Inflammation can be affected by fatty acid intake. Asthma is a chronic inflammatory disease, and rates of the disorder have been increasing around the world. While there are effective asthma treatments, not everyone with asthma can get relief; it's estimated that about ten percent of asthma patients do not respond to available medicines, which are usually inhaled corticosteroids. Recent studies have shown that fatty acids also affect asthma. Higher intake of omega-3 fatty acids has been associated with a reduction in asthma incidence while the intake of omega-6 or monosaturated fatty acids has been linked to an increase in inflammation and asthma.
Scientists are now starting to decipher the connection between fatty acids and asthma. New work reported in the Journal of Allergy and Clinical Immunology has shown that an enzyme called ELOVL6 is involved. This enzyme helps produce long-chain fatty acids in people, and ELOVL6 dysfunction has been associated with a variety of immune disorders, including atopic dermatitis. This condition is similar to asthma, noted senior study author Yuko Morishima of the University of Tsukuba.
The research ream developed a mouse model of asthma in which ELOVL6 was eliminated. In this study, the "fatty acid profile and allergen response of the mouse airways" were assessed, along with ELOVL6 levels in people with severe asthma.
This work revealed that ELOVL6 expression is abnormally low in severe asthmatics who do not get relief from available treatments. Airway inflammation, airway response to allergens, and goblet cell hyperplasia were all increased in mice that lacked ELOVL6 compared to mice with functional ELOVL6.
The body mass index (BMI) of severe asthmatics was not different from non-asthmatics, nor were the BMIs of the different groups of mice, suggesting that the loss of functional ELOVL6 was not influencing weight gain.
In mice without ELOVL6, the levels of a type of lipid called ceramides were elevated, along with a ceramide metabolite known as S1P.
"S1P is known to be potentially related to allergic inflammation, thus we wondered what effect inhibiting its synthesis would have on our ELOVL6-deficient mouse model," noted Morishima. "Fascinatingly, we found that drug-induced inhibition of ceramide and S1P synthesis reduced not only airway inflammation in our model but also reduced the migration of immune cells out of lymph nodes and their cytokine production."
Lipid composition seems to be crucial to inflammatory responses in treatment-resistant asthma, and modulating that composition could be a way to make asthma treatments effective.
Sources: University of Tsukuba, Journal of Allergy and Clinical Immunology