Japanese researchers have made a new step toward understanding—and learning how to stop—runaway inflammation for both chronic obstructive pulmonary disorder (COPD) and allergic asthma. In a new report appearing in the August 2013 issue of 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, called "BLT1," promotes inflammation, while the second receptor, called "BLT2," has a potential to weaken inflammation during an allergic reaction. This discovery also is important because until now, BLT2 was 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, M.D., study author from the Department of Pulmonary Medicine at the Graduate School of Medical and Dental Sciences at Kagoshima University in Kagoshima, Japan. "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." To make this discovery, scientists compared the allergic reactions in BLT2-gene deleted mice to those in normal mice. Then an allergic asthma reaction was provoked by inhalation of allergens. BLT2-gene deleted mice showed more inflammatory cells in the lung compared to normal mice. Without the BLT2 gene, lung allergic inflammation was stronger than that of normal mice. The production of interleukin-13, an important mediator of allergic inflammation from T lymphocytes, was increased in the group without the BLT2 gene.
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