| First Author | Yang C | Year | 2015 |
| Journal | Infect Immun | Volume | 83 |
| Issue | 8 | Pages | 3293-301 |
| PubMed ID | 26056380 | Mgi Jnum | J:229114 |
| Mgi Id | MGI:5750822 | Doi | 10.1128/IAI.00440-15 |
| Citation | Yang C, et al. (2015) TREM-1 signaling promotes host defense during the early stage of infection with highly pathogenic Streptococcus suis. Infect Immun 83(8):3293-301 |
| abstractText | 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. |
