ArticleScientific reports2024
Progesterone modulates the immune microenvironment to suppress ovalbumin-induced airway inflammation by inhibiting NETosis.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Sex Differences in Cancer Immunotherapy-Clinical Evidence and Mechanisms With a Focus on NSCLC.Immunological reviews · 2026Review
- DNMT3A-mediated Methylation of IRF4 Alleviates Inflammatory Response in Allergic Rhinitis Mice.Applied biochemistry and biotechnology · 2026Article
- Inhaled biologics for respiratory diseases: clinical potential and emerging technologies.Drug delivery and translational research · 2025Review
- Sex-dependent effects of peptidylarginine deiminases on neutrophil function and long-term outcomes after spinal cord injury.Experimental neurology · 2025Article
- Immunotropic Effects of Steroid Hormone Medicines in Combination with Plasma-Treated Solution in Women of a Reproductive Age and Postmenopausal Women.Medical sciences (Basel, Switzerland) · 2025Article
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Authors and funding
8 authors.
Funding
Abstract
Studies have demonstrated that prior to puberty, girls have a lower incidence and severity of asthma symptoms compared to boys. This study aimed to explore the role of progesterone (P4), a sex hormone, in reducing inflammation and altering the immune microenvironment in a mouse model of allergic asthma induced by OVA. Female BALB/c mice with or without ovariectomy to remove the influence of sex hormones were used for the investigations. Serum, bronchoalveolar lavage fluid (BALF), and lung tissue samples were collected for analysis. The results indicated that P4 treatment was effective in decreasing inflammation and mucus secretion in the lungs of OVA-induced allergic asthma mice. P4 treatment also reduced the influx of inflammatory cells into the BALF and increased the levels of Th1 and Th17 cytokines while decreasing the levels of Th2 and Treg cytokines in both BALF and lung microenvironment CD45
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