PMID- 15606618
OWN - NLM
STAT- MEDLINE
DCOM- 20050302
LR  - 20231103
IS  - 0009-9104 (Print)
IS  - 1365-2249 (Electronic)
IS  - 0009-9104 (Linking)
VI  - 139
IP  - 1
DP  - 2005 Jan
TI  - Role of p38 MAPK and NF-kB for chemokine release in coculture of human 
      eosinophils and bronchial epithelial cells.
PG  - 90-100
AB  - Eosinophils are principal effector cells of inflammation in allergic asthma, 
      characterized by their accumulation and infiltration at inflammatory sites 
      mediated by the chemokine eotaxin and their interaction with adhesion molecules 
      expressed on bronchial epithelial cells. We investigated the modulation of 
      nuclear factor-kappaB (NF-kappaB) and the mitogen-activated protein kinase (MAPK) 
      pathway on the in vitro release of chemokines including regulated upon activation 
      normal T cell expressed and secreted (RANTES), monokine induced by 
      interferon-gamma (MIG), monocyte chemoattractant protein-1 (MCP-1), interleukin 
      (IL)-8, and interferon-inducible protein-10 (IP-10) upon the interaction of human 
      bronchial epithelial BEAS-2B cells and eosinophils. Gene expression of chemokines 
      was evaluated by RT-PCR and the induction amount of chemokines quantified by 
      cytometric bead array. NF-kappaB and p38 MAPK activities were assessed by 
      electrophoretic mobility shift assay and Western blot, respectively. The 
      interaction of eosinophils and BEAS-2B cells was found to up-regulate the gene 
      expression of the chemokines IL-8, MCP-1, MIG, RANTES and IP-10 expression in 
      BEAS-2B cells, and to significantly elevate the release of the aforementioned 
      chemokines except RANTES in a coculture of BEAS-2B cells and eosinophils. 
      IkappaB-alpha phosphorylation inhibitor, BAY 11-7082, and p38 MAPK inhibitor, SB 
      203580 could decrease the release of IL-8, IP-10 and MCP-1 in the coculture. 
      Together, the above results show that the induction of the release of chemokines 
      in a coculture of epithelial cells and eosinophils are regulated by p38 MAPK and 
      NF-kappaB activities of BEAS-2B cells, at least partly, through intercellular 
      contact. Our findings therefore shed light on the future development of more 
      effective agents for allergic and inflammatory diseases.
FAU - Wong, C K
AU  - Wong CK
AD  - Department of Chemical Pathology, The Chinese University of Hong Kong, Prince of 
      Wales Hospital, Shatin, NT, Hong Kong.
FAU - Wang, C B
AU  - Wang CB
FAU - Ip, W K
AU  - Ip WK
FAU - Tian, Y P
AU  - Tian YP
FAU - Lam, C W K
AU  - Lam CW
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Clin Exp Immunol
JT  - Clinical and experimental immunology
JID - 0057202
RN  - 0 (3-(4-methylphenylsulfonyl)-2-propenenitrile)
RN  - 0 (CCL2 protein, human)
RN  - 0 (CXCL10 protein, human)
RN  - 0 (CXCL9 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CCL5)
RN  - 0 (Chemokine CXCL10)
RN  - 0 (Chemokine CXCL9)
RN  - 0 (Chemokines)
RN  - 0 (Chemokines, CXC)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Fixatives)
RN  - 0 (Imidazoles)
RN  - 0 (Intercellular Signaling Peptides and Proteins)
RN  - 0 (Interleukin-8)
RN  - 0 (NF-kappa B)
RN  - 0 (Nitriles)
RN  - 0 (Polymers)
RN  - 0 (Pyridines)
RN  - 0 (Sulfones)
RN  - 1HG84L3525 (Formaldehyde)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
RN  - OU13V1EYWQ (SB 203580)
RN  - Y19UC83H8E (paraform)
SB  - IM
MH  - Bronchi/*immunology
MH  - Cells, Cultured
MH  - Chemokine CCL2/immunology
MH  - Chemokine CCL5/immunology
MH  - Chemokine CXCL10
MH  - Chemokine CXCL9
MH  - Chemokines/*immunology
MH  - Chemokines, CXC/immunology
MH  - Coculture Techniques/methods
MH  - Enzyme Inhibitors/immunology
MH  - Eosinophils/*immunology
MH  - Epithelial Cells/immunology
MH  - Fixatives
MH  - Formaldehyde
MH  - Gene Expression Regulation/immunology
MH  - Humans
MH  - Imidazoles/immunology
MH  - Intercellular Signaling Peptides and Proteins/immunology
MH  - Interleukin-8/immunology
MH  - NF-kappa B/antagonists & inhibitors/*immunology
MH  - Nitriles/immunology
MH  - Polymers
MH  - Pyridines/immunology
MH  - Reverse Transcriptase Polymerase Chain Reaction/methods
MH  - Sulfones/immunology
MH  - p38 Mitogen-Activated Protein Kinases/*immunology
PMC - PMC1809270
EDAT- 2004/12/21 09:00
MHDA- 2005/03/03 09:00
PMCR- 2006/01/01
CRDT- 2004/12/21 09:00
PHST- 2004/12/21 09:00 [pubmed]
PHST- 2005/03/03 09:00 [medline]
PHST- 2004/12/21 09:00 [entrez]
PHST- 2006/01/01 00:00 [pmc-release]
AID - CEI2678 [pii]
AID - 10.1111/j.1365-2249.2005.02678.x [doi]
PST - ppublish
SO  - Clin Exp Immunol. 2005 Jan;139(1):90-100. doi: 10.1111/j.1365-2249.2005.02678.x.