Inflammation is a type of immune system response to injury or irritation.  This response is problematic to the individuals who have asthma and chronic obstructive pulmonary disorder (COPD), though.  Asthma is a lung disease that causes inflammation and narrowing of the bronchi of the lungs, which makes it hard for people with asthma to breathe.  COPD is also a lung disease which causes poor air flow to the lungs due to inflammation, also making it hard for the individual to breathe.  Japanese researchers have gained knowledge on two specific receptors that respond to an inflammatory molecule known as “leukotriene B4,” which is found within individuals who have allergic asthma and COPD.  Prior to their findings, they believed that BLT1 and BLT2 receptors promoted this inflammation, when in fact, they actually have opposite roles.  BLT1 does promote inflammation, but the new finding is that BLT2 weakens the inflammation.

To test their findings, the deletion of BLT2-gene in mice versus normal mice was observed.  The mice had to inhale allergens in order to stimulate an allergic asthma reaction.  There were more inflammatory cells, along with an increase of interleukin-13, in the lungs of the BLT2-gene deleted mice than there were in the normal mice.  Interleukin-13 is a “mediator of allergic inflammation from T lymphocytes.”  Because of the results, it is believed that a more effective anti-leukotriene B4 drug can be made.  The leukotriene B4 drug right now blocks the pathways caused by the two different receptors; but since there is a better understanding of the roles of the receptors, creating a drug to target the two receptors differently and or separately will be more effective.