Expression of Toll‐like receptors in nasal epithelium in allergic rhinitis

Toll‐like receptors (TLRs) are important in barrier homeostasis, but their role in airborne allergies is not fully understood. The aim was to evaluate baseline and allergen‐induced expression of TLR proteins in nasal epithelium during allergic rhinitis. Nineteen otherwise healthy non‐smoking volunteers both allergic to birch pollen and non‐allergic controls were enrolled. We took nasal biopsies before and after off‐seasonal intranasal birch pollen or diluent challenge. The expression of epithelial TLR1‐7, TLR9‐10, and MyD88 proteins was immunohistochemically evaluated from the nasal biopsies. The TLR1‐3 and TLR5‐10 mRNAs were observed by RNA‐microarray. Baseline epithelial expression of TLR proteins was wide and identical in controls and atopics. After off‐seasonal intranasal birch pollen challenge, a negative change in the expression score of TLR1 and TLR6 proteins was detected in the atopic group. TLR mRNA expression was not affected by birch pollen challenge. Nasal epithelium seems to express all known TLRs. The mechanisms by which TLR1, and TLR6 proteins could affect pollen allergen transport need further studies.     

PAP treatment in patients with OSA does not induce long‐term nasal obstruction

We hypothesized that positive airway pressure treatment would induce nasal obstruction and decrease nasal cavity due to mucosal swelling. We further hypothesized that subjective and objective nasal obstruction at baseline would negatively affect positive airway pressure adherence. A total of 728 patients with sleep apnea were investigated in the Icelandic Sleep Apnea Cohort at baseline and 2 years after starting positive airway pressure. Patients underwent home sleep apnea testing at baseline. Questionnaires were answered and acoustic rhinometry was completed at baseline and follow‐up. The proportion of patients reporting subjective nocturnal nasal obstruction was reduced (baseline: 35% versus follow‐up: 24%; p < 0.001). Small interior nasal dimensions increased (p < 0.001) independent of adherence to treatment. Small nasal volume at baseline was a determinant for becoming a non‐user of positive airway pressure treatment (odds ratio 2.22, confidence interval 95% 1.35–3.67, p = 0.002). Subjective nasal obstruction decreased 2 years after initiating positive airway treatment in sleep apnea, and objectively small nasal dimensions increased. Small nasal volume at baseline was a negative predictor for positive airway pressure treatment adherence. Maybe most importantly, positive airway pressure treatment did not cause long‐term objective or subjective nasal obstruction.     

Frequent BCOR aberrations in extranodal NK/T‐Cell lymphoma,nasal type

Extranodal natural killer/T cell lymphoma (ENKTL) is a rare subtype of lymphoma. Recurrent mutations in the JAK‐STAT pathway, recently reported in ENKTL cases, are interesting in terms of both pathogenesis and inhibitor therapy. However, the frequencies of these mutations are low and variable among reports, and other pathognomonic mutations in ENKTL remain to be elucidated. In the present study, targeted capture sequencing of 602 cancer‐related genes from 25 frozen ENKTL samples was performed, 11 of which were matched to normal samples. Several recurrent somatic mutations involving BCOR (32%), TP53 (16%), DDX3X (12%), FAT4 (8%), NRAS (8%), MLL3 (12%), and MIR17HG (8%) were identified. The pattern of BCOR aberrations (1 nonsense and 5 frame‐shift mutations, a mutation leading to a splicing error, and gene loss) suggested that loss of function of BCOR was the functionally important outcome of such changes. The literature was reviewed and the public data on BCOR aberrations was reanalyzed and it was found that the aberrations were frequently found in myeloid neoplasms, but, interestingly, were highly specific to ENKTL among lymphoid malignancies. Given the high frequency and pattern of aberration, BCOR is likely to play an important role in ENKTL pathogenesis as a tumor suppressor gene. © 2016 Wiley Periodicals, Inc.