Whether airway hyperresponsiveness is a symptom of airway inflammation or airway remodeling, or whether it is the cause of long-term loss of lung function, remains controversial. Some investigators have hypothesized that aggressive treatment with anti-inflammatory therapies improves the long-term course of asthma beyond their salutary effects on parameters of asthma control and rates of exacerbation over time. 13 This contention has been supported by an observational study 14 that found long-term exposure to ICS was associated with an attenuation of the accelerated decline in lung function previously reported in asthmatics; more studies are required to substantiate these findings.
An antileukotriene is a drug which functions as a leukotriene -related enzyme inhibitor ( arachidonate 5-lipoxygenase ) or leukotriene receptor antagonist ( cysteinyl leukotriene receptors ) and consequently opposes the function of these inflammatory mediators; leukotrienes are produced by the immune system and serve to promote bronchoconstriction , inflammation, microvascular permeability, and mucus secretion in asthma and COPD .  Leukotriene receptor antagonists are sometimes colloquially referred to as leukasts .
Omega-3 fatty acids have been shown to disrupt inflammation cell signaling pathways by binding to the GPR120 receptor.  This benefit however can be inhibited or even reversed if the ratio of Omega-6 / Omega-3 is too high as Omega-6 serves as a precursor to inflammatory chemicals ( prostaglandin and leukotriene eicosanoids ) in the body.   A high proportion of omega-6 to omega-3 fat in the diet shifts the physiological state in the tissues toward the pathogenesis of many diseases: prothrombotic, proinflammatory and proconstrictive.  Omega-6 competes with Omega-3 for the same rate limiting factor which is required for the health-benefits of Omega-3, directly reducing the action of Omega-3 in addition to pharmacologically counteracting Omega-3 benefits through its own action as a pro-inflammatory agent.