TREM‐1 deficiency attenuates the inflammatory responses in LPS‐induced murine endometritis

Abstract

Summary 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‐1β (IL‐1β), IL‐6, and tumour necrosis factor‐α (TNF‐α) 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.

Soluble TREM‐1, as a new ligand for the membrane receptor Robo2, promotes hepatic stellate cells activation and liver fibrosis

“… 31 TREM‐1 deficiency attenuates endometritis induced by lipopolysaccharide in mice. 32 HIV or HCV infection stimulates Kuffer cells that upregulates TREM‐1. 33 In non‐alcoholic fatty liver disease, inhibition of TREM‐1 reduces the inflammation and lipid accumulation.…”

Extracellular matrix stiffness mediates uterine repair via the Rap1a/ARHGAP35/RhoA/F-actin/YAP axis

“…To explore the mechanisms through which endometrial repair occurs, we used a pathological mouse uterine injury model generated by intrauterine injection of LPS. Although the LPS-induced mouse endometritis model has been widely recognized, most research using this model has focused on the damage phase, and the pathological characteristics of the repair phase have not been clearly explained [ 21 , 22 ]. First, we evaluated the levels of white blood cells (WBCs) in the peripheral blood of mice with bacterially induced uterine injury by routine blood b examination (Fig.…”

Predicting the course of early onset neonatal sepsis in pretern infants

“…Доведено багаторазове посилення продукції цитокінів при сумісній активації TREM 1 на моноцитах анти TREM антитілами за участі бактеріальних ліпополісахаридів (LPS). Отже, у випадку мікробного впливу, спільна стимуля ція TREM 1 та LPS може викликати як ком пенсаторну, так і надмірну системну запальну реакцію, що призводить до поліорганного пошкодження [9,17]. TREM 1 також продуку ється в розчинній формі (sTREM 1), яка вивіль няється після впливу ендотоксину, вимірюється в біологічних рідинах і може бути корисна в яко сті діагностичного інструменту [5].…”