Biomarkers of airway inflammation and immunotherapy

allergy is the most common food- related trigger of anaphy-lactic reactions in the United States and some other countires. 1 Probiotic and Peanut Oral Immunotherapy (PPOIT) was shown to be effective at inducing desensitization and promoting sustained unresponsiveness (SU), however, there is an apparent lack of data on the long- term effectiveness and safety. 2 Hsiao and colleagues aimed to evaluate the mechanism by which PPOIT altered peanut- specific humoral immunity and how these mechanisms relate to SU induction. 3– The study is a double- blinded placebo- controlled randomized trial that included 62 children with peanut allergy. Plasma levels of whole peanut and peanut components were measured, along with specific- IgE (sIgE) and specific- IgG4 (sIgG4) using ImmunoCAP, in addition to measuring salivary peanut- specific- IgA (sIgA) quantified by ELISA. sIgE levels were significantly reduced post treatment, while sIgG4 levels, like sIgA levels, were significantly increased by end- of- treatment, but were lowered to placebo levels once treatment stopped. This study was the first to evaluate the long- term immunologic effects of PPOIT and resulted in two main novel find-ings. The first being that peanut and peanut component sIgG4 levels were directly proportional to the amount of peanut ingested post-treatment; increased peanut sIgG4 levels being reflective of an ac-tive allergen exposure. The second observation was that peanut and peanut component sIgG4 levels were significantly lower in subjects with persistent SU compared to those without. The study also pro-vides evidence on the important role that allergen specific- IgE plays in the attainment and persistence of SU. The authors highlighted intrapulmonal cellular and humoral inflammatory pattern in patients with humoral immunodeficiency associated with lung function parameters. This is mirrored by gene regulation and secretion of proinflammatory secreted mediators IL- 1 β , IL- 6, CXCL- 8 and TNF- α , which were induced in lower airway cells along with local neutrophil counts. In addition, bronchiectasis- related airway dysfunction was associated with higher levels of proinflammatory cell load and increased levels of proinflammatory- secreted mediators IL- 1 β , IL- 6, CXCL- 8 and TNF- α .