Pcyox1L Controls Immune Dynamics through Neutrophil Differentiation and Functionality

Abstract

Autophagy is a cellular function that is essential in maintaining homeostasis at the molecular level. Over the years, autophagy has defined its role in neutrophil biology and innate immunity. Understanding the role of autophagy at the cellular level will prove very useful for future therapies in immunology. In this study, the functional significance of Pcyox1L and its influence on autophagy is explored to assess the Pcyox1L regulated neutrophil functions. While Pcyox1L is a known protein-coding gene, it currently has no know function. To examine the role of Pcyox1L on neutrophil function and differentiation, in vivo and in vitro experiments were demonstrated with mouse neutrophil cell lines and using a corneal mouse infection model. This study indicates that Pcyox1L alters the process of innate immunity by affecting neutrophil autophagy, which in turn affects the bactericidal capabilities, maturation, and viability of the neutrophil. Data from my studies highlight intracellular pathways influenced by commensal colonization induced an increase in Pcyox1L levels in PMNs. Conversely, Pcyox1L KO mice demonstrate an altered commensal microbiome in the gut and distant sites, such as the eye, and elevated susceptibility to P. aeruginosa.