Inhibition of phosphoinositide 3-kinase activity attenuates neutrophilic airway inflammation and inhibits pyrin domain-containing 3 inflammasome activation in an ovalbumin-lipopolysaccharide-induced asthma murine model.

Qun Li, Guiyun Jiang, Yunxiang Lv

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Article in Molecular biology reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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1 citing paper in PubMed.

Modulation of the NF-κB signaling pathway by the combined strategy of tocilizumab and dexamethasone for asthma therapy.Respiratory research · 2026
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Authors and funding

3 authors.

Qun LiDepartment of Pulmonary and Critical Care Medicine, The Second Affiliated Hospital of Bengbu Medical University, Anhui, China.

Guiyun JiangDepartment of Clinical Laboratory, The First Affiliated Hospital of Bengbu Medical University, Bengbu, 233000, Anhui, China.

Yunxiang LvDepartment of Pulmonary and Critical Care MedicineAnhui Clinical and Preclinical Key Laboratory of Respiratory DiseaseMolecular Diagnosis Center, The First Affiliated Hospital of Bengbu Medical University, Bengbu, 233000, Anhui, China. yunxianglv@126.com.ORCID http://orcid.org/0000-0003-0417-1141

Funding

Key Project of Natural Science of Colleges and University in Anhui Province KJ2021A0750Key Research and Development Plan of Anhui Province 211094057061

6 · The paper itself

Abstract

backgroundExisting investigations suggest that the blockade of phosphoinositide 3-kinase (PI3K) activity contributes to inflammatory solution in allergic asthma, but whether this inhibition directly attenuates neutrophilic airway inflammation in vivo is still unclear. We explored the pharmacological effects of LY294002, a specific inhibitor of PI3K on the progression of neutrophilic airway inflammation and investigated the underlying mechanism. METHODS AND

resultsFemale C57BL/6 mice were intranasally sensitized with ovalbumin (OVA) together with lipopolysaccharide (LPS) on days 0 and 6, and challenged with OVA on days 14-17 to establish a neutrophilic airway disease model. In the challenge phase, a subset of mice was treated intratracheally with LY294002. We found that treatment of LY294002 attenuates clinic symptoms of inflammatory mice. Histological studies showed that LY294002 significantly inhibited inflammatory cell infiltration and mucus production. The treatment also significantly inhibited OVA-LPS induced increases in inflammatory cell counts, especially neutrophil counts, and IL-17 levels in bronchoalveolar lavage fluid (BALF). LY294002 treated mice exhibited significantly increased IL-10 levels in BALF compared to the untreated mice. In addition, LY294002 reduced the plasma concentrations of IL-6 and IL-17. The anti-inflammatory effects of LY29402 were correlated with the downregulation of NLRP3 inflammasome.

conclusionsOur findings suggested that LY294002 as a potential pharmacological target for neutrophilic airway inflammation.

Indexed as

AsthmaBronchoalveolar Lavage FluidChromonesDisease Models, AnimalInflammasomesLipopolysaccharidesMice, Inbred C57BLMorpholinesNeutrophilsNLR Family, Pyrin Domain-Containing 3 ProteinOvalbuminPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsAnimalsFemaleInflammation2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneChromonesInflammasomesInterleukin-17LipopolysaccharidesMorpholinesNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseOvalbuminPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsInterleukin-17LY294002Neutrophilic airway inflammationNLRP3Phosphoinositide 3-kinase

Identifiers

PMID38811424

DOI10.1007/s11033-024-09360-5

PMCPMC11136729

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