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Prostaglandin D 2 as a Mediator of Allergic Asthma

2000; American Association for the Advancement of Science; Volume: 287; Issue: 5460 Linguagem: Inglês

10.1126/science.287.5460.2013

1095-9203

Toshiyuki Matsuoka, Masakazu Hirata, Hiroyuki Tanaka, Yoshimasa Takahashi, Tatsunori Murata, Kenji Kabashima, Yukihiko Sugimoto, Takuya Kobayashi, Fumitaka Ushikubi, Yoshiya Aze, Naomi Eguchi, Yoshihiro Urade, Nobuaki Yoshida, Kazushi Kimura, Akira Mizoguchi, Yoshihito Honda, Hiroichi Nagai, Shuh Narumiya,

Mast cells and histamine

Allergic asthma is caused by the aberrant expansion in the lung of T helper cells that produce type 2 (T H 2) cytokines and is characterized by infiltration of eosinophils and bronchial hyperreactivity. This disease is often triggered by mast cells activated by immunoglobulin E (IgE)–mediated allergic challenge. Activated mast cells release various chemical mediators, including prostaglandin D 2 (PGD 2 ), whose role in allergic asthma has now been investigated by the generation of mice deficient in the PGD receptor (DP). Sensitization and aerosol challenge of the homozygous mutant (DP −/− ) mice with ovalbumin (OVA) induced increases in the serum concentration of IgE similar to those in wild-type mice subjected to this model of asthma. However, the concentrations of T H 2 cytokines and the extent of lymphocyte accumulation in the lung of OVA-challenged DP −/− mice were greatly reduced compared with those in wild-type animals. Moreover, DP −/− mice showed only marginal infiltration of eosinophils and failed to develop airway hyperreactivity. Thus, PGD 2 functions as a mast cell–derived mediator to trigger asthmatic responses.