Bacterial secretion of histamine in the gut can influence allergic inflammation in the lung. Both H2Rdependent and -independent effects are observed, while murine expression of histamine metabolising enzymes may also alter the effects of histamine within the lung.

Suppressed expression and production of IL-27 were identified in serum, cervical lymph nodes, and conjunctiva in a murine model of experimental allergic conjunctivitis (EAC) with TSLP-driven Th2-dominant inflammation. The aggravated allergic inflammation was associated with enhanced Th17 hyperresponse and reduced Th1 and Treg cytokines via imbalanced activation of STAT1/STAT6 in WSX-1^−/−-EAC mice deficient for IL-27 signaling. The findings uncovered novel anti-inflammatory roles and signaling pathways of IL-27 in allergic inflammation.

Prostaglandin E2 decreases in induced sputum of hypersensitive asthmatics during oral challenge with aspirin. In nonsteroidal anti-inflammatory drug–exacerbated respiratory disease (NERD), sputum eosinophilic count is elevated as compared to aspirin-tolerant asthmatics with chronic rhinosinusitis with nasal polyposis (ATACRSwNP) or heathy controls (HC). Prostaglandin E2 (PGE2) levels in the induced sputum are higher in asthmatics (NERD and ATA-CRSwNP) reflecting chronic inflammation of bronchi despite control of the disease. During oral aspirin challenge, cyclooxygenases are inhibited. Aspirin-provoked bronchoconstriction in NERD is accompanied by decrease of PGE2 and rise of leukotriene E4 in the induced sputum.

In humans, CCR10 is highly expressed by blood ILC2s in severe asthmatic patients. CCR10⁺ ILC2s secrete little TH2 cytokines, but exhibit ILC1-like properties, including a capacity to produce IFN-γ. T-bet expression is increased in CCR10⁺ ILC2s when compared to CCR10⁻ ILC2s, whereas GATA3 expression is reduced.

Chronic hypersensitivity pneumonitis is a severe disease with a bad mid-term prognosis. Lymphocyte values in BAL and DLCO values at baseline, presence of honeycomb in HRCT, and UIP histologic pattern were found to be predictors of survival. At follow-up, all patients presented an EuroQol-5D score < 0.8 and a probable anxiety and depressive syndrome.

Risk for poor asthma outcomes varied between cluster-based asthma phenotypes defined 20 years earlier. The clinical prognosis of the cluster-based asthma phenotypes was stronger as compared to classical phenotypes. There was a tracking of asthma activity and lung function over the life course for each asthma cluster.

We found an inverted U-shaped relationship between ever-report of eczema and serum 25(OH)D level among US adults. There is a racial difference, as this relationship was observed among nonHispanic white population, but not nonHispanic black population. We see more reduction in risk of eczema beyond 75 nmol/L of vitamin D sufficiency level.

Allergen-specific immunotherapy induces an increase in activated Treg cells, IL-10-producing Treg cells, IL-22- producing Th cells, and reduces dysfunctional ILT3+ CD25+ Treg cells. Increased number of FOXP3⁺Helios⁺, IL-10⁺ and decreased ILT3⁺ Treg cell responses correlated with improved allergic symptoms. Allergen-specific immunotherapy improves clinical symptoms which relates to the correction of dysregulated T cell responses.

A modified peanut extract (MPE), made by reduction and alkylation, followed by aluminum hydroxide (Al(OH)₃) adsorption was similar or more immunogenic than unmodified peanut extract (PE). MPE demonstrated strongly improved safety compared to PE in relevant in vitro and in vivo assays. MPE showed efficacy in a murine model for immunotherapy, which supports further development of modified peanut allergens for subcutaneous immunotherapy.