xRead - Nasal Obstruction (September 2024) Full Articles

20426984, 2021, 3, Downloaded from https://onlinelibrary.wiley.com/doi/10.1002/alr.22741 by Stanford University, Wiley Online Library on [01/07/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License

383

Orlandi et al.

delineating many of the immunologic responses to respi ratory viral infection in acute URI, these have involved healthy controls or patients with lower respiratory dis ease such as asthma, making direct application to CRS problematic. In vitro studies with sinonasal epithelial cells derived from CRS patients can elucidate the response to res piratory viral infection. In 1 study, 1017 sinus air-liquid interface epithelial cells were differentiated from patients who underwent ESS for CRS. Cultures were chal lenged with RV-A, RV-B, and RV-C species. Viral yield, cytokine/chemokine production, and markers of cellu lar cytotoxicity were measured. RV-B strains had lower viral yield, decreased host immune viral response, and were less cytotoxic compared to RV-A and RV-C strains. This supports clinical observations that RV-A and RV-C result in more severe upper respiratory infections than RV B. Another group 383 inoculated commercial ALI cultures from nasal polyp cells with RV-A, RV-B, and RV-C species. RV-A and RV-C species again provoked greater epithelial response, as characterized by decreased MCC, cytokine secretion, and induced gene expression compared to RV-B. These data suggest that identification of RV species at the time of RS infection could help to predict disease severity. Another group 386 also derived nasal epithelial cells from CRS patients and controls. The cultures were infected with RV-16. While no difference was found by this study in IL-6 and IL-8 levels when comparing CRS and control cultures following RV infection, IFN- β induction was not noted in the CRS group. The authors speculate that this could lead to delayed viral clearance. Overall, invitro studies support the idea that rhinovirus can lead to alterations in the nasal epithelial cell immuno logic homeostasis in CRS and that different RV species may have differential severity. In summary, the epidemiologic data predominantly sup port an association between higher rates of viral infection in CRS patients than in controls; however, the data are inconsistent, particularly regarding genus of virus isolated and association with polyp status. The invitro studies sug gest that infection by RV leads to alterations in immuno logic homeostasis, but additional studies are needed to clarify the extent to which viral insults are an antecedent factor, chronically present, or merely result in exacerba tions of a patient’s underlying sinonasal symptoms. Recent findings 754 suggest that CRSsNP patients with viral infec tion have worse endoscopic and radiographic measures of disease severity. Combined with previous studies such as the identification of a missense mutation in CDHR3 (the viral receptor for rhinovirus-C) as a risk factor for development of CRS. 1018 These data suggest that additional research is needed to elucidate the potential for virome host genome interactions as a risk for development of CRS.

Viruses as a Contributing Factor for CRS Aggregate Grade of Evidence: C (level 3: 1 study; level 4: 12 studies; level 5: 5 studies; Table IX-22).

IX.C.17 Contributing Factors for CRS: Occupational and Environmental Factors Because of limited data, CRSsNP and CRSwNP are com bined in this analysis. Occupational and environmental exposures can con tribute to the development of CRS and lead to worsen ing disease severity. 1020–1022 Mucosa lining the nasal cav ity and paranasal sinuses is the first area to interact with smoke, pollutants, or toxins during respiration. 1023 Expo sure to particulates in upper airway diseases may relate to alterations of the sinonasal barrier, microbiome changes, and/or propagation of inflammation. 156,1021 There is high-level evidence that cigarette smoke con tributes to CRS, in addition to lower airway diseases such as asthma. 1023–1025 Tobacco smoke reduces MCC by altering chloride secretion and CBF, and tobacco smoke inhibits ciliogenesis in animal models. 896,1026 Both active and passive smoking have been shown to contribute to the development of CRS throughout childhood and adulthood. 15,1023,1025,1027 In a large, population based analy sis, current smoking was associated with increased odds of several symptoms of CRS, including facial pain and pres sure (odds ratio [OR] 1.52, 95% confidence interval [CI] 1.03-2.24) and smell loss (OR, 1.8; 95% CI, 1.01-3.11), and former smoking was associated with smell loss (OR, 1.9; 95% CI, 1.24-2.89). 13 A case control study showed that an increased likelihood of CRS was associated with passive smoke exposure at work (OR, 2.81; 95% CI, 1.42-5.57) and at private functions (OR, 2.60; 95% CI, 1.74-3.89). 1027 Fur ther, the odds of having CRS increased with second-hand smoke exposure in multiple venues, including at home andwork. 1027 To the best of our knowledge, smoking has not been reported to be associated with reduced thera peutic efficacy of recommended treatment for CRS nor failure of ESS. Limited research into the impacts of non conventional cigarette smoking exists, including on elec tronic cigarettes, however cannabis in combination with tobacco smoke appears to further worsen CRS severity compared to tobacco smoke alone. 1028 Public health inter ventions that limit smoking would likely serve to reduce the morbidity of CRS. Beyond tobacco smoke exposure, fewer conclusions on other occupational and environmental factors could be