title: TREM-1 signaling promotes host defense during the early stage of infection with highly pathogenic Streptococcus suis.
abstract: Infection with highly pathogenic Streptococcus suis can cause septic shock, which is characterized by high levels of inflammatory cytokines and a high mortality rate. Our previous study indicated that TREM-1 (triggering receptor expressed on myeloid cells 1) was upregulated in swine spleen cells in response to S. suis infection. The role of TREM-1 signaling in enhancement of the proinflammatory response promoted us to examine its effect on the outcome of S. suis infection. In the present study, the recombinant extracellular domain of TREM-1 (rTREM-1) and an agonistic TREM-1 antibody were used to inhibit and activate TREM-1 signaling to evaluate its role in neutrophil activation, pathogen clearance, proinflammatory cytokine response, and the outcome of highly pathogenic S. suis infection in a mouse model. Blockage of TREM-1 signaling caused a more severe proinflammatory response to S. suis infection and increased the mortality rate, while its activation had the opposite effect. Blockage or activation of TREM-1 signaling lowered or raised the number of neutrophils in the blood, which correlated well with host clearance of S. suis. In conclusion, the TREM-1-mediated innate immune response played an essential role in the activation of neutrophils and S. suis clearance, which further reduced severe inflammation and finally benefited the outcome of the infection.
authors.affiliation: National Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan, Hubei, China College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, Hubei, China.
authors.forename: Chao
authors.initials: C
authors.lastname: Yang
authors.affiliation: National Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan, Hubei, China Department of Microbiology and Molecular Genetics, University of Texas Medical School at Houston, Houston, Texas, USA.
authors.forename: Bo
authors.initials: B
authors.lastname: Chen
authors.affiliation: National Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan, Hubei, China College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, Hubei, China.
authors.forename: Jianqing
authors.initials: J
authors.lastname: Zhao
authors.affiliation: College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, Hubei, China.
authors.forename: Lan
authors.initials: L
authors.lastname: Lin
authors.affiliation: College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, Hubei, China.
authors.forename: Li
authors.initials: L
authors.lastname: Han
authors.affiliation: College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, Hubei, China.
authors.forename: Shan
authors.initials: S
authors.lastname: Pan
authors.affiliation: College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, Hubei, China.
authors.forename: Lei
authors.initials: L
authors.lastname: Fu
authors.affiliation: National Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan, Hubei, China College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, Hubei, China.
authors.forename: Meilin
authors.initials: M
authors.lastname: Jin
authors.affiliation: National Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan, Hubei, China College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, Hubei, China.
authors.forename: Huanchun
authors.initials: H
authors.lastname: Chen
authors.affiliation: National Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan, Hubei, China College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, Hubei, China andye8019@mail.hzau.edu.cn.
authors.forename: Anding
authors.initials: A
authors.lastname: Zhang
mesh_terms: D000818:Animals; D005260:Female; D007113:Immunity, Innate; D008562:Membrane Glycoproteins / Q000235:genetics / Q000276:immunology*; D051379:Mice; D008810:Mice, Inbred C57BL; D009504:Neutrophils / Q000276:immunology; D011971:Receptors, Immunologic / Q000235:genetics / Q000276:immunology*; D015398:Signal Transduction; D013290:Streptococcal Infections / Q000235:genetics / Q000276:immunology / Q000382:microbiology / Q000662:veterinary*; D017011:Streptococcus suis / Q000235:genetics / Q000472:pathogenicity / Q000502:physiology*; D013552:Swine; D013553:Swine Diseases / Q000235:genetics / Q000276:immunology* / Q000382:microbiology; D000073871:Triggering Receptor Expressed on Myeloid Cells-1; D014774:Virulence
chemical_list: D008562:Membrane Glycoproteins; D011971:Receptors, Immunologic; C517262:TREM1 protein, mouse; D000073871:Triggering Receptor Expressed on Myeloid Cells-1