IL-22 Is Deleterious along with IL-17 in Allergic Asthma but Is Not Detrimental in the Comorbidity Asthma and Acute Pneumonia

• Published in: International journal of molecular sciences 2023-06, Vol.24 (13), p.10418
• Main Authors: Goulart, Amanda, Boko, Mèdéton Mahoussi Michaël, Martins, Nubia Sabrina, Gembre, Ana Flávia, de Oliveira, Rômulo Silva, Palma-Albornoz, Sandra Patrícia, Bertolini, Thais, Ribolla, Paulo Eduardo Martins, Ramalho, Leandra Naira Zambelli, Fraga-Silva, Thais Fernanda de Campos, Bonato, Vânia Luiza Deperon
• Format: Article
• Language: English
• Subjects: Allergens; Allergies; Animals; Apoptosis; Asthma; Asthma - pathology; Bacterial pneumonia; Bronchoalveolar Lavage Fluid; CD11b antigen; CD11c antigen; Comorbidity; Computer software industry; Cytokines; Dendritic cells; Disease Models, Animal; Eosinophils; Helper cells; Immunotherapy; Inflammation; Interleukin 13; Interleukin 17; Interleukin 22; Interleukin 5; Interleukin-17 - genetics; Leukocytes (eosinophilic); Leukocytes (neutrophilic); Lung - pathology; Lungs; Lymphocytes; Lymphocytes T; Mice; Mice, Inbred BALB C; Ovalbumin; Pneumonia; Pneumonia - pathology
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms241310418

There is evidence that IL-22 and IL-17 participate in the pathogenesis of allergic asthma. To investigate the role of IL-22, we used IL-22 deficient mice (IL-22 KO) sensitized and challenged with ovalbumin (OVA) and compared with wild type (WT) animals exposed to OVA. IL-22 KO animals exposed to OVA showed a decreased number and frequency of eosinophils, IL-5 and IL-13 in the airways, reduced mucus production and pulmonary inflammation. In addition, IL-22 KO animals exhibited a decreased percentage and number of lung CD11c CD11b cells and increased apoptosis of eosinophils. Th17 cell transfer generated from IL-22 KO to animals previously sensitized and challenged with OVA caused a reduction in eosinophil frequency and number in the airways compared to animals transferred with Th17 cells generated from WT mice. Therefore, IL-22 is deleterious with concomitant secretion of IL-17. Our findings show a pro-inflammatory role for IL-22, confirmed in a model of allergen-free and allergen-specific immunotherapy. Moreover, during the comorbidity asthma and pneumonia that induces neutrophil inflammation, IL-22 was not detrimental. Our results show that targeting IL-22 would negatively affect the survival of eosinophils, reduce the expansion or migration of CD11c CD11b cells, and negatively regulate allergic asthma.