| First Author | Zhu H | Year | 2019 |
| Journal | Microb Biotechnol | Volume | 12 |
| Issue | 6 | Pages | 1337-1345 |
| PubMed ID | 31365951 | Mgi Jnum | J:293368 |
| Mgi Id | MGI:6435909 | Doi | 10.1111/1751-7915.13467 |
| Citation | Zhu H, et al. (2019) TREM-1 deficiency attenuates the inflammatory responses in LPS-induced murine endometritis. Microb Biotechnol 12(6):1337-1345 |
| abstractText | Endometritis, which is usually caused by bacterial infection, is characterized by high levels of pro-inflammatory cytokines and a high infertility rate. Triggering receptor expressed on myeloid cells-1 (TREM-1) has been recognized as a potent amplifier of inflammatory reactions. Studies have demonstrated reduced inflammatory responses and mortality rates of animals with bacterial infection due to the blocking of TREM-1 expression. However, whether TREM-1 deficiency could alleviate the inflammatory reaction in bacterial endometritis is still unclear. Here, TREM-1 knock-out (Trem-1(-/-) ) mice were used to inhibit TREM-1 signalling to evaluate its role in inflammatory reactions after a highly pathogenic LPS infection in mice uteri. The results demonstrated that TREM-1 deficiency attenuated the inflammation in mice uteri; markedly reduced the number of polymorphonuclear neutrophils; and suppressed interleukin-1beta (IL-1beta), IL-6, and tumour necrosis factor-alpha (TNF-alpha) concentrations in serum as well as their production in inflamed uteri after LPS stimulation. Our results illustrate an anticipated pathogenic impact of TREM-1 on endometritis during LPS infection and indicate that blocking of TREM-1 in LPS-induced endometritis holds considerable promise for blunting excessive inflammation. |
