FPIES primarily affects infants and young children and is characterized by the delayed onset of gastrointestinal symptoms, predominantly repetitive vomiting, in response to a trigger food. Symptoms are often severe and can lead to shock. Diagnosis can be challenging due to a wide differential diagnoses and lack of disease biomarkers. FPIES is a clinical diagnosis, with allergy testing playing a very limited role, if any. Medically supervised oral food challenges are used to monitor resolution of disease, which generally occurs in early childhood. FPIES is an important condition presenting to clinicians in a variety of settings. Recent international consensus guidelines and a growing body of literature can better equip practitioners to care for these often-challenging patients.
RATIONALE: Nei-like 2 (NEIL2) is a DNA glycosylase enzyme that can excise oxidized damaged DNA bases like 5-hydroxyuracil. Neil2-null mice show more innate inflammatory response in the lungs stimulated by oxidative stress-inducing challenges. Here we hypothesized that NEIL2 regulates cat dander extract (CDE)-induced allergic airway inflammation and sensitization. METHODS: Wild-type (WT) and Neil2 KO mice were sensitized with 5 intranasal doses of CDE and challenged with CDE to elucidate allergic airway inflammation. Allergic airway inflammation and the lung mRNA expression of 84 genes known to be associated with allergic-inflammation were quantified. RESULTS: Multiple challenge with CDE in WT mice induced allergic inflammation characterized by an increase in eosinophilic airway inflammation, stimulation of mucin in airway epithelial cells, and levels of cat dander specific IgE in serum at 72-hours post challenge. Multiple CDE challenges in Neil2 KO mice enhanced these increases observed in WT mice. PCR array and qPCR identified Ccl11 and Il5ra as two eosinophilia-associated genes that were higher 4 h-post challenge in Neil2 KO mice. CONCLUSIONS: These observations indicates that NEIL2 suppress CDE-induced eosinophilic airway inflammation. NEIL2 may be a novel target for attenuating eosinophilic airway inflammation and antigenspecific IgE.
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