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Retinoic Acid Treatment Mitigates PM2.5-Induced Type 2 Inflammation: Insights into Modulation of Innate Immune
Hyun-Joo Lee1, Dong-Kyu Kim1,2
1Institute of New Frontier Research, Hallym University College of Medicine, Chuncheon 24252, Republic of Korea.
International Journal of Molecular Sciences
|April 13, 2024
Summary
Fine dust (PM2.5) worsens chronic rhinosinusitis with nasal polyps (CRSwNP) by increasing type 2 inflammation. Retinoic acid (RA) treatment may reduce this inflammation by modulating innate lymphoid cells (ILCs).
Area of Science:
- Immunology
- Environmental Health
- Otorhinolaryngology
Background:
- Particulate matter (PM) is linked to chronic rhinosinusitis with nasal polyps (CRSwNP).
- The role of PM in innate lymphoid cell (ILC) immunology and retinoic acid's (RA) therapeutic mechanisms in nasal polypogenesis are not fully understood.
Purpose of the Study:
- To investigate the impact of fine dust (PM2.5) on CRSwNP-related inflammation.
- To elucidate the mechanisms behind RA's therapeutic effects in this context.
Main Methods:
- Mice models with nasal polyps were exposed to PM2.5.
- Expression of type 2 cytokines, epithelial-derived cytokines (IL-33, IL-25), and ILC populations were analyzed.
- The effect of RA supplementation on ILCreg and IL-10 levels was assessed in human nasal polyp-derived epithelial cells (HNECs).
Main Results:
- PM2.5 exposure aggravated nasal mucosal damage in mice, upregulating type 2 inflammation.
- PM2.5 significantly increased type 2 and epithelial-derived cytokines (IL-33, IL-25) and ILC populations in HNECs.
- RA supplementation increased ILCreg expression and subsequent anti-inflammatory IL-10 levels.
Conclusions:
- PM2.5 exposure exacerbates type 2 inflammation in CRSwNP.
- RA treatment shows potential to ameliorate PM2.5-induced inflammation by modulating the innate immune response, specifically ILCs.
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