title: Immune modulatory effects of IL-22 on allergen-induced pulmonary inflammation.
abstract: IL-22 is a Th17/Th22 cytokine that is increased in asthma. However, recent animal studies showed controversial findings in the effects of IL-22 in allergic asthma. To determine the role of IL-22 in ovalbumin-induced allergic inflammation we generated inducible lung-specific IL-22 transgenic mice. Transgenic IL-22 expression and signaling activity in the lung were determined. Ovalbumin (OVA)-induced pulmonary inflammation, immune responses, and airway hyperresponsiveness (AHR) were examined and compared between IL-22 transgenic mice and wild type controls. Following doxycycline (Dox) induction, IL-22 protein was readily detected in the large (CC10 promoter) and small (SPC promoter) airway epithelial cells. IL-22 signaling was evidenced by phosphorylated STAT3. After OVA sensitization and challenge, compared to wild type littermates, IL-22 transgenic mice showed decreased eosinophils in the bronchoalveolar lavage (BAL), and in lung tissue, decreased mucus metaplasia in the airways, and reduced AHR. Among the cytokines and chemokines examined, IL-13 levels were reduced in the BAL fluid as well as in lymphocytes from local draining lymph nodes of IL-22 transgenic mice. No effect was seen on the levels of serum total or OVA-specific IgE or IgG. These findings indicate that IL-22 has immune modulatory effects on pulmonary inflammatory responses in allergen-induced asthma.
authors.affiliation: Respiratory Department, The Second Affiliated Hospital, Xi'an Jiaotong University School of Medicine, Xi'an, Shaanxi, China; Division of Allergy and Clinical Immunology, Department of Internal Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America.
authors.forename: Ping
authors.initials: P
authors.lastname: Fang
authors.affiliation: Division of Allergy and Clinical Immunology, Department of Internal Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America.
authors.forename: Li
authors.initials: L
authors.lastname: Zhou
authors.affiliation: Division of Allergy and Clinical Immunology, Department of Internal Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America.
authors.forename: Yuqi
authors.initials: Y
authors.lastname: Zhou
authors.affiliation: Division of Pediatric Rheumatology, Children's Hospital of Pittsburgh, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, United States of America.
authors.forename: Jay K
authors.initials: JK
authors.lastname: Kolls
authors.affiliation: Division of Allergy and Clinical Immunology, Department of Internal Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America.
authors.forename: Tao
authors.initials: T
authors.lastname: Zheng
authors.affiliation: Division of Allergy and Clinical Immunology, Department of Internal Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America.
authors.forename: Zhou
authors.initials: Z
authors.lastname: Zhu
mesh_terms: D000485:Allergens / Q000276:immunology*; D000818:Animals; D018925:Chemokines / Q000378:metabolism; D005786:Gene Expression Regulation / Q000187:drug effects; D006967:Hypersensitivity / Q000150:complications; D056747:Immunomodulation; D007378:Interleukins / Q000235:genetics / Q000378:metabolism*; D051379:Mice; D008822:Mice, Transgenic; D009928:Organ Specificity; D010047:Ovalbumin / Q000009:adverse effects; D011014:Pneumonia / Q000150:complications / Q000235:genetics / Q000276:immunology* / Q000378:metabolism*; D050796:STAT3 Transcription Factor / Q000378:metabolism; D000097043:Interleukin-22
chemical_list: D000485:Allergens; D018925:Chemokines; D007378:Interleukins; D010047:Ovalbumin; D050796:STAT3 Transcription Factor; D000097043:Interleukin-22