NimB2 Enhances Staphylococcus aureus Recognition by Macrophages in Drosophila

Abstract

The innate immune system relies on rapid recognition and clearance of pathogens to maintain homeostasis. Phagocytosis, a crucial defence mechanism, enables the elimination of both microbial invaders and apoptotic cells. In Drosophila melanogaster, haemocytes act as professional phagocytes, coordinating immune responses against infections. While several regulators of phagocytosis have been identified, the role of NimB2 in this process remains unexplored. Here, we investigate the function of NimB2 in bacterial clearance, specifically its role in recognizing and eliminating Staphylococcus aureus. Using NimB2 null mutant and infection assays, we show that the loss of NimB2 significantly impairs S. aureus clearance, leading to increased bacterial load and heightened susceptibility to infection. Flow cytometry and microscopy analyses confirm a phagocytic defect in NimB2 mutants, highlighting its role in haemocyte-mediated bacterial uptake. Furthermore, our findings suggest that NimB2 functions as an opsonin, facilitating the recognition of S. aureus by haemocytes and promoting efficient bacterial clearance. This study identifies NimB2 as a secreted Nimrod protein essential for S. aureus phagocytosis and provides new insights into its role in cellular immunity.