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BackgroundThe aim was to elucidate the function of IL‐37 in middle east respiratory syndrome coronavirus (MERS‐CoV) infection, thereby providing a novel therapeutic strategy for managing the clinical treatment of inflammatory response caused by respiratory virus infection.MethodsWe investigated the development of MERS by infecting hDPP4 mice with hCoV‐EMC (107 TCID50 [50% tissue culture infectious dose]) intranasally. We infected A549 cells with MERS‐CoV, which concurrently interfered with IL‐37, detecting the viral titer, viral load, and cytokine expression at certain points postinfection. Meanwhile, we administered IL‐37 (12.5 μg/kg) intravenously to hDPP4 mice 2 h after MERS‐CoV‐2 infection and collected the serum and lungs 5 days after infection to investigate the efficacy of IL‐37 in MERS‐CoV infection.ResultsThe viral titer of MERS‐CoV‐infected A549 cells interfering with IL‐37 was significantly reduced by 4.7‐fold, and the viral load of MERS‐CoV‐infected hDPP4 mice was decreased by 59‐fold in lung tissue. Furthermore, the administration of IL‐37 suppressed inflammatory cytokine and chemokine (monocyte chemoattractant protein 1, interferon‐γ, and IL‐17A) expression and ameliorated the infiltration of inflammatory cells in hDPP4 mice.ConclusionIL‐37 exhibits protective properties in severe pneumonia induced by MERS‐CoV infection. This effect is achieved through attenuation of lung viral load, suppression of inflammatory cytokine secretion, reduction in inflammatory cell infiltration, and mitigation of pulmonary injury.
BackgroundThe aim was to elucidate the function of IL‐37 in middle east respiratory syndrome coronavirus (MERS‐CoV) infection, thereby providing a novel therapeutic strategy for managing the clinical treatment of inflammatory response caused by respiratory virus infection.MethodsWe investigated the development of MERS by infecting hDPP4 mice with hCoV‐EMC (107 TCID50 [50% tissue culture infectious dose]) intranasally. We infected A549 cells with MERS‐CoV, which concurrently interfered with IL‐37, detecting the viral titer, viral load, and cytokine expression at certain points postinfection. Meanwhile, we administered IL‐37 (12.5 μg/kg) intravenously to hDPP4 mice 2 h after MERS‐CoV‐2 infection and collected the serum and lungs 5 days after infection to investigate the efficacy of IL‐37 in MERS‐CoV infection.ResultsThe viral titer of MERS‐CoV‐infected A549 cells interfering with IL‐37 was significantly reduced by 4.7‐fold, and the viral load of MERS‐CoV‐infected hDPP4 mice was decreased by 59‐fold in lung tissue. Furthermore, the administration of IL‐37 suppressed inflammatory cytokine and chemokine (monocyte chemoattractant protein 1, interferon‐γ, and IL‐17A) expression and ameliorated the infiltration of inflammatory cells in hDPP4 mice.ConclusionIL‐37 exhibits protective properties in severe pneumonia induced by MERS‐CoV infection. This effect is achieved through attenuation of lung viral load, suppression of inflammatory cytokine secretion, reduction in inflammatory cell infiltration, and mitigation of pulmonary injury.
Medical personnel and family members of patients with acute respiratory diseases (ARD) are at increased risk of infection during epidemics or pandemics. In this regard, it is necessary to develop and implement accessible preventive measures. The aim of the study was to evaluate the effectiveness of the use of IFNα-2b for the prevention of acute respiratory viral infections in persons located at the source of infection (medical personnel and members of their families). Patients (n = 31) with acute respiratory infections and 117 people from their environment (family members in constant contact with patients) were examined. The subjects underwent a clinical examination and laboratory tests a clinical blood test and a study of the content of the main populations and subpopulations of lymphocytes in the blood. Persons in contact with ARD patients were divided into three groups: persons who received the drug “Grippferon” for 7 days; persons who received the drug “Grippferon” in a prophylactic dose for 7 days; persons in contact with patients with ARD but who have not received the drug “Grippferon”. When assessing the state of the immune system, it was found that the most common type of immune reaction in patients and their people around was activation of innate immunity (48.39% and 66.67%, respectively). At the same time, immunodeficiency in the group of patients with ARD was detected much more often than in persons in contact with them. In addition, patients were more likely to have monocytosis (1.4 times), T lymphocytopenia (2.1 times) and an increase in the number of regulatory T lymphocytes (7.6 times). More than 50% of those examined in both groups showed an increase in the number of NK cells in the blood. An examination of persons in contact with patients with ARD after 7 days of using the “Grippferon” in different doses revealed that the lowest frequency of acute respiratory viral infections symptoms was found in the group receiving IFN at a therapeutic dose. In the group receiving IFN in a prophylactic dose, the frequency of acute respiratory viral infection (ARVI) symptoms was detected in almost 40% of those examined. More than 80% of people from the group who did not receive the “Grippferon” had symptoms of ARVI after a week of contact with patients with ARD. Thus, the use of IFN in therapeutic doses during the epidemic for persons in contact with patients is proposed as a new concept for the prevention of ARD.
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