PMID- 9893039
OWN - NLM
STAT- MEDLINE
DCOM- 19990205
LR  - 20190512
IS  - 0019-2805 (Print)
IS  - 1365-2567 (Electronic)
IS  - 0019-2805 (Linking)
VI  - 95
IP  - 4
DP  - 1998 Dec
TI  - Distinct functions of interferon-gamma for chemokine expression in models of 
      acute lung inflammation.
PG  - 512-21
AB  - Challenge of the immune system with bacterial superantigens or endotoxin induces 
      the systemic release of cytokines followed by lethal septic shock. The lung is 
      particularly susceptible to systemic toxin exposure resulting in acute leucocyte 
      infiltration and vascular damage. In the present study, the functions of 
      interferon-gamma (IFN-gamma) and tumour necrosis factor (TNF) for chemokine 
      regulation during acute lung inflammation were examined. Following administration 
      of the superantigen, staphylococcal enterotoxin B (SEB), lung mRNA levels of the 
      chemokines cytokine-induced neutrophil chemo-attractant (KC), 
      lipopolysaccharide-induced CXC chemokine (LIX), macrophage chemotactic protein-1 
      (MCP-1), macrophage inflammatory protein (MIP)-1alpha and MIP-2 were increased to 
      a similar extent both in controls and in mice deficient for the IFN-gamma or 55 
      000 MW TNF receptors. In contrast, interferon-inducible protein-10 (IP-10) and 
      monokine induced by IFN-gamma (Mig) mRNA expression was markedly reduced in mice 
      deficient for IFN-gamma or IFN-gamma receptor, but not in 55 000 MW TNF receptor 
      knockout mice. In situ hybridization experiments demonstrated that IP-10 was 
      highly expressed in lung interstitial macrophages of C57BL/6, but not of 
      IFN-gamma receptor-deficient mice. In contrast to SEB administration, treatment 
      with lipopolysaccharide resulted in a strong induction of IP-10 and Mig in 
      IFN-gamma receptor-deficient mice. Together, these results establish a critical 
      function of IFN-gamma for chemokine induction in acute lung inflammation that is 
      dependent on the nature of the inflammatory stimulus.
FAU - Neumann, B
AU  - Neumann B
AD  - Department of Surgery, Klinikum rechts der Isar, Technical University of Munich, 
      Munich, Germany.
FAU - Emmanuilidis, K
AU  - Emmanuilidis K
FAU - Stadler, M
AU  - Stadler M
FAU - Holzmann, B
AU  - Holzmann B
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Immunology
JT  - Immunology
JID - 0374672
RN  - 0 (Chemokine CXCL10)
RN  - 0 (Chemokines)
RN  - 0 (Chemokines, CC)
RN  - 0 (Chemokines, CXC)
RN  - 0 (Enterotoxins)
RN  - 0 (Receptors, Interferon)
RN  - 0 (Superantigens)
RN  - 39424-53-8 (enterotoxin B, staphylococcal)
RN  - 82115-62-6 (Interferon-gamma)
SB  - IM
MH  - Acute Disease
MH  - Animals
MH  - Chemokine CXCL10
MH  - Chemokines/analysis/*biosynthesis
MH  - Chemokines, CC/analysis/biosynthesis
MH  - Chemokines, CXC/analysis/biosynthesis/immunology
MH  - Enterotoxins/*pharmacology
MH  - In Situ Hybridization
MH  - Interferon-gamma/*physiology
MH  - Lung/*immunology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Pneumonia, Bacterial/*immunology
MH  - Receptors, Interferon/metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Staphylococcal Infections/*immunology
MH  - Staphylococcus aureus
MH  - Superantigens/pharmacology
PMC - PMC1364346
EDAT- 1999/01/20 00:00
MHDA- 1999/01/20 00:01
PMCR- 1999/12/01
CRDT- 1999/01/20 00:00
PHST- 1999/01/20 00:00 [pubmed]
PHST- 1999/01/20 00:01 [medline]
PHST- 1999/01/20 00:00 [entrez]
PHST- 1999/12/01 00:00 [pmc-release]
AID - 10.1046/j.1365-2567.1998.00643.x [doi]
PST - ppublish
SO  - Immunology. 1998 Dec;95(4):512-21. doi: 10.1046/j.1365-2567.1998.00643.x.