PMID- 9022006
OWN - NLM
STAT- MEDLINE
DCOM- 19970305
LR  - 20131121
IS  - 0014-2980 (Print)
IS  - 0014-2980 (Linking)
VI  - 27
IP  - 1
DP  - 1997 Jan
TI  - Regulated production of the interferon-gamma-inducible protein-10 (IP-10) 
      chemokine by human neutrophils.
PG  - 111-5
AB  - Interferon-gamma (IFN-gamma)-inducible protein-10 (IP-10), a member of the C-X-C 
      sub-family of chemokines, is known to be produced by monocytes, lymphocytes, 
      keratinocytes and endothelial cells in response to IFN-gamma. Here, we show that 
      human polymorphonuclear neutrophils (PMN) also have the ability to produce IP-10. 
      IFN-gamma alone had a modest effect on IP-10 mRNA accumulation, whereas tumor 
      necrosis factor-alpha (TNF-alpha), yeast particles opsonized with IgG (Y-IgG), 
      lipopolysaccharide (LPS), and formyl-methionyl-leucyl-phenylalanine (fMLP) all 
      failed to up-regulate IP-10 gene expression. However, stimulation of neutrophils 
      with IFN-gamma in combination with either TNF-alpha or LPS (but not with Y-IgG or 
      fMLP) resulted in a considerable induction of IP-10 mRNA transcripts, as well as 
      in the extracellular release of the protein. In contrast, the best inducer of 
      IP-10 release from peripheral blood mononuclear cells was IFN-gamma alone. 
      Furthermore, mRNA stabilization analyses demonstrated that IP-10 mRNA isolated 
      from PMN stimulated with IFN-gamma only, or with IFN-gamma plus either TNF-alpha 
      or LPS, had similar half-lives. Finally, we found that interleukin-10, a known 
      inhibitor of chemokine production in PMN, moderately suppressed the extracellular 
      production of IP-10 in neutrophils stimulated with IFN-gamma plus either LPS or 
      TNF-alpha. Since IP-10 is a potent chemoattractant for activated T lymphocytes, 
      the ability of neutrophils to produce IP-10 might contribute to the evolution and 
      progression of the inflammatory response.
FAU - Cassatella, M A
AU  - Cassatella MA
AD  - Department of General Pathology, University of Verona, Italy. 
      MCNCSS@borgoroma.univr.it
FAU - Gasperini, S
AU  - Gasperini S
FAU - Calzetti, F
AU  - Calzetti F
FAU - Bertagnin, A
AU  - Bertagnin A
FAU - Luster, A D
AU  - Luster AD
FAU - McDonald, P P
AU  - McDonald PP
LA  - eng
GR  - R01-CA69212/CA/NCI 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  - Germany
TA  - Eur J Immunol
JT  - European journal of immunology
JID - 1273201
RN  - 0 (Chemokine CXCL10)
RN  - 0 (Chemokines, CXC)
RN  - 0 (Cytokines)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (RNA, Messenger)
RN  - 1CC1JFE158 (Dactinomycin)
RN  - 82115-62-6 (Interferon-gamma)
SB  - IM
MH  - Cells, Cultured
MH  - Chemokine CXCL10
MH  - *Chemokines, CXC
MH  - Cytokines/*biosynthesis
MH  - Dactinomycin/pharmacology
MH  - Gene Expression/drug effects
MH  - Humans
MH  - Interferon-gamma/pharmacology
MH  - Lipopolysaccharides/pharmacology
MH  - Neutrophils/*metabolism
MH  - RNA, Messenger/genetics
MH  - Time Factors
EDAT- 1997/01/01 00:00
MHDA- 1997/01/01 00:01
CRDT- 1997/01/01 00:00
PHST- 1997/01/01 00:00 [pubmed]
PHST- 1997/01/01 00:01 [medline]
PHST- 1997/01/01 00:00 [entrez]
AID - 10.1002/eji.1830270117 [doi]
PST - ppublish
SO  - Eur J Immunol. 1997 Jan;27(1):111-5. doi: 10.1002/eji.1830270117.