Obesity is an asthma comorbidity associated with increased severity, poor control, reduced steroid responsiveness and greater exacerbation and healthcare utilization rates. The obese asthma phenotype defined in several cluster studies, has paradoxically reduced levels of Type 2 T helper (Th2) cytokines, sputum eosinophils and exhaled nitric oxide (FeNO). As this cluster is refractory to steroid therapy, it is imperative that an intervention is sufficiently pleiotropic to reduce inflammation and restore airway •NO levels. We hypothesize that treatment with conjugated linolenic acid (cLA), nitrate (NO3‒) and nitrite (NO2‒) will restore •NO airway bio-availability and reduce inflammation via nitro-cLA (NO2-cLA) signaling, leading to improved airway hyperresponsiveness (AHR). In a pilot study, obese asthmatic subjects taking 1 gm NO3‒, 20 mg NO2‒ and 3 gm of cLA for 8 weeks demonstrated a 3 fold increase in free NO2-cLA plasma levels that tracked with increases in plasma cLA. FeNO values increased from an average of 19.3 ± 9.9 to 39.5 ± 10.4 ppb. Clinically there is a trending decrease in PC20 indicating a decrease in AHR as well as decreased asthma control questionnaire scores, indicative of better controlled asthma. Inflammatory markers including plasma tumor necrosis factor α and alveolar macrophage CD36 mRNA expression decreased after supplementation whereas interleukin (IL)-10 and glucocorticoid receptor expression (NR3C1) in alveolar macrophages increased. IL-10 and NR3C1 are both implicated in the inhibition of Th1 cytokine expression via suppression of nuclear factor κB. Further analyses of a larger clinical “n” as well as complimentary cell culture and animal model studies are needed to address the clinical changes seen after NO3‒/ NO2‒+cLA supplementation in obese asthmatics.