Allergy Asthma Respir Dis.
2022 Jul;10(3):145-152. 10.4168/aard.2022.10.3.145.
Cigarette smoke extract contributes to the inception and aggravation of asthmatic inflammation by stimulating innate immunity
- Affiliations
-
- 1Department of Translational Medicine, Seoul National University College of Medicine, Seoul, Korea
- 2Institute of Allergy and Clinical Immunology, Seoul National University Medical Research Center, Seoul, Korea
- 3Department of Internal Medicine, Chung-Ang University Hospital, Seoul, Korea
- 4Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Korea
- KMID: 2532268
- DOI: http://doi.org/10.4168/aard.2022.10.3.145
Abstract
- Purpose
Smoking is a risk factor for the development of asthma and worsens the long-term prognosis of asthma. This study investigated the effect of cigarette smoke extract (CSE) on innate immune cells such as innate lymphoid cells (ILCs) and macrophages in a murine model of induced asthma.
Methods
Six-week-old female BALB/C mice were exposed to ovalbumin (OVA) via an intranasal route with or without CSE for 8 weeks to establish a chronic murine asthma model. Airway hyperresponsiveness (AHR), airway inflammatory cells from bronchoalveolar lavage fluid, and the population of CD4 + T cells, ILCs, and macrophages in the lungs were studied to evaluate the effect of chronic CSE exposure on asthma.
Results
Mice intranasally exposed to CSE along with OVA treatment (CSE/OVA) had significantly enhanced AHR, eosinophilic inflammation, increased IL-13 and IL-17 producing CD4 + T cells compared to mice intranasally exposed to OVA only. On the contrary, the frequency of Foxp3 + in CD4 + T cells was reduced in the CSE/OVA group. CSE enhanced the dendritic cell (DC) population, especially MHCII + DC with antigen-presenting capacity. Among ILCs, the CSE/OVA group showed a significant increase of IL-13-producing type 2 ILCs, but not interferon-γ+ ILC1s and IL-17 + ILC3s. . Among macrophages, alveolar macrophage and Ym-1 and FIZZ1 positive M2 macrophage populations were significantly induced by CSE exposure alone and when combined with OVA treatment.
Conclusion
In this study, we showed that long-term exposure to cigarette smoke contributes to the inception and aggravation of asthmatic inflammation by enhancing DCs, ILC2, and M2 alveolar macrophage populations in the mouse model.
