Abstract: Neuroinflammation has been identified as a crucial element in several neurological disorders. Glial cells play a critical role in directing neuroinflammation, both in deleterious and beneficial ways. They communicate with one another, nearby neurons, and infiltrating cells following central nervous system (CNS) insult. Hence, understanding cellular crosstalk has become fundamental to comprehending neurodegenerative conditions at the micro level (Bhusal et al., 2023). In recent times, scientists have used various transcriptomics and proteomics analyses to identify molecules that are responsible for this cellular communication and to determine the resulting functional outcomes. Various molecules involved in interglial crosstalk have been identified to date. However, the role of peptidoglycan recognition proteins (PGRPs) in the nervous system has received considerably less attention. PGRPs are a unique class of innate immune pattern recognition molecules that bind to bacterial peptidoglycans (PGN) and act as antibacterial agents (Dziarski, 2004). Studies have demonstrated that PGRPs affect host-pathogen interactions not only through antibacterial activity but also through the regulation of inflammatory response. Mammals have four PGRPs initially named PGRP-S, PGRP-L, PGRP-Ia, and PGRP-Ib (for “short,” “long,” and “intermediate” transcripts, respectively), similar to the naming convention used for insect PGRPs. The Human Genome Organization Gene Nomenclature Committee later standardized the nomenclature of human PGRPs to peptidoglycan recognition protein 1 (PGLYRP1), PGLYRP2, PGLYRP3, and PGLYRP4, respectively, and this nomenclature has been adopted for all mammalian PGRPs (Dziarski and Gupta, 2010).