Toll-like receptor 2 (TLR2) functions as a key regulator of inflammatory responses to Vibrio parahaemolyticus infection in the Manila clam (Ruditapes philippinarum).
TL;DR
Findings indicate that RpTLR2 acts as a positive regulator of V. parahaemolyticus-induced inflammatory responses and improve understanding of TLR2-mediated innate immunity in mollusks and provide a molecular basis for studying host-pathogen interactions in bivalves.
Abstract
Toll-like receptor 2 (TLR2) is a pivotal pattern-recognition receptor in innate immunity. It is well characterized in vertebrates but remains poorly understood in mollusks. In this study, we identified a TLR2 homolog (RpTLR2) in Ruditapes philippinarum encoding a 575-amino acid protein with a canonical Toll/interleukin-1 receptor (TIR) domain. Phylogenetic analysis placed RpTLR2 within the molluscan TLR2 clade, confirming its evolutionary conservation. RpTLR2 was constitutively expressed in all examined tissues, with the highest transcript levels in the gill and mantle. After Vibrio parahaemolyticus challenge, RpTLR2 mRNA and protein levels were significantly upregulated. Functional assays showed that RpTLR2 overexpression intensified inflammatory responses and increased the expression of key inflammation-related genes, whereas RNA interference-mediated RpTLR2 knockdown markedly reduced V. parahaemolyticus-induced inflammation in gill cells. Overall, our findings indicate that RpTLR2 acts as a positive regulator of V. parahaemolyticus-induced inflammatory responses. These results improve understanding of TLR2-mediated innate immunity in mollusks and provide a molecular basis for studying host-pathogen interactions in bivalves.