PMID- 11336536
OWN - NLM
STAT- MEDLINE
DCOM- 20010726
LR  - 20131121
IS  - 0026-2862 (Print)
IS  - 0026-2862 (Linking)
VI  - 61
IP  - 3
DP  - 2001 May
TI  - Histamine-induced production of interleukin-6 and interleukin-8 by human coronary 
      artery endothelial cells is enhanced by endotoxin and tumor necrosis 
      factor-alpha.
PG  - 253-62
AB  - In this study, we tested the synergy between histamine and LPS, and histamine and 
      TNF-alpha, on endothelial cell production of interleukin-6 (IL-6), interleukin-8 
      (IL-8), and monocyte chemoattractant protein-1 (MCP-1). Human coronary artery 
      endothelial cells (HCAEC) were cultured in vitro with histamine (0.1 to 1000 
      microM) in the presence or absence of LPS or TNF-alpha for 24 h, and the secreted 
      IL-6, IL-8 and MCP-1 were quantified. Unactivated HCAEC produced minimal levels 
      of IL-6, IL-8, or MCP-1. The incubation of HCAEC with histamine resulted in low 
      level induction of IL-6 and IL-8 production, which was dose-dependent and 
      attained a plateau at a concentration of 10 microM. On the other hand, histamine 
      failed to induce MCP-1 production. Stimulation of HCAEC with LPS or TNF-alpha 
      caused dose-dependent increase in cytokine production. In the presence of all 
      stimulatory concentrations of LPS and TNF-alpha tested, histamine was shown to 
      further enhance IL-6 and IL-8 production. The effect of histamine on endothelial 
      cell production of cytokines was completely inhibited by the H-1 receptor 
      antagonist, diphenhydramine, and not by the H-2 antagonist, famotidine. 
      Electrophoretic mobility shift assays of nuclear proteins extracted from HCAEC 
      treated with histamine and LPS, or histamine and TNF-alpha, revealed amplified 
      translocation of NF-kappaB proteins to the nuclei. Since both LPS and TNF-alpha 
      potentiated histamine-induced cytokine production, it is possible that these 
      activators stimulate H-1 receptor expression and/or augment the signal 
      transduction pathways leading to the expression of IL-6 and IL-8. These results 
      indicate the importance of synergy between histamine and other inflammatory 
      stimuli on endothelial cell activation and implicate their cooperative 
      participation in vascular leak and inflammation.
CI  - Copyright 2001 Academic Press.
FAU - Li, Y
AU  - Li Y
AD  - Division of Allergy, Department of Medicine, Kansas City, Kansas 66160, USA.
FAU - Chi, L
AU  - Chi L
FAU - Stechschulte, D J
AU  - Stechschulte DJ
FAU - Dileepan, K N
AU  - Dileepan KN
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Microvasc Res
JT  - Microvascular research
JID - 0165035
RN  - 0 (Chemokine CCL2)
RN  - 0 (Histamine H1 Antagonists)
RN  - 0 (Histamine H2 Antagonists)
RN  - 0 (Interleukin-6)
RN  - 0 (Interleukin-8)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (NF-kappa B)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 5QZO15J2Z8 (Famotidine)
RN  - 820484N8I3 (Histamine)
RN  - 8GTS82S83M (Diphenhydramine)
SB  - IM
MH  - Cells, Cultured
MH  - Chemokine CCL2/biosynthesis
MH  - Coronary Vessels/cytology/drug effects/immunology
MH  - Diphenhydramine/pharmacology
MH  - Drug Synergism
MH  - Endothelium, Vascular/cytology/*drug effects/*immunology
MH  - Famotidine/pharmacology
MH  - Histamine/administration & dosage/*pharmacology
MH  - Histamine H1 Antagonists/pharmacology
MH  - Histamine H2 Antagonists/pharmacology
MH  - Humans
MH  - Interleukin-6/*biosynthesis
MH  - Interleukin-8/*biosynthesis
MH  - Lipopolysaccharides/administration & dosage/pharmacology
MH  - NF-kappa B/metabolism
MH  - Tumor Necrosis Factor-alpha/administration & dosage/pharmacology
EDAT- 2001/05/05 10:00
MHDA- 2001/07/28 10:01
CRDT- 2001/05/05 10:00
PHST- 2001/05/05 10:00 [pubmed]
PHST- 2001/07/28 10:01 [medline]
PHST- 2001/05/05 10:00 [entrez]
AID - S0026-2862(01)92304-0 [pii]
AID - 10.1006/mvre.2001.2304 [doi]
PST - ppublish
SO  - Microvasc Res. 2001 May;61(3):253-62. doi: 10.1006/mvre.2001.2304.