On-Off Switch For Inflammation In Allergic Asthma and COPD Identified

Research shows that two receptors of an inflammatory molecule play opposite roles in inflammation, suggesting new strategies for treatment.

Asian Scientist (Aug. 6, 2013) – Japanese researchers have taken a step towards understanding why there is runaway inflammation in both chronic obstructive pulmonary disorder (COPD) and allergic asthma.

In their study published in the FASEB Journal, the scientists show that two receptors of an inflammatory molecule, called leukotriene B4, play opposing roles in turning inflammation on and off for allergic asthma and COPD.

The first receptor, BLT1, promotes inflammation, while the second receptor, BLT2, has the potential to weaken inflammation during an allergic reaction. BLT2 was previously believed to increase inflammatory reaction.

“Leukotriene B4 levels are elevated in the airways of the patients with asthma and COPD, and the opposite role of BLT1 and BLT2 in allergic inflammation implies that drug development should target BLT1 and BLT2 differently,” said Hiromasa Inoue, senior author of the study.

“We hope that better anti-asthma drugs or anti-COPD drugs will be produced in the future to treat millions of patients who suffer from severe asthma and COPD.”

In their study, the scientists compared the allergic reactions in BLT2-gene deleted mice to those in normal mice after an allergic asthma reaction was provoked by inhalation of allergens.

They found that BLT2-gene deleted mice displayed more inflammatory cells in the lung compared to normal mice. Without the BLT2 gene, lung allergic inflammation was stronger than that of normal mice.

Results suggest that targeting these two receptors differently and/or separately could achieve vastly different outcomes.

Conventional anti-leukotriene B4 drugs block both of the pathways induced by BLT1 and BLT2. By manipulating the specific target, it may be possible to develop more effective anti-leukotriene B4 drugs.

“This is one case where BLT isn’t a sandwich! Distinguishing between BLT1 and BLT2 is an important step forward to developing more effective drugs for lung inflammation,” said Dr Gerald Weissmann, who was not involved in the study.

“Understanding the specific roles of these and other receptors allow researchers to identify new drug targets, which in turn can lead to new and more effective drugs.”

The article can be found at: Matsunaga et al. (2013) Leukotriene B4 Receptor BLT2 Negatively Regulates Allergic Airway Eosinophilia.


Source: FASEB; Photo: lamdogjunkie/Flickr/CC.
Disclaimer: This article does not necessarily reflect the views of AsianScientist or its staff.

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