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A characteristic feature of the cytokine storm in coronavirus disease 2019 (COVID-19) is the dramatic elevation of serum interleukin 10 (IL-10). This may be a negative feedback mechanism to suppress inflammation. However, this IL-10 elevation may contribute to COVID-19 severity. In our study, we aimed to evaluate the effect of serum IL-10 level on patients' clinical outcome and the incidence of post-COVID19 pulmonary fibrosis. This was a prospective observational study, included 100 patients, confirmed to have COVID-19, Of these, 50 patients had COVID-19 without evidence of pneumonia in computed tomography (CT) scans (group I) and the other 50 patients had COVID-19 pneumonia (group II). Our results showed a significant increase in serum ferritin level in patients with COVID pneumonia. However, no difference was found in serum C-reactive protein (CRP) nor D-Dimer between both groups. There was a statistically significant increase in serum IL-10 in patients with COVID pneumonia compared with COVID patients without pneumonia (p < 0.001). Fibrosis was developed in 35 patients (70%) with COVID pneumonia after 3 months and 4 of them died, however, all patients without pneumonia survived. Among age, serum IL-10, aspartate aminotransferase (AST), alanine transaminase (ALT), elevated serum IL-10 was found to be an independent predictor of pneumonia (p=0.32). However, there was no significant effect for IL-10 on patients' clinical outcome. There was a statistically significant correlation between serum IL-10 levels and oxygen (O2) demand, CRP and D-Dimer (p= 0.015, p=0.034 and p=0.042, respectively). The higher the level of IL-10 the less fibrosis detected in follow up CT scans (p=0.038). In conclusion, even though IL-10 was significantly associated with disease severity (higher in pneumonia), elevated serum Il-10 has an independent role in decreasing the incidence of post-COVID-19 pulmonary fibrosis., (Copyright© by the Egyptian Association of Immunologists.)

Stroke is long known to be followed by a series of immunosuppressive events, and infections might be a cause of death after an acute insult of stroke. The aim of our work was to assess the percentage of neutrophils showing spontaneous oxidative burst in patients with acute ischemic stroke. The study included 30 patients with acute cerebral infarction subjected to the following: magnetic resonance imaging of the brain immediately on admission, and blood sampling on day one of admission (baseline) and after 3 days of admission. Blood samples were used for the assessment of: differential leucocyte count and percentage of neutrophils showing spontaneous oxidative burst, performed by flow cytometry. Thirty age and gender matched controls were also recruited. Neutrophil respiratory burst percentage was significantly lower in stroke patients in comparison to controls (P < 0.001), and stroke patients had significantly lower neutrophil respiratory burst percent on day 3 of admission compared to the baseline (P < 0.001). Stroke-induced immune alterations including impairment of the first-line defense performed by neutrophils against bacteria. The hypothesis that these changes enhance susceptibility to acquired infections is supported by our observation that oxidative burst in neutrophils was more impaired in patients with stroke who exhibited subsequent stroke-associated infections., (Copyright© by the Egyptian Association of Immunologists.)