Abstract
BACKGROUND: Neutrophils are key players in the innate immune system, responsible for rapid responses to infections through mechanisms such as phagocytosis and the release of reactive oxygen species (ROS). Beyond their role in host defense, neutrophils also contribute to the pathogenesis of various diseases, including infections, metabolic disorders, autoimmune diseases, and cancer. Understanding the immunosuppressive role of neutrophils, particularly through markers like human neutrophil lipocalin (HNL) and the chemokine receptor CXCR3, is crucial for developing targeted therapeutic strategies. MATERIALS AND METHODS: This study involved 200 participants divided into four groups: 50 patients with acute respiratory infection, 50 COVID-19 recovered patients, 50 oncology patients, and 50 healthy donors as controls. Peripheral blood samples were collected and analyzed using enzyme-linked immunoassay (ELISA) to quantify levels of HNL and CXCR3. Data were analyzed using SPSS version 25.0, employing descriptive statistics, the Shapiro-Wilk test for normality, one-way ANOVA for normally distributed variables, and the Kruskal-Wallis test for non-normally distributed variables. Post-hoc comparisons were conducted using Tukey's HSD and Dunn's tests. RESULTS: CXCR3 levels were stable across groups, with no significant differences found. Acute respiratory infection patients had an average CXCR3 level of 150 ± 20 pg/ml, while COVID-19 recovered patients had slightly lower levels at 140 ± 18 pg/ml. Oncology patients had elevated CXCR3 levels at 160 ± 22 pg/ml, similar to healthy donors at 150 ± 19 pg/ml. HNL levels varied more, with COVID-19 recovered patients showing notably lower levels (100 ± 12 ng/ml) compared to other groups. Oncology patients exhibited higher HNL levels, especially those with prostate cancer (150 ± 20 ng/ml). CONCLUSION: The findings highlight the consistent expression of CXCR3 across various conditions, making it a reliable marker for immune response assessment. The distinct HNL profiles, particularly the lower levels in COVID-19 recovered patients and higher levels in prostate cancer patients, suggest unique neutrophil activities and immune responses. These insights into neutrophil-mediated immunosuppression and inflammation could inform the development of targeted therapies for infections, cancer, and autoimmune diseases. Further research is needed to elucidate the specific mechanisms underlying neutrophil-induced immunosuppression.