title: Interleukin-22 produced by alveolar macrophages during activation of the innate immune response.
abstract: OBJECTIVE
  Interleukin (IL)-22 is important for mucosal host defense. Whereas previous studies focus on lymphocytes as sources of IL-22, we determined whether IL-22 is produced by inflammatory cells in the lungs other than T-lymphocytes during the activation of the innate immune response.
  
  
  METHODS
  Inflammatory cells in the lungs of Balb/c mice were primed by endotoxin (LPS, 10 μg) or peptidoglycan (PG, 40 μg) intranasally (3 days). After CD3 + cell depletion, lung homogenates were re-stimulated 24 h with LPS (100 ng/ml), PG (10 μg/ml), IL-23 (100 ng/ml) or vehicle. Human BAL macrophages were stimulated 24 h with PG (50 μg/ml) and IL-23 (100 ng/ml) or vehicle. The release of IL-22 was measured with ELISA and intracellular IL-22 with immunostaining. For statistics, either Dunnett or Students t test method was employed (n = 3-8).
  
  
  RESULTS
  Re-stimulation in vitro increased concentrations of mouse IL-22 protein irrespective of priming in vivo. A majority of macrophages in mouse lung and BAL samples displayed immunostaining for IL-22. In analogy, human BAL macrophages released IL-22 protein, and a third of these cells displayed immunostaining for IL-22.
  
  
  CONCLUSIONS
  Alveolar macrophages can produce and release IL-22 during the activation of the innate immune response and thereby constitute a potentially important regulator of mucosal host defence in the lungs.
authors.affiliation: Lung Immunology Group, Department of Internal Medicine and Clinical Nutrition/Respiratory Medicine and Allergology, Institute of Medicine, Sahlgrenska Academy at Gothenburg University, Guldhedsgatan 10A, Box 480, 405 30 Gothenburg, Sweden. marit.hansson@gu.se
authors.forename: Marit
authors.initials: M
authors.lastname: Hansson
authors.forename: Elin
authors.initials: E
authors.lastname: Silverpil
authors.forename: Anders
authors.initials: A
authors.lastname: Lindén
authors.forename: Pernilla
authors.initials: P
authors.lastname: Glader
mesh_terms: D000818:Animals; D000943:Antigens, Differentiation / Q000276:immunology; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology / Q000276:immunology; D017252:CD3 Complex / Q000276:immunology; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology; D002478:Cells, Cultured; D005260:Female; D006801:Humans; D007113:Immunity, Innate / Q000276:immunology*; D053759:Interleukin-23 / Q000494:pharmacology; D007378:Interleukins / Q000276:immunology*; D008070:Lipopolysaccharides / Q000494:pharmacology; D016676:Macrophages, Alveolar / Q000276:immunology*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D010457:Peptidoglycan / Q000494:pharmacology; D000097043:Interleukin-22
chemical_list: D000943:Antigens, Differentiation; D017252:CD3 Complex; D053759:Interleukin-23; D007378:Interleukins; D008070:Lipopolysaccharides; D010457:Peptidoglycan; D000097043:Interleukin-22; C036763:monocyte-macrophage differentiation antigen