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Cryptococcosis is a disease caused by the pathogenic fungi Cryptococcus neoformans and Cryptococcus deuterogattii, and is responsible for causing primary infections. C. deuterogattii, unlike other species of the same genus, affects mostly immunocompetent individuals, having considerably increased its endemic area in recent years. Furthermore, infection caused by C. deuterogattii induces increased production of the cytokine IL-22 during pulmonary cryptococcosis. IL-22 regulates inflammatory responses, promotes tissue repair and contributes to the maintenance of the pulmonary barrier. Thus, IL-22 may influence the regulation of the inflammatory response and, therefore, the pulmonary pathophysiology during the progression of cryptococcosis. In order to investigate the impact of the absence of this cytokine on the pulmonary pathophysiology of C57Bl/6 mice during infection by C. deuterogattii, we used IL-22-deficient mice, infected by this fungus for 16 days, and evaluated collagen deposition, mucus production and cellular infiltration in the airways by histopathology. The use of animals was approved by the CEUA 092/21. Furthermore, we investigated the lung capacity of the animals through a pulmonary resistance test. We observed that animals deficient in the cytokine IL-22 have high inflammatory infiltrate in the lungs. In this sense, the high deposition of collagen in the lungs combined with the high production of mucus characterizes a state of greater lung damage and functional impairment of the lungs of IL-22 deficient animals. In the pulmonary resistance tests we saw that the worsening of the inflammatory response and destruction of the lung parenchyma increased the basal resistance of the airways, indicating a loss of respiratory capacity. The cytokine IL-22 is crucial for maintaining pulmonary homeostasis, ensuring the regulation of the inflammatory response during cryptococcosis and the integrity of the lung tissue of infected animals.
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