpha, 
      interferon-gamma, interleukin-1alpha/beta (IL-1alpha/beta), IL-2 and IL-6 
      production correlated with up-regulation of MyD88 after treatment of spleen cells 
      and mice with SEA alone or in combination with lipopolysaccharide (LPS). The 
      SEA-induced lethality was also observed in (LPS-independent) 
      D-galactosamine-sensitized mice. While LPS potentiated SEA-induced cytokine 
      responses, D-galactosamine treatment had no additive effect. Most importantly, 
      our results demonstrated that MyD88(-/-) mice were resistant to SEA-induced toxic 
      shock and had reduced pro-inflammatory cytokine responses. These results suggest 
      that SEA-induced lethality is primarily dependent on MyD88. Our findings offer an 
      important insight on potential therapeutic treatment of SEA-induced toxic shock 
      targeting MyD88.
FAU - Kissner, Teri L
AU  - Kissner TL
AD  - Department of Immunology, United States Army Medical Research Institute of 
      Infectious Diseases, Frederick, MD, USA.
FAU - Cisney, Emily D
AU  - Cisney ED
FAU - Ulrich, Robert G
AU  - Ulrich RG
FAU - Fernandez, Stefan
AU  - Fernandez S
FAU - Saikh, Kamal U
AU  - Saikh KU
LA  - eng
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
DEP - 20100503
PL  - England
TA  - Immunology
JT  - Immunology
JID - 0374672
RN  - 0 (Cytokines)
RN  - 0 (Enterotoxins)
RN  - 0 (Myd88 protein, mouse)
RN  - 0 (Myeloid Differentiation Factor 88)
RN  - 0 (NF-kappa B)
RN  - 37337-57-8 (enterotoxin A, Staphylococcal)
SB  - IM
MH  - Animals
MH  - Cells, Cultured
MH  - Cytokines/biosynthesis/*immunology
MH  - Enterotoxins/*toxicity
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Myeloid Differentiation Factor 88/deficiency/*immunology
MH  - NF-kappa B/immunology/metabolism
MH  - Spleen/immunology
MH  - Staphylococcus/drug effects/*immunology
PMC - PMC2913262
EDAT- 2010/05/15 06:00
MHDA- 2010/08/17 06:00
PMCR- 2011/08/01
CRDT- 2010/05/15 06:00
PHST- 2010/05/15 06:00 [entrez]
PHST- 2010/05/15 06:00 [pubmed]
PHST- 2010/08/17 06:00 [medline]
PHST- 2011/08/01 00:00 [pmc-release]
AID - IMM3249 [pii]
AID - 10.1111/j.1365-2567.2010.03249.x [doi]
PST - ppublish
SO  - Immunology. 2010 Aug;130(4):516-26. doi: 10.1111/j.1365-2567.2010.03249.x. Epub 
      2010 May 3.