We explored the effects of eicosapentaenoic acid (EPA) on asthma, focusing particularly on its ability to alleviate eosinophilic airway inflammation. Through a well-structured experiment, male C57BL6 mice were sensitized and challenged with ovalbumin, simulating allergic airway responses. After treating these mice with EPA, we measured various outcomes, including cell counts in bronchoalveolar lavage fluid and mRNA expressions in the lungs.
Our findings were encouraging! We observed that EPA not only reduced eosinophil accumulation in the airway but also lowered the expression of certain inflammatory mediators in the lungs. Moreover, when analyzing the metabolites of EPA, we identified 12-hydroxy-17,18-epoxyeicosatetraenoic acid (12-OH-17,18-EpETE) as a significant player in these processes. This metabolite's production increased with EPA treatment and allergic inflammation.
Notably, administering 12-OH-17,18-EpETE directly into the bloodstream helped in decreasing airway eosinophilic inflammation by downregulating a specific inflammatory signal in the lungs. In our in vitro studies, this compound also inhibited the release of an inflammatory substance known as CCL11 from human airway cells that were stimulated by interleukin-4.
Overall, these results suggest that EPA has a favorable impact against asthma by converting into beneficial metabolites. Specifically, 12-OH-17,18-EpETE appears to be a promising therapeutic agent for asthma sufferers.