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    <responseDate>2026-10-13T13:38:45Z</responseDate>
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    <identifier>10.57760/sciencedb.j00217.14231</identifier>
    <datestamp>2026-07-24T17:40:29Z</datestamp>
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  <dc:date>2026-07-24</dc:date>
  <dc:title>Expression and Potential Role of FGL2 in Allergic Rhinitis- and Asthma-Related Airway Inflammation</dc:title>
  <dc:identifier>doi:10.57760/sciencedb.j00217.14231</dc:identifier>
  <dc:language>en</dc:language>
  <dc:description>To investigate the expression characteristics of fibrinogen-like protein 2 (FGL2) in allergic rhinitis- and asthma-related airway inflammation, and to preliminarily explore its effects on ADAM10 and allergy-related gene expression in human nasal epithelial cells.Bioinformatics analysis combined with reverse transcription-polymerase chain reaction (RT-qPCR) was used to detect the expression levels of FGL2 and a disintegrin and metalloproteinase 10 (ADAM10) in nasal mucosa of AR patients and AR model mice, as well as lung tissues of asthmatic mice. Human nasal epithelial cells (HNECs) were stimulated with recombinant FGL2 protein in vitro to evaluate ADAM10 expression. Transcriptomic sequencing was performed on primary epithelial cells after FGL2 stimulation, and intersected with a Th2-high epithelial RNA-seq dataset from asthma to identify key genes, which were further validated by RT-qPCR.FGL2 expression was significantly upregulated in the nasal mucosa of AR patients and mice, as well as in lung tissues of asthmatic mice. Recombinant FGL2 stimulation induced increased ADAM10 expression in HNECs. Intersection analysis identified 17 commonly upregulated allergic-related genes, among which sphingosine kinase 1 (SPHK1) was significantly upregulated in AR nasal mucosa and validated by RT-qPCR.This study found that FGL2 expression was increased in the nasal mucosa of patients with allergic rhinitis (AR), the nasal mucosa of AR model mice, and the lung tissues of asthmatic mice. In vitro experiments showed that recombinant FGL2 stimulation induced upregulation of ADAM10 expression in human nasal epithelial cells. Transcriptomic intersection analysis further identified SPHK1 and other candidate genes overlapping with the Th2-high asthmatic epithelial phenotype, and SPHK1 upregulation was validated in AR nasal mucosa. These findings suggest that FGL2 may participate in epithelial responses during allergic airway inflammation and provide candidate molecular evidence for understanding the shared inflammatory features of AR and asthma.</dc:description>
  <dc:subject>Allergic rhinitis; Asthma; Fibrinogen-like protein 2; A disintegrin and metalloproteinase 10; Sphingosine kinase 1; Epithelial cells; Transcriptomic sequencing</dc:subject>
  <dc:creator>Xinyu.Zhang</dc:creator>
  <dc:creator>Aoxing.Zhang</dc:creator>
  <dc:creator>Nadia •.Ablikmu</dc:creator>
  <dc:creator>Kewei.Lin</dc:creator>
  <dc:creator>Yin.Yao</dc:creator>
  <dc:creator>Yang.Liu</dc:creator>
  <dc:rights>EMBARGO</dc:rights>
  <dc:rights>https://creativecommons.org/licenses/by-nc/4.0/</dc:rights>
  <dc:type>dataset</dc:type>
  <dc:publisher>Science Data Bank</dc:publisher>
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