PMID- 8597869
OWN - NLM
STAT- MEDLINE
DCOM- 19960423
LR  - 20081121
IS  - 1078-7852 (Print)
IS  - 1078-7852 (Linking)
VI  - 45
IP  - 3
DP  - 1995
TI  - Regulation of GRO alpha production in human granulocytes.
PG  - 143-51
AB  - GRO alpha, a member of the chemokine superfamily, exerts potent stimulatory 
      actions on granulocytes. In this report, we show that activated human 
      polymorphonuclear leukocytes (PMN) are able to produce significant amounts of GRO 
      alpha. Lipopolysaccharide (LPS), tumor necrosis factor-alpha (TNF alpha), and 
      yeast particles opsonized with IgG (Y-IgG) had the ability to induce GRO alpha 
      release, with Y-IgG being the most potent stimulus. The extracellular production 
      of GRO alpha was also modulated by both interferon-gamma (IFN gamma) and 
      interleukin-10 (IL-10). IFN gamma significantly inhibited the production of GRO 
      alpha by PMN stimulated for 2 hr with LPS, TNF alpha, or Y-IgG, but potentiated 
      the production of GRO alpha in cells stimulated for 18 hr with LPS and TNF alpha. 
      IL-10 moderately suppressed the Y-IgG-induced production of GRO alpha, but 
      strongly inhibited the action of LPS and potentiated the effect of TNF alpha. As 
      revealed by Northern blot analysis, the extracellular production of GRO alpha 
      under the experimental conditions used did not always correlate with parallel 
      changes at the level GRO alpha mRNA expression, suggesting that production of GRO 
      alpha by PMN might be regulated at post-transcriptional, translational, or 
      post-translational level. These findings identify a novel biological function of 
      PMN, likely involved in the modulation of the acute inflammatory response.
FAU - Gasperini, S
AU  - Gasperini S
AD  - Department of General Pathology, University of Verona, Italy.
FAU - Calzetti, F
AU  - Calzetti F
FAU - Russo, M P
AU  - Russo MP
FAU - De Gironcoli, M
AU  - De Gironcoli M
FAU - Cassatella, M A
AU  - Cassatella MA
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Inflamm
JT  - Journal of inflammation
JID - 9511967
RN  - 0 (CXCL1 protein, human)
RN  - 0 (Chemokine CXCL1)
RN  - 0 (Chemokines, CXC)
RN  - 0 (Chemotactic Factors)
RN  - 0 (Growth Inhibitors)
RN  - 0 (Growth Substances)
RN  - 0 (Immunoglobulin G)
RN  - 0 (Intercellular Signaling Peptides and Proteins)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Opsonin Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 130068-27-8 (Interleukin-10)
RN  - 82115-62-6 (Interferon-gamma)
SB  - IM
MH  - Chemokine CXCL1
MH  - *Chemokines, CXC
MH  - Chemotactic Factors/*biosynthesis/genetics
MH  - Drug Synergism
MH  - Gene Expression
MH  - Growth Inhibitors/*biosynthesis/genetics
MH  - Growth Substances/*biosynthesis/genetics
MH  - Humans
MH  - Immunoglobulin G/pharmacology
MH  - *Intercellular Signaling Peptides and Proteins
MH  - Interferon-gamma/pharmacology
MH  - Interleukin-10/pharmacology
MH  - Lipopolysaccharides/pharmacology
MH  - Neutrophils/*metabolism
MH  - Opsonin Proteins
MH  - RNA, Messenger/metabolism
MH  - Saccharomyces cerevisiae
MH  - Tumor Necrosis Factor-alpha/pharmacology
EDAT- 1995/01/01 00:00
MHDA- 1995/01/01 00:01
CRDT- 1995/01/01 00:00
PHST- 1995/01/01 00:00 [pubmed]
PHST- 1995/01/01 00:01 [medline]
PHST- 1995/01/01 00:00 [entrez]
PST - ppublish
SO  - J Inflamm. 1995;45(3):143-51.