IMMUNE ALTERATIONS DURING CHEMOTHERAPY

Abstract

Neutropenia is an established risk factor for Invasive Aspergillosis (IA) in Acute Myeloid Leukemia (AML) patients. The aim was to investigate the role of neutrophils in modulating host response to A. fumigatus. Neutrophils intrinsically down-modulated TNF-α and IL-1β cytokines production cytokines production of Peripheral Blood Mononuclear Cells (PBMC), in response to A. fumigatus. The suppression of IL-1β was dependent on contact through Complement Receptor 3 (CR3). On the other hand, modulation of TNF-α was contact-independent, and possibly through the release of Myeloperoxidase (MPO). AML patients were able to elicit pro-inflammatory and anti-inflammatory response to fungal pathogens prior and after chemotherapy. A decrease of CD14+CD16- monocytes was observed throughout the course of chemotherapy. The expression of toll-like receptor 2 (TLR2) and toll-like receptor 4 (TLR4) in CD14+CD16- monocytes population, decreased after chemotherapy. The observation here has provided the understanding that different populations of immune cells are affected differently by chemotherapy.