PMID- 8095960
OWN - NLM
STAT- MEDLINE
DCOM- 19930422
LR  - 20190723
IS  - 0022-202X (Print)
IS  - 0022-202X (Linking)
VI  - 100
IP  - 4
DP  - 1993 Apr
TI  - Induction of intercellular adhesion molecule 1 (ICAM-1) expression in normal 
      human eosinophils by inflammatory cytokines.
PG  - 417-23
AB  - Intercellular adhesion molecule-1 (ICAM-1) functions as a ligand for lymphocyte 
      function-associated antigen-1 (LFA-1), and thereby plays a crucial role in 
      mediating cell-cell interactions in inflammatory reactions. Human eosinophils 
      represent important effector cells in allergic skin diseases. To gain more 
      insight into the capacity of eosinophils to physically interact with 
      LFA-1-positive inflammatory leukocytes, in the present study ICAM-1 expression in 
      eosinophils was investigated. Using fluorescence-activated cell sorter analysis, 
      it could be shown that highly purified (> or = 95%) eosinophils from peripheral 
      blood of non-atopic individuals do not constitutively express ICAM-1 molecules. 
      However, stimulation of eosinophils with interferon gamma (IFN gamma), 
      tumor-necrosis factor alpha (TNF alpha), or interleukin 3 (IL-3) markedly 
      upregulated ICAM-1 surface expression in a time- and dose-dependent manner. 
      Cytokine-induced ICAM-1 expression in human eosinophils was corroborated by 
      Northern blot analysis. Accordingly, unstimulated eosinophils did not express 
      significant amounts of ICAM-1 mRNA, but ICAM-1 mRNA expression could be markedly 
      induced in these cells upon stimulation with IFN gamma plus TNF alpha. The 
      combination of TNF alpha with either IFN gamma, IL-3, IL-5, or 
      granulocyte/macrophage colony-stimulating factor (GM-CSF) increased ICAM-1 
      expression in a synergistic fashion, whereas IL-5 or GM-CSF by itself did not 
      induce ICAM-1 expression. Cytokine-induced ICAM-1 expression was specific, 
      because IL-1 alpha, IL-1 beta, IL-2, IL-4, IL-6, IL-7, IL-8, C5a, and 
      platelet-activating factor did not significantly affect eosinophil ICAM-1 surface 
      expression. In summary, these studies indicate that eosinophils may be activated 
      to express the adhesion molecule ICAM-1 upon stimulation with selected 
      inflammatory cytokines, which may allow adhesion-mediated cross-talk between 
      eosinophils and LFA-1-positive cells. In addition, these data demonstrate for the 
      first time a role for IL-3, IL-5, and GM-CSF in regulation of ICAM-1 expression 
      in human cells.
FAU - Czech, W
AU  - Czech W
AD  - Department of Dermatology, University of Freiburg, Germany.
FAU - Krutmann, J
AU  - Krutmann J
FAU - Budnik, A
AU  - Budnik A
FAU - Schopf, E
AU  - Schopf E
FAU - Kapp, A
AU  - Kapp A
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Invest Dermatol
JT  - The Journal of investigative dermatology
JID - 0426720
RN  - 0 (Antigens, CD)
RN  - 0 (Cell Adhesion Molecules)
RN  - 0 (Cytokines)
RN  - 0 (ICAM2 protein, human)
RN  - 0 (Interleukin-3)
RN  - 0 (Lymphocyte Function-Associated Antigen-1)
RN  - 0 (RNA, Messenger)
RN  - 0 (Recombinant Proteins)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - 82115-62-6 (Interferon-gamma)
SB  - IM
MH  - *Antigens, CD
MH  - Blotting, Northern
MH  - Cell Adhesion Molecules/*blood/genetics
MH  - Cytokines/*pharmacology
MH  - Eosinophils/*chemistry
MH  - Humans
MH  - Hypersensitivity, Immediate/blood
MH  - Intercellular Adhesion Molecule-1
MH  - Interferon-gamma/pharmacology
MH  - Interleukin-3/pharmacology
MH  - Lymphocyte Function-Associated Antigen-1/blood
MH  - RNA, Messenger/analysis/drug effects
MH  - Recombinant Proteins/pharmacology
MH  - Stimulation, Chemical
MH  - Tumor Necrosis Factor-alpha/pharmacology
MH  - Up-Regulation/physiology
EDAT- 1993/04/01 00:00
MHDA- 1993/04/01 00:01
CRDT- 1993/04/01 00:00
PHST- 1993/04/01 00:00 [pubmed]
PHST- 1993/04/01 00:01 [medline]
PHST- 1993/04/01 00:00 [entrez]
AID - S0022-202X(93)91195-S [pii]
AID - 10.1111/1523-1747.ep12472082 [doi]
PST - ppublish
SO  - J Invest Dermatol. 1993 Apr;100(4):417-23. doi: 10.1111/1523-1747.ep12472082.