Send to

Choose Destination
See comment in PubMed Commons below
Eur J Immunol. 2007 Apr;37(4):1107-15.

Mast cells play a key role in the development of late airway hyperresponsiveness through TNF-alpha in a murine model of asthma.

Author information

Department of Immunology, Chonbuk National University Medical School, Chonju, Republic of Korea.


We have investigated the role of TNF-alpha in mast cell-mediated late airway hyperresponsiveness (AHR) using mast cell-deficient WBB6F1-W/W(v) (W/W(v)) mice in a murine model of asthma, which exhibits a biphasic increase in AHR. TNF-alpha levels in the airway and magnitude of late AHR in response to airway allergen challenge were severely impaired in W/W(v) mice compared to their littermates. In addition to TNF-alpha, cytosolic phospholipase A(2) (cPLA(2)) phosphorylation and enzymatic activity in the lungs were also impaired in W/W(v) mice. Either anti-TNF-alpha antibody or an inhibitor of cPLA(2) abolished late AHR in congeneic +/+ mice. Intratracheal administration of TNF-alpha resulted in increases in late AHR, cPLA(2 )phosphorylation, cPLA(2 )activity, and phosphorylation of mitogen-activated protein kinases. Mast cell replacement restored airway TNF-alpha level, cPLA(2 )phosphorylation and enzymatic activity in the lungs as well as late AHR in W/W(v) mice. These data indicate that mast cells play a key role in the development of late AHR through liberation of TNF-alpha.

[Indexed for MEDLINE]
Free full text
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Wiley
    Loading ...
    Support Center