Kim MA, et al. Allergy Asthma Immunol Res. 2018 Nov;10(6):648-661. https://doi.org/10.4168/aair.2018.10.6.648

Background: Prominent expression of YKL-40 has been associated with pathological conditions characterized by tissue remodeling. We determined the expression level and distribution pattern of YKL-40 in allergic nasal mucosa and evaluated the effect of YKL-40 on the proliferation and migration of fibroblasts, the production of the mediators related to tissue remodeling, and collagen production. Additionally, the cytokine-driven regulation of YKL-40 expression was evaluated in cultured epithelial cells. Methods: The expression of YKL-40 in normal, mild, and moderate/severe allergic nasal mucosa was evaluated using real-time polymerase chain reaction (PCR), Western blot, and immunohistochemistry. Fibroblast migration was observed using a scratch wound method, and proliferation was determined by the MTT methods. Expression of proteoglycans, transforming growth factor (TGF) beta1, MMP2, MMP9, TIMP1, TIMP2, and collagen concentration were analyzed in fibroblasts treated with YKL-40. The expression levels of YKL-40 in cultured epithelial cells were examined after stimulation with mediators including Th2 cytokines, interferon (IFN)gamma, and TNF-alpha with real-time PCR and ELISA. Results: The expression of YKL-40 was up-regulated in allergic rhinitis and distributed in superficial epithelium, submucosal glands, and vascular endothelium, in addition to infiltrating cells. TGF-beta1, TIMP1, MMP9, and biglycan were up-regulated in fibroblasts on stimulation with YKL-40, accompanying increased proliferation and migration, and collagen production. IL-13, IFN-gamma, and TNF-alpha induced the increased production of YKL-40 in cultured epithelial cells. Conclusion: YKL-40 is up-regulated in mild and moderate/severe persistent allergic rhinitis, and its expression can be regulated differentially by different cytokines, possibly contributing to the remodeling of nasal mucosa in allergic rhinitis.

Kim M, et al. Yonsei Med J. 2019 Oct;60(10):960-968. https://doi.org/10.3349/ymj.2019.60.10.960

We discuss the effects of air pollutants on upper airway disease; the topic has hitherto received little attention. Several epidemiological studies have shown that air pollutants aggravate airway diseases including asthma, bronchitis, and chronic obstructive pulmonary disorder. Pollutants also have negative effects on other upper airway diseases such as allergic and nonallergic rhinitis, sinusitis, and otitis media. Traffic-related air pollutants (diesel exhaust particles and nitrogen dioxide and tobacco smoke) have been widely studied in this context. Increasing evidence suggests that particulate matter, photochemical pollutants, and ozone are associated with such conditions. Young children and the obese are more vulnerable. Work in vivo and in vitro has explored the relationships between pollutants and disease, and possible pathophysiological mechanisms. Reactive oxygen species, apoptosis, and inflammation are all in play. Traffic-derived materials and tobacco smoke are major air pollutants that aggravate upper airway disease. Novel mechanisms of action have been suggested and risk factors have been defined. However, the data are conflicting, and controlled prospective studies are required.