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Abstract
Small proline-rich proteins (SPRRs), components of cornified cell envelope precursors, have recently been found to participate in airway diseases. However, their role in allergic airway inflammatory conditions remains unknown. Here, we explored the expression of SPRR3 in house dust mite (HDM)-sensitized/challenged mice and attempted to elucidate the regulatory role of SPRR3 in allergic airway inflammation. SPRR3 was identified via bioinformatics analysis of Gene Expression Omnibus (GEO) databases and further confirmed to be upregulated in the lungs of asthmatic mice. Knockdown of SPRR3 via the intratracheal route significantly inhibited eosinophils in bronchoalveolar lavage fluid (BALF) and suppressed the expressions of type 2 cytokines (IL-4, IL-5, and IL-13) in BALF and lung tissues. Further, SPRR3 knockdown reduced the expression of IL-33 and further attenuated the activation of the PI3K/AKT/NF-κB signaling pathway in the recruitment of group 2 innate lymphoid cells (ILC2s) to inhibit allergic airway inflammation. In vitro, SPRR3 siRNA could alleviate HDM-induced inflammatory responses in BEAS-2B cells. This study reveals the regulatory role of SPRR3 in allergic airway inflammation, identifying this protein as a potential novel therapeutic target for asthma.
Highlights
Asthma, a chronic airway disease, is characterized by airway inflammation and airway hyperresponsiveness
Screening with a threshold of p-value
Twenty candidate DEGs were found in the above two datasets. The heatmap of these 20 candidate DEGs in airway epithelial cells treated with IL-13 and asthmatic bronchial epithelial cells are shown in Figures 1B, C
Summary
A chronic airway disease, is characterized by airway inflammation and airway hyperresponsiveness. It is a heterogeneous disease with complex endotypes, among which type 2 high inflammation accounts for the majority of asthma cases [1, 2]. Many of the identified susceptibility genes for asthma are expressed in the SPRR3 Promotes Experimental Asthma airway epithelium, supporting the notion that airway epithelial cells are critical for the development of the disease [7]. The epithelial cell-derived alarmins, including IL-25, IL-33, and TSLP, play pivotal roles in connecting adaptive immunity and innate immunity [8]. Identifying the epithelial-derived mediator that regulates the expression of these cytokines is of great significance for understanding the molecular mechanism by which asthma is initiated
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