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Summary

Neutrophils, the most abundant white blood cells, are essential defenders against infections—but not all neutrophils function alike. This thesis reveals that distinct neutrophil subsets vary in both appearance and function and they appear in blood during different stages of inflammation, such as the acute and sub-acute phases following severe trauma, endotoxemia, and COVID-19. By analyzing surface markers like CD16 and CD62L, we distinguished between these subsets.

In an acute inflammatory response, a subset called CD16dim (or banded) neutrophils predominates, showing strong bacterial killing ability. In contrast, during the sub-acute phase, CD62Ldim (hypersegmented) neutrophils become more common; however, they have a markedly reduced capacity to kill bacteria. This suggests that while CD16dim neutrophils primarily serve an antibacterial role, CD62Ldim cells may instead have a regulatory function. The downside is that their impaired bacterial killing may allow them to act as “Trojan horses”, harboring intracellular bacteria and potentially increasing infection risk in vulnerable patients. Our work also highlights that bacteria residing within neutrophils can complicate antibiotic treatment.

In addition to the functional differences, markers such as CD10 and CD64 provide insight into the inflammatory state. We showed that low CD10 levels during inflammation—and its gradual return to baseline—could serve as a biomarker for recovery. Furthermore, the diagnostic potential of neutrophil CD64 was explored for its role in identifying bacterial infections rapidly in emergency settings.
Overall, these findings enhance our understanding of neutrophil dynamics and functions during inflammation. They offer promising avenues for refining diagnostics and treatment strategies, which could ultimately improve infection management and patient outcomes for critically ill patients.