Pglyrp3, short for peptidoglycan recognition protein 3, is a bactericidal innate immunity protein. It plays a role in antibacterial innate immunity, recognizing bacterial peptidoglycan. The gene is associated with the NF-κB signaling pathway, where its anti-inflammatory effects involve negative regulation of this pathway, including up-regulation of IκB-α and down-regulation of NF-κB and COX-2 [2,3]. Pglyrp3 is important for maintaining gut homeostasis and protecting against certain inflammatory conditions [1,4]. Gene knockout mouse models have been valuable in studying its functions.

In Pglyrp3 knockout (Pglyrp3-/-) mice, the additive protective effect of Pglyrp3 and Bifidobacterium adolescentis on DSS-induced colitis was investigated. The results showed that Pglyrp3 facilitates recognition of bifidobacterial cell wall-derived peptidoglycan, leading additively to a reduction of meta-inflammation through an increase in the number of bifidobacteria, which mitigated intestinal immunopathology in the context of Pglyrp3 blockade [1]. Also, combined deficiency of Pglyrp3 and Nod2 in mice resulted in higher sensitivity to dextran sodium sulfate-induced colitis compared with single deficiency, indicating that both are required for maintaining gut homeostasis and protection against colitis, though their protective mechanisms differ [4].

In conclusion, Pglyrp3 is crucial for antibacterial innate immunity and maintaining gut homeostasis. The study of Pglyrp3 knockout mouse models has revealed its role in reducing meta-inflammation and protecting against DSS-induced colitis, providing insights into the mechanisms of gut-related inflammatory diseases and potential therapeutic strategies.