Exposure to environmental black carbon exacerbates nasal epithelial inflammation via the reactive oxygen species (ROS)–nucleotide‐binding, oligomerization domain–like receptor family, pyrin domain containing 3 (NLRP3)–caspase‐1–interleukin 1β (IL‐1β) pathway

Abstract

Background Allergic rhinitis AR is an increasing challenge to public health worldwide Exposure to environmental black carbon BC is associated with increased risk of allergic rhinitis but the molecular mechanisms underlying its toxicity have not been fully elucidated The aims of the present study were therefore to determine the effect of BC on the expression of interleukin β IL-β and to investigate the mechanism underlying BC-induced IL-β production in pollen-sensitized human nasal epithelial cells hNECs Methods Nasal mucosal samples collected from patients undergoing nasal surgery were used to isolate and culture epithelial cells as air-liquid interface ALI cultures Cultures exposed to BC ± pollen allergen for hours were assessed for the presence of IL-β the production of reactive oxygen species ROS and activation of the nucleotidebinding oligomerization domain-like receptor family pyrin domain containing NLRP inflammasome Furthermore the mechanisms underlying BC ± pollen allergen-induced IL-β in hNECs were evaluated Results Exposure to BC significantly increased the production of IL-β and ROS and the expression of NLRP in hNECs compared with control all of which were significantly increased further by exposure to a combination of BC and pollen Incubation of hNECs with N-acetyl-L-cysteine NAC significantly attenuated BC ± polleninduced expression of ROS NLRP and IL-β NLRP and Caspase-inhibitors MCC and YVAD significantly inhibited IL-β expression and NLRP activation but not NLRP expression following exposure to BC ± pollen Conclusion These findings suggest that exposure to BC and pollen can exaggerate oxidative stress and significantly increase the expression of IL-β in hNECs and that this may involve a pathway integrating ROS-NLRP-Caspase-IL-β signaling © 2020 ARS-AAOA, LLC.

The NLRP3 inflammasome as a new target in respiratory disorders treatment

“…This suggested that the development of AR could be dependent on the ROS increase, which in turn, led to the activation of NLRP3 inflammasome and increased the level of IL-1b in nasal epithelial cells (27). Consistent results were obtained by Li et al on human nasal mucosa samples (hNEC) (28) showing that an ozone-oxidised black carbon (BC) and pollen exposure led to oxidative stress by increasing the level of ROS production. Consequently, it increased the mRNA and protein levels of NLRP3 and IL-1b.…”

Impact of Air Pollutants and Pollen on the Severity of Nonallergic Rhinitis: A Data-Oriented Analysis

“…Li et al reported that black carbon and pollen were associated with oxidative stress in the nasal mucosa and the combination of these two could even aggregate the inflammation. 28 In fact, NO 2 is a relatively weak oxidant, while O 3 is a strong oxidant. In mice and rat models, ozone induced nasal type 2 immunity and aggravated eosinophilic inflammation.…”

“…The risk was expressed as an odds ratio (OR) per one interquartile range (IQR, Q3 minus Q1) of each air pollutant. During the study period, the IQR levels of air pollutants were 2 (Q1-Q3;2-4) μg/m 3 for sulfur dioxide (SO 2 ), 16 (23)(24)(25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35)(36)(37)(38)(39) μg/m 3 for nitrogen dioxide (NO 2 ), 44 (60-104) μg/m 3 for ozone (O 3 ), 54 (32-86) μg/m 3 for particulate matter ≤10 μm in aerodynamic diameter (PM 10 ), 40(15-55) μg/m 3 for particulate matter ≤2.5 μm in aerodynamic diameter (PM 2.5 ), and 0.44 (0.4-0.84) μg/m 3 for carbon monoxide (CO).…”

Association between Concentration of Air Pollutants and Prevalence of Inflammatory Sinonasal Diseases: A Nationwide Cross-sectional Study

“…[38][39][40] This may be due to the effect of PM 10 to AR in terms of "nonspecific nasal hyperreactivity" rather than allergic sensitization; it has been proposed that PM 10 could exacerbate the inflammatory response of the nasal epithelial cells by increasing the oxidate distress in patients with AR when exposed to an aeroallergen. 11,41 The more specific mechanism of action by which air pollutants have effects on inflammatory sinonasal diseases including AR needs further investigation and research.…”