PMID- 2838424
OWN - NLM
STAT- MEDLINE
DCOM- 19880801
LR  - 20210526
IS  - 0019-9567 (Print)
IS  - 1098-5522 (Electronic)
IS  - 0019-9567 (Linking)
VI  - 56
IP  - 7
DP  - 1988 Jul
TI  - Inhibition of the inflammatory action of interleukin-1 and tumor necrosis factor 
      (alpha) on neutrophil function by pentoxifylline.
PG  - 1722-9
AB  - Inflammatory cytokines, including interleukin-1 and tumor necrosis factor, are 
      produced by monocytes and macrophages in response to microorganisms and microbial 
      products such as endotoxins. The cytokines stimulate neutrophil adherence, 
      degranulation, and superoxide production but inhibit neutrophil migration. We 
      studied the modulation of cytokine-induced neutrophil activation by 
      pentoxifylline and its principle metabolites. Lipopolysaccharide-stimulated 
      mononuclear-leukocyte-conditioned medium containing inflammatory cytokines, 
      purified human interleukin-1, or recombinant human tumor necrosis factor 
      increased neutrophil adherence to nylon fiber, primed neutrophils for increased 
      superoxide production in response to 
      N-formyl-L-methionyl-L-leucyl-L-phenylalanine (FMLP), increased neutrophil 
      lysozyme release stimulated by FMLP, and decreased directed migration of 
      neutrophils to FMLP. Pentoxifylline and its principle metabolites at or near 
      therapeutically achievable levels were able to counteract these effects. 
      Pentoxifylline inhibited the increase in free intracellular calcium in 
      polymorphonuclear leukocytes stimulated by FMLP and increased binding of FMLP to 
      neutrophils at 37 degrees C but not at 4 degrees C. By blocking the inflammatory 
      action of interleukin-1 and tumor necrosis factor on neutrophils, pentoxifylline 
      may diminish the tissue damage caused by neutrophils in such conditions as septic 
      shock, adult respiratory distress syndrome, cardiopulmonary bypass lung damage, 
      and myocardial reperfusion injury.
FAU - Sullivan, G W
AU  - Sullivan GW
AD  - Department of Internal Medicine, University of Virginia Medical Center, 
      Charlottesville 22908.
FAU - Carper, H T
AU  - Carper HT
FAU - Novick, W J Jr
AU  - Novick WJ Jr
FAU - Mandell, G L
AU  - Mandell GL
LA  - eng
GR  - AI09504-17/AI/NIAID 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  - United States
TA  - Infect Immun
JT  - Infection and immunity
JID - 0246127
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Culture Media)
RN  - 0 (Free Radicals)
RN  - 0 (Interleukin-1)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Receptors, Formyl Peptide)
RN  - 0 (Receptors, Immunologic)
RN  - 0 (Recombinant Proteins)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 11062-77-4 (Superoxides)
RN  - 59880-97-6 (N-Formylmethionine Leucyl-Phenylalanine)
RN  - OBD445WZ5P (Theobromine)
RN  - SD6QCT3TSU (Pentoxifylline)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Anti-Inflammatory Agents/*pharmacology
MH  - Calcium
MH  - Cell Adhesion/drug effects
MH  - Cell Movement/drug effects
MH  - Culture Media/pharmacology
MH  - Cytoplasmic Granules/enzymology
MH  - Cytosol/metabolism
MH  - Free Radicals
MH  - Humans
MH  - Interleukin-1/*antagonists & inhibitors/pharmacology
MH  - Leukocytes, Mononuclear/physiology
MH  - Lipopolysaccharides/pharmacology
MH  - N-Formylmethionine Leucyl-Phenylalanine/metabolism
MH  - Neutrophils/*drug effects/metabolism/physiology
MH  - Pentoxifylline/*pharmacology
MH  - Receptors, Formyl Peptide
MH  - Receptors, Immunologic/drug effects
MH  - Recombinant Proteins/antagonists & inhibitors/pharmacology
MH  - Superoxides/biosynthesis
MH  - Theobromine/*analogs & derivatives
MH  - Tumor Necrosis Factor-alpha/*antagonists & inhibitors/pharmacology
PMC - PMC259468
EDAT- 1988/07/01 00:00
MHDA- 2001/03/28 10:01
PMCR- 1988/07/01
CRDT- 1988/07/01 00:00
PHST- 1988/07/01 00:00 [pubmed]
PHST- 2001/03/28 10:01 [medline]
PHST- 1988/07/01 00:00 [entrez]
PHST- 1988/07/01 00:00 [pmc-release]
AID - 10.1128/iai.56.7.1722-1729.1988 [doi]
PST - ppublish
SO  - Infect Immun. 1988 Jul;56(7):1722-9. doi: 10.1128/iai.56.7.1722-1729.1988.