title: LECT2 protects mice against bacterial sepsis by activating macrophages via the CD209a receptor.
abstract: Leukocyte cell-derived chemotaxin 2 (LECT2) is a multifunctional cytokine and reduced plasma levels were found in patients with sepsis. However, precise functions and mechanisms of LECT2 remain unclear. The aim of the present study was to determine the role of LECT2 in modulating immune responses using mouse sepsis models. We found that LECT2 treatment improved outcome in mice with bacterial sepsis. Macrophages (MΦ), but not polymorphonuclear neutrophils, mediated the beneficial effect of LECT2 on bacterial sepsis. LECT2 treatment could alter gene expression and enhance phagocytosis and bacterial killing of MΦ in vitro. CD209a was identified to specifically interact with LECT2 and mediate LECT2-induced MΦ activation. CD209a-expressing MΦ was further confirmed to mediate the effect of LECT2 on sepsis in vivo. Our data demonstrate that LECT2 improves protective immunity in bacterial sepsis, possibly as a result of enhanced MΦ functions via the CD209a receptor. The modulation of MΦ functions by LECT2 may serve as a novel potential treatment for sepsis.
authors.affiliation: Laboratory of Biochemistry and Molecular Biology, Ningbo University, Ningbo 315211, China.
authors.forename: Xin-Jiang
authors.initials: XJ
authors.lastname: Lu
authors.forename: Jiong
authors.initials: J
authors.lastname: Chen
authors.forename: Chao-Hui
authors.initials: CH
authors.lastname: Yu
authors.forename: Yu-Hong
authors.initials: YH
authors.lastname: Shi
authors.forename: Yu-Qing
authors.initials: YQ
authors.lastname: He
authors.forename: Rui-Cheng
authors.initials: RC
authors.lastname: Zhang
authors.forename: Zuo-An
authors.initials: ZA
authors.lastname: Huang
authors.forename: Ji-Neng
authors.initials: JN
authors.lastname: Lv
authors.forename: Shun
authors.initials: S
authors.lastname: Zhang
authors.forename: Lei
authors.initials: L
authors.lastname: Xu
mesh_terms: D000818:Animals; D016470:Bacteremia / Q000235:genetics / Q000276:immunology* / Q000378:metabolism / Q000382:microbiology / Q000473:pathology; D015815:Cell Adhesion Molecules / Q000235:genetics / Q000378:metabolism*; D004927:Escherichia coli Infections / Q000188:drug therapy / Q000276:immunology / Q000401:mortality / Q000473:pathology; D005786:Gene Expression Regulation; D036341:Intercellular Signaling Peptides and Proteins / Q000235:genetics / Q000276:immunology / Q000378:metabolism* / Q000494:pharmacology; D037181:Lectins, C-Type / Q000235:genetics / Q000378:metabolism*; D008262:Macrophage Activation; D008264:Macrophages / Q000187:drug effects / Q000276:immunology* / Q000378:metabolism*; D051379:Mice; D008807:Mice, Inbred BALB C; D008817:Mice, Mutant Strains; D010587:Phagocytosis / Q000187:drug effects; D011956:Receptors, Cell Surface / Q000235:genetics / Q000378:metabolism*; D000099215:DC-Specific ICAM-3 Grabbing Nonintegrin
chemical_list: D015815:Cell Adhesion Molecules; D036341:Intercellular Signaling Peptides and Proteins; D037181:Lectins, C-Type; D011956:Receptors, Cell Surface; D000099215:DC-Specific ICAM-3 Grabbing Nonintegrin; C491213:Lect2 protein, mouse