title: IL-4R suppresses airway inflammation in bronchial asthma by inhibiting the IL-4/STAT6 pathway.
abstract: This study aims to explore the mechanisms of how IL-4R suppresses airway inflammation in bronchial asthma by inhibiting the IL-4/STAT6 pathway.
  
  
  
  A total of 27 BALB/c male mice were selected and divided into control, asthma and IL-4R groups. Ovalbumin-induced mouse asthma model was established. Maximal pulmonary resistance was recorded. Hematoxylin and eosin (HE) and periodic acid Schiff (PAS) staining were conducted to observe the pathological changes in lung tissue. Optical microscope was used to detect numbers of total cells, mastocytes, eosinophils (EOS), neutrophils, and lymphocytes. Enzyme-linked immunosorbent assay (ELISA) was adopted for the levels of immunoglobulin (IgE), IL-4, IL-5, IL-13 and interferon (IFN)-γ, flow cytometry for the percentages of IL-4+CD4+, IFN-γ+CD4+and IFN-γ+/IL-4+in total thymus-derived (T) cells, qRT-PCR for the mRNA expressions of IL-4, IL-5, IL-13, STAT6, pSTAT6, suppressor of cytokine signaling (SOCS), inducible nitric oxide synthase (iNOS) and vascular cell adhesion molecule (VCAM)-1, and Western blotting for the protein expressions of STAT6 and pSTAT6.
  
  
  
  Compared with the control group, the asthma group had irregular tissue structure and severe inflammation, increases in maximal pulmonary resistance, numbers of total cells, EOS, neutrophils, and lymphocytes, levels of IgE, IL-4, IL-5 and IL-13, percentages of IFN-γ+CD4+and IFN-γ+/IL-4+in total T cells, mRNA expressions of IL-4, IL-5, IL-13, STAT6, pSTAT6, SOCS, iNOS and VCAM-1, and protein expressions of STAT6 and pSTAT6, but decreases in IFN-γ level and percentage of IL-4+CD4+in total T cells. Compared with the asthma group, the IL-4R group had relatively regular tissue structure and light inflammation, declined maximal RL, numbers of total cells, EOS, neutrophils, and lymphocytes, contents of IgE, IL-4, IL-5 and IL-13, percentages of IFN-γ+CD4+and IFN-γ+/IL-4+in total T cells, mRNA expressions of IL-4, IL-5, IL-13, STAT6, pSTAT6, SOCS, iNOS and VCAM-1, and protein expressions of STAT6 and pSTAT6, but elevated IFN-γ content and percentage of IL-4+CD4+in total T cells.
  
  
  
  Our results demonstrate that IL-4R can suppress airway inflammation in bronchial asthma by inhibited the IL-4/STAT6 pathway, which may provide a new therapeutic approach for the treatment of bronchial asthma.
authors.affiliation: Department of Respiration Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, PR China. Electronic address: liuying03341237@126.com.
authors.forename: Ying
authors.initials: Y
authors.lastname: Liu
authors.affiliation: Department of Respiration Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, PR China.
authors.forename: Hui
authors.initials: H
authors.lastname: Zhang
authors.affiliation: Department of Respiration Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, PR China.
authors.forename: Ran
authors.initials: R
authors.lastname: Ni
authors.affiliation: Department of Respiration Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, PR China.
authors.forename: Wen-Qing
authors.initials: WQ
authors.lastname: Jia
authors.affiliation: Department of Respiration Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, PR China.
authors.forename: Yuan-Yuan
authors.initials: YY
authors.lastname: Wang
mesh_terms: D000818:Animals; D001249:Asthma / Q000503:physiopathology*; D015153:Blotting, Western; D004195:Disease Models, Animal; D004797:Enzyme-Linked Immunosorbent Assay; D004804:Eosinophils / Q000378:metabolism; D007249:Inflammation / Q000473:pathology; D015847:Interleukin-4 / Q000378:metabolism*; D008214:Lymphocytes / Q000378:metabolism; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D009504:Neutrophils / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D010047:Ovalbumin / Q000008:administration & dosage; D019948:Receptors, Interleukin-4 / Q000378:metabolism*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D050800:STAT6 Transcription Factor / Q000378:metabolism*; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism
chemical_list: D019948:Receptors, Interleukin-4; D050800:STAT6 Transcription Factor; D019010:Vascular Cell Adhesion Molecule-1; D015847:Interleukin-4; D010047:Ovalbumin; D052247:Nitric Oxide Synthase Type II
keywords: Airway inflammation; Bronchial asthma; IL-4; IL-4R; STAT6