PMID- 20502734
OWN - NLM
STAT- MEDLINE
DCOM- 20110525
LR  - 20110408
IS  - 0300-0729 (Print)
IS  - 0300-0729 (Linking)
VI  - 48
IP  - 1
DP  - 2010 Mar
TI  - Nasal polyp fibroblasts produce MIP-3alpha in response to toll-like receptor 
      ligands and cytokine stimulation.
PG  - 41-6
LID - 10.4193/Rhin09.019 [doi]
AB  - OBJECTIVE: Dendritic cells (DCs) play important roles in the development and 
      perpetuation of immune responses. DCs are present in upper airway diseases such 
      as chronic rhinosinusitis with nasal polyps. However, the mechanisms of how DCs 
      migrate into the upper airway mucosa during upper airway inflammatory diseases 
      remains unclear. Macrophage inflammatory protein-3alpha (MIP-3alpha) is known to 
      be a migratory factor for immature DCs. There have been very few reports 
      regarding cells producing this chemokine in the airways. To investigate this, we 
      stimulated fibroblasts cultured from the nasal polyps with various toll-like 
      receptor (TLR) ligands, which are derived from microorganisms, and IL-beta1 and 
      TNF-alpha, which are proinflammatory cytokines, and analyzed their ability to 
      produce MIP-3alpha. METHODS: Fibroblast lines were established from nasal polyps 
      and stimulated with TLR2, 3, 4, 5, 7/8 and 9 ligands, IL-beta1 and TNF-alpha. 
      MIP-3alpha mRNA expression in nasal polyp fibroblasts (NPF) was evaluated by 
      real-time RT-PCR and the protein levels of MIP-3alpha in the supernatants of 
      stimulated NPF was measured by ELISA. RESULTS: Stimulation with TLR2, 3, 4 and 5 
      ligands, IL-beta1 and TNF-alpha, induced MIP-3alpha gene expression and protein 
      production in the cultured NPF This response was dose- and time-dependent. 
      CONCLUSION: NPF possibly play an important role in the recruitment of DCs in 
      upper airway diseases such as chronic rhinosinusitis with nasal polyps through 
      the production of MIP-3alpha.
FAU - Nonaka, Manabu
AU  - Nonaka M
AD  - Department of Otolaryngology, Nippon Medical School, Sendagi, Tokyo, Japan. 
      nonaka@nms.ac.jp
FAU - Ogihara, Nozomu
AU  - Ogihara N
FAU - Fukumoto, Akira
AU  - Fukumoto A
FAU - Sakanushi, Atsuko
AU  - Sakanushi A
FAU - Kusama, Kaoru
AU  - Kusama K
FAU - Pawankar, Ruby
AU  - Pawankar R
FAU - Yagi, Toshiaki
AU  - Yagi T
LA  - eng
PT  - Journal Article
PL  - Netherlands
TA  - Rhinology
JT  - Rhinology
JID - 0347242
RN  - 0 (CCL20 protein, human)
RN  - 0 (Chemokine CCL20)
RN  - 0 (Interleukin-1beta)
RN  - 0 (Ligands)
RN  - 0 (Toll-Like Receptors)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Chemokine CCL20/*metabolism
MH  - Dendritic Cells/physiology
MH  - Fibroblasts/*metabolism
MH  - Humans
MH  - Interleukin-1beta/physiology
MH  - Ligands
MH  - Nasal Polyps/*metabolism/pathology
MH  - Toll-Like Receptors/*physiology
MH  - Tumor Necrosis Factor-alpha/physiology
EDAT- 2010/05/27 06:00
MHDA- 2011/05/26 06:00
CRDT- 2010/05/27 06:00
PHST- 2010/05/27 06:00 [entrez]
PHST- 2010/05/27 06:00 [pubmed]
PHST- 2011/05/26 06:00 [medline]
AID - 09.019 [pii]
AID - 10.4193/Rhin09.019 [doi]
PST - ppublish
SO  - Rhinology. 2010 Mar;48(1):41-6. doi: 10.4193/Rhin09.019.