PMID- 18303186
OWN - NLM
STAT- MEDLINE
DCOM- 20080408
LR  - 20190911
IS  - 1880-3989 (Electronic)
IS  - 0388-1350 (Linking)
VI  - 33
IP  - 1
DP  - 2008 Feb
TI  - Role of TNF-alpha and extracellular ATP in THP-1 cell activation following 
      allergen exposure.
PG  - 71-83
AB  - Dendritic cells (DCs), including Langerhans cells (LCs), play a critical role in 
      the induction phase of allergic contact hypersensitivity. Following exposure to 
      chemical allergens in the skin, LCs undergo a maturation process leading to the 
      up-regulation of expression of co-stimulatory molecules, such as CD86, CD54 and 
      CD40. Our previous study revealed that chemical allergens induce phenotype 
      alterations (e.g., CD86, CD54 and CD40) and cytokine production (TNF-alpha and 
      IL-8) in THP-1 cells that possibly reflect the maturation of dendritic cells 
      during skin sensitization. However, the physiological signals for phenotypic 
      alterations by chemical allergens are still not fully understood. Therefore, in 
      this study, we investigated the effect of TNF-alpha and extracellular ATP on 
      THP-1 cell activation induced by chemical allergens. Kinetic studies revealed 
      that TNF-alpha and IL-8 release occurred in a time-dependent manner with release 
      of two cytokines beginning at 3 hr post-exposure to well-known haptens, DNCB and 
      NiSO(4). While recombinant human TNF-alpha augmented CD54 and CD40 expression in 
      a dose-dependent manner, rhTNF-alpha did not increase CD86 expression. 
      Furthermore, neutralization of TNF-alpha activity strongly inhibited CD54 and 
      CD40 expression induced by allergens. On the contrary, extracellular ATP induced 
      the up-regulation of both CD86 and CD54 expression. In the presence of the P2 
      receptor antagonist suramin, the up-regulation of CD86 and CD54 expression by 
      allergens was in part suppressed. Therefore, we postulate that not only TNF-alpha 
      but also extracellular ATP may contribute to cell activation following allergen 
      stimulation, which might reflect the mechanism by which DCs respond to allergens.
FAU - Miyazawa, Masaaki
AU  - Miyazawa M
AD  - Kao Corporation, Safety Science Research Laboratories, Haga-Gun, Tochigi, Japan. 
      miyazawa.masaaki@kao.co.jp
FAU - Ito, Yuichi
AU  - Ito Y
FAU - Kosaka, Nanae
AU  - Kosaka N
FAU - Nukada, Yuko
AU  - Nukada Y
FAU - Sakaguchi, Hitoshi
AU  - Sakaguchi H
FAU - Suzuki, Hiroyuki
AU  - Suzuki H
FAU - Nishiyama, Naohiro
AU  - Nishiyama N
LA  - eng
PT  - Journal Article
PL  - Japan
TA  - J Toxicol Sci
JT  - The Journal of toxicological sciences
JID - 7805798
RN  - 0 (Allergens)
RN  - 0 (B7-2 Antigen)
RN  - 0 (CD40 Antigens)
RN  - 0 (CD86 protein, human)
RN  - 0 (Haptens)
RN  - 0 (Interleukin-8)
RN  - 0 (Purinergic P2 Receptor Antagonists)
RN  - 0 (Recombinant Proteins)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - 6032D45BEM (Suramin)
RN  - 8L70Q75FXE (Adenosine Triphosphate)
SB  - IM
MH  - Adenosine Triphosphate/*immunology/pharmacology
MH  - Allergens/*toxicity
MH  - B7-2 Antigen/immunology
MH  - CD40 Antigens/immunology
MH  - Cell Line
MH  - Cell Survival/drug effects
MH  - Dendritic Cells/*drug effects/immunology
MH  - Haptens/*toxicity
MH  - Humans
MH  - Intercellular Adhesion Molecule-1/immunology
MH  - Interleukin-8/genetics/immunology/pharmacology
MH  - Phenotype
MH  - Purinergic P2 Receptor Antagonists
MH  - Recombinant Proteins/pharmacology
MH  - Suramin/pharmacology
MH  - Tumor Necrosis Factor-alpha/genetics/*immunology/pharmacology
EDAT- 2008/02/28 09:00
MHDA- 2008/04/09 09:00
CRDT- 2008/02/28 09:00
PHST- 2008/02/28 09:00 [pubmed]
PHST- 2008/04/09 09:00 [medline]
PHST- 2008/02/28 09:00 [entrez]
AID - JST.JSTAGE/jts/33.71 [pii]
AID - 10.2131/jts.33.71 [doi]
PST - ppublish
SO  - J Toxicol Sci. 2008 Feb;33(1):71-83. doi: 10.2131/jts.33.71.