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Peptidoglycan recognition receptor proteins (PGRPs), a group of pattern recognition receptors (PRRs), can recognize peptidoglycan (PGN) of the bacteria cell wall and play an important role in host immune defense against pathogen infection. They are highly structurally conserved through evolution, but with different function in innate immunity between invertebrates and vertebrates. In teleost fish, several PGRPs have been characterized recently. They have both amidase activity and bactericidal activity and are involved in indirectly killing bacteria and regulating multiple signaling pathways. However, the knowledge of PGRPs in mucosal immunity of teleost fish is still limited. In this study, we identified a PGRPs gene ( SmPGRP2 ) of turbot and investigated its expression patterns in mucosal tissues after challenge with Gram-positive bacteria Streptococcus iniae and Gram-negative bacteria Vibrio anguillarum . Phylogenetic analysis showed the strongest relationship of turbot PGRP to halibut, which was consistent with their phylogenetic relationships. In addition, SmPGRP2 was ubiquitously expressed in turbot tissues, and constitutive expression levels were higher in classical immune tissues (including liver, spleen, and head-kidney) than mucosal tissues (intestine, gill and skin). After bacterial challenge, the expression of SmPGRP2 was induced and showed a general trend of up-regulation in mucosal tissues, except in intestine following V . anguillarum infection. These different expression patterns varied depending on both pathogen and tissue type, suggesting its distinct roles in the host immune response to bacterial pathogen. [ABSTRACT FROM AUTHOR]

The class A scavenger receptors play important roles in innate immunity and are distributed on plasma membrane of macrophages and other cell types. Notably, the class A scavenger receptor 4 (SCARA4) contains a typical C-type (calcium-dependent) lectin domain, which belongs to the collectin family of pattern recognition receptors and is involved in the immune response against infection. Here, one turbot SCARA4 gene was identified with a 2,292 bp open reading frame (ORF) encoding 763 amino acid residues. Multiple sequence analysis and phylogenetic analysis confirmed that Sm SCARA4 gene was more close to that of P. olivaceus. Gene structure and syntenic analysis showed conserved exon/intron organization pattern and syntenic pattern across selected vertebrate species. Tissue distribution analysis showed Sm SCARA4 was expressed in all the tested healthy tissues with the relative high expression levels in skin, gill and spleen. Following both E. tarda and V. anguillarum challenge in vivo , Sm SCARA4 was significantly repressed in gill and intestine. Remarkably, Sm SCARA4 showed the strongest binding ability to LPS and strongest upregulation in turbot head kidney macrophages in response to LPS. Knockdown and overexpression of Sm SCARA4 revealed its interactions with the two pro-inflammatory cytokines, TNF-α and IL-1β. Finally, repression of Sm SCARA4 via combined treatment of LPS and overexpression of Sm SCARA4 construct in turbot head kidney macrophages further indicated an inhibitory role of Sm SCARA4 in LPS-stimulated inflammation. Taken together, turbot Sm SCARA4 plays an important role in turbot immunity, especially in the mucosa-related systems; Sm SCARA4 possesses strong binding specificity to LPS, and exerts protective roles in response to LPS infection by reducing the release of pro-inflammatory cytokines. The mechanisms of inhibitory role of Sm SCARA4 in LPS-elicited inflammation await further investigation. • Gene structure and syntenic analysis of SCARA4 showed conserved patterns across selected vertebrate species. • Sm SCARA4 was expressed in all the tested healthy tissues with the relative high expression levels in skin, gill and spleen. • Following both E. tarda and V. anguillarum challenge, Sm SCARA4 was significantly repressed in gill and intestine. • Sm SCARA4 showed the strongest binding ability to LPS and strongest upregulation in turbot head kidney macrophages in response to LPS. • Knockdown and overexpression of Sm SCARA4 revealed its interactions with TNF-α and IL-1β. [ABSTRACT FROM AUTHOR]