PMID- 20412419
OWN - NLM
STAT- MEDLINE
DCOM- 20101116
LR  - 20161125
IS  - 1600-0765 (Electronic)
IS  - 0022-3484 (Linking)
VI  - 45
IP  - 4
DP  - 2010 Aug
TI  - Interleukin-1 receptor-associated kinase-M in gingival epithelial cells 
      attenuates the inflammatory response elicited by Porphyromonas gingivalis.
PG  - 512-9
LID - 10.1111/j.1600-0765.2009.01266.x [doi]
AB  - BACKGROUND AND OBJECTIVE: Recent studies have revealed that negative regulatory 
      molecules, including interleukin-1 receptor-associated kinase-M (IRAK-M), control 
      the overactivation of Toll-like receptor (TLR) signaling. The role of IRAK-M in 
      human gingival epithelial cells (HGECs), which express TLRs, remains unclear. The 
      present study examined the role of IRAK-M on interleukin-8 and macrophage 
      chemoattractant protein-1 (MCP-1) expression in HGECs stimulated with 
      Porphyromonas gingivalis and TLR ligands. MATERIAL AND METHODS: Primary HGECs and 
      an SV40 T-antigen-immortalized HGEC line (epi 4) were stimulated with live or 
      heat-killed P. gingivalis, P. gingivalis lipopolysaccharide or the synthetic 
      lipopeptide PAM(3)CSK(4), and subsequent expression of IRAK-M, interleukin-8 and 
      MCP-1 was evaluated at the mRNA and protein levels. The effects of IRAK-M on 
      interleukin-8 and MCP-1 expressions were evaluated by IRAK-M-specific RNA 
      interference (RNAi)-based loss-of-function assay. RESULTS: All tested stimulants 
      up-regulated the expression of IRAK-M in HGECs. The P. gingivalis 
      lipopolysaccharide or PAM(3)CSK(4) increased MCP-1 expression, whereas live P. 
      gingivalis down-regulated the MCP-1 expression in HGECs. However, IRAK-M RNAi 
      increased the expression of MCP-1 irrespective of up- or down-regulation mediated 
      by the respective stimulants. Interleukin-8 gene expression, up-regulated by all 
      tested stimulants, was further enhanced by IRAK-M RNAi. In contrast, IRAK-M RNAi 
      had no effect on the interleukin-8 protein levels, irrespective of the stimulant, 
      indicating that post-translational modification, not IRAK-M, controls 
      interleukin-8 protein expression. CONCLUSION: Interleukin-1 receptor-associated 
      kinase-M appeared to have distinct regulatory roles on the interleukin-8 and 
      MCP-1 produced by HGECs, further suggesting an important role for interleukin-8 
      in the immune response to periodontopathic bacteria.
FAU - Takahashi, N
AU  - Takahashi N
AD  - Center for Transdisciplinary Research, Niigata University, Niigata, Japan.
FAU - Honda, T
AU  - Honda T
FAU - Domon, H
AU  - Domon H
FAU - Nakajima, T
AU  - Nakajima T
FAU - Tabeta, K
AU  - Tabeta K
FAU - Yamazaki, K
AU  - Yamazaki K
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20100419
PL  - United States
TA  - J Periodontal Res
JT  - Journal of periodontal research
JID - 0055107
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Interleukin-8)
RN  - 0 (Ligands)
RN  - 0 (Lipopeptides)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Pam(3)CSK(4) peptide)
RN  - 0 (RNA, Small Interfering)
RN  - 0 (SOCS1 protein, human)
RN  - 0 (Suppressor of Cytokine Signaling 1 Protein)
RN  - 0 (Suppressor of Cytokine Signaling Proteins)
RN  - 0 (Toll-Like Receptors)
RN  - EC 2.7.11.1 (IRAK3 protein, human)
RN  - EC 2.7.11.1 (Interleukin-1 Receptor-Associated Kinases)
RN  - EC 3.1.3.2 (Phosphoric Monoester Hydrolases)
RN  - EC 3.1.3.56 (Inositol Polyphosphate 5-Phosphatases)
SB  - IM
MH  - Cell Line
MH  - Cells, Cultured
MH  - Chemokine CCL2/*immunology
MH  - Down-Regulation/immunology
MH  - Epithelial Cells/immunology/microbiology
MH  - Gene Silencing
MH  - Gingiva/cytology/*immunology/microbiology
MH  - Humans
MH  - Inositol Polyphosphate 5-Phosphatases
MH  - Interleukin-1 Receptor-Associated Kinases/genetics/*immunology
MH  - Interleukin-8/*immunology/metabolism
MH  - Ligands
MH  - Lipopeptides/immunology
MH  - Lipopolysaccharides/immunology
MH  - Phosphoric Monoester Hydrolases/analysis
MH  - Porphyromonas gingivalis/*immunology
MH  - Protein Processing, Post-Translational/immunology
MH  - RNA Interference
MH  - RNA, Small Interfering/pharmacology
MH  - Signal Transduction/immunology
MH  - Suppressor of Cytokine Signaling 1 Protein
MH  - Suppressor of Cytokine Signaling Proteins/analysis
MH  - Toll-Like Receptors/agonists/immunology
MH  - Up-Regulation/immunology
EDAT- 2010/04/24 06:00
MHDA- 2010/11/17 06:00
CRDT- 2010/04/24 06:00
PHST- 2010/04/24 06:00 [entrez]
PHST- 2010/04/24 06:00 [pubmed]
PHST- 2010/11/17 06:00 [medline]
AID - JRE1266 [pii]
AID - 10.1111/j.1600-0765.2009.01266.x [doi]
PST - ppublish
SO  - J Periodontal Res. 2010 Aug;45(4):512-9. doi: 10.1111/j.1600-0765.2009.01266.x. 
      Epub 2010 Apr 19.