Aim: Neutrophils are thought to play a role in the pathogenesis of tuberculosis (Tb). This study aimed to evaluate the function and activation markers of peripheral neutrophils in Tb patients to clarify their involvement in disease progression.
Materials and Methods: The study included three groups: seven untreated Tb patients, seven cystic fibrosis (CF) patients, and seven healthy controls. Neutrophils were isolated from peripheral blood using Ficoll-Histopaque gradient centrifugation and cultured in RPMI 1640 medium with L-glutamine. Inactivated Mycobacterium tuberculosis was added both in the presence and absence of recombinant interleukin (IL)-17. Neutrophil functions—including phagocytosis, chemotaxis, and oxidative burst—as well as surface activation markers, such as CD11b, CD63, and CD66b, were analyzed via flow cytometry.
Results: Neutrophil functions and activation markers in response to IL-17 and bacilli stimulation in Tb patients were similar to those in healthy controls, but were significantly reduced in CF patients. Surface CD11b and CD66b expression, as well as the oxidative burst index of neutrophils from patients with Tb and CF, were inhibited by IL-17.
Conclusion: Neutrophil functions and activation markers in patients with mycobacterial infections were comparable to those in healthy subjects. In contrast, neutrophil functions were reduced in CF patients compared to both healthy subjects and Tb patients, though this difference lacked statistical significance. Notably, IL-17 was found to suppress the expression of CD11b, CD66b, and the oxidative burst index on neutrophil surfaces in both Tb and CF patients. These findings highlight the need for further research with larger cohorts to investigate neutrophil apoptosis and cytokine receptor expression in cell culture supernatants, offering deeper insights into neutrophil roles in Tb infection.
Key words: Neutrophils, interleukin-17, tuberculosis, cystic fibrosis, flow cytometry
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