Patterns of Inflammatory Cell Infiltration and Expression of STAT6 in the Lungs of Patients With COVID-19: An Autopsy...

Severe acute respiratory syndrome coronavirus 2 causes diffuse alveolar damage (DAD), lymphocyte infiltration in the lungs and a cytokine storm. In this study we examined inflammatory cell infiltrates and the expression of signal transducer and activator of transcription (STAT) 6 in the lungs of patients with coronavirus disease 2019 (COVID-19).

Eighteen COVID-19 autopsy cases, 9 non-COVID cases with DAD, and 11 controls without lung diseases were included. Immunostainings for STAT6, CD3, CD4, CD8, CD68, and broad-spectrum keratins were performed.

The average age of COVID-19 patients was 64.4±2.1 years. The disease duration was 7 to 53 days. The number of pneumocytes, macrophages or CD3+ T cells was significantly increased in the lungs of patients with COVID-19. Patients' age above 67 years, blood troponin levels >0.2 ng/mL, platelet count >100×109/L, lung macrophages >130/high-power field (HPF), CD3+ T cells >145/HPF, CD8+ T cells <30/HPF, and CD8/CD4 ratio <1 were associated with shorter survival duration after onset of symptoms. In addition, STAT6 staining was much stronger in pneumocytes and lymphocytes in the lungs of patients with COVID-19 than non-COVID DAD patients or controls.

Older age, high blood troponin level and platelet count, more macrophages and fewer CD8+ T cells in the lungs of COVID-19 were associated with poorer outcome. STAT6 expression was increased in pneumocytes and lymphocytes in the lungs of patients with COVID-19, implying a role of STAT6 in cytokine storms.