scholarly journals Triggering receptor expressed on myeloid Cells-2 (TREM2) inhibits steroidogenesis in adrenocortical cell by macrophage-derived exosomes in lipopolysaccharide-induced septic shock

2021 ◽  
Vol 525 ◽  
pp. 111178
Author(s):  
Hui Ye ◽  
Qian Zhai ◽  
Ping Fang ◽  
Shiyue Yang ◽  
Yaqi Sun ◽  
...  
2005 ◽  
Vol 31 (4) ◽  
pp. 594-597 ◽  
Author(s):  
S�bastien Gibot ◽  
Pol-Edern Le Renard ◽  
Pierre-Edouard Bollaert ◽  
Marie-Nathalie Kolopp-Sarda ◽  
Marie-Christine B�n� ◽  
...  

Life Sciences ◽  
1981 ◽  
Vol 28 (17) ◽  
pp. 1917-1923 ◽  
Author(s):  
G. Keri ◽  
V. Parameswaran ◽  
Donald D. Trunkey ◽  
J. Ramachandran

2004 ◽  
Vol 200 (11) ◽  
pp. 1419-1426 ◽  
Author(s):  
Sébastien Gibot ◽  
Marie-Nathalie Kolopp-Sarda ◽  
Marie-C. Béné ◽  
Pierre-Edouard Bollaert ◽  
Alain Lozniewski ◽  
...  

The triggering receptor expressed on myeloid cells (TREM)-1 is a recently discovered receptor expressed on the surface of neutrophils and a subset of monocytes. Engagement of TREM-1 has been reported to trigger the synthesis of proinflammatory cytokines in the presence of microbial products. Previously, we have identified a soluble form of TREM-1 (sTREM-1) and observed significant levels in serum samples from septic shock patients but not controls. Here, we investigated its putative role in the modulation of inflammation during sepsis. We observed that sTREM-1 was secreted by monocytes activated in vitro by LPS and in the serum of animals involved in an experimental model of septic shock. Both in vitro and in vivo, a synthetic peptide mimicking a short highly conserved domain of sTREM-1 appeared to attenuate cytokine production by human monocytes and protect septic animals from hyper-responsiveness and death. This peptide seemed to be efficient not only in preventing but also in down-modulating the deleterious effects of proinflammatory cytokines. These data suggest that in vivo modulation of TREM-1 by sTREM peptide might be a suitable therapeutic tool for the treatment of sepsis.


2020 ◽  
Author(s):  
Hui Ye ◽  
Pinhao Li ◽  
Qian Zhai ◽  
Ping Fang ◽  
Shiyue Yang ◽  
...  

Abstract Background: Endogenously produced glucocorticoids exhibit immunomodulating properties and are of pivotal importance for sepsis outcome. Uncontrolled activation of the immune-adrenal crosstalk increases the risk of sepsis-related death. Triggering receptor expressed on myeloid cells-2 (TREM2) is richly expressed on macrophages and has been demonstrated to improve outcome of sepsis by enhancing elimination of pathogens. However, the role and mode of action of macrophage TREM2 on adrenocortical steroidogenesis remains unclear in septic shock.Methods: The acute septic shock model was established by intraperitoneally challenging wild-type (WT) and TREM2 knock-out (Trem2-/-) mice with lipopolysaccharide (30 mg/kg). The mice were assessed for TREM2 expression and local inflammation in adrenal gland and synthesis of corticotropin releasing hormone (CRH) and adrenocorticotropic hormone (ACTH) in vivo. Bone marrow-derived macrophages or macrophage-derived exosomes were isolated from WT and Trem2-/- mice and co-cultured with adrenocortical cells. The expression of steroidogenic enzymes and corticosterone production were assessed.Results: Genetic deficiency of TREM2 caused significantly higher corticosterone levels (326.6 ± 73.0 ng/ml in Trem2-/- mice vs. 151.1 ± 58.9 ng/ml in WT mice; p < 0.001) at the early stage of LPS-induced septic shock. While TREM2 deficiency neither increased CRH and ACTH, nor exacerbated the inflammation in adrenocortical tissue during septic shock. Ex vivo study revealed that Trem2-/- macrophages significantly promoted the expression of steroidogenic enzymes and increased production of corticosterone (27.73 ± 1.78 ng/ml in Trem2-/- mice vs. 22.96 ± 1.94 ng/ml in W T mice; p < 0.01). Furthermore, Trem2-/- macrophage-derived exosomes were able to mimic Trem2-/- macrophages in enhancing adrenocortical steroidogenesis. Conclusions: At the early stage of lipopolysaccharide-induced septic shock, macrophage TREM2 inhibited the steroid synthesis and corticosterone production in adrenocortical cells, which may be partially associated with macrophage-derived exosomes.


Shock ◽  
2004 ◽  
Vol 21 (Supplement) ◽  
pp. 100
Author(s):  
A Nierhaus ◽  
B Montag ◽  
D Frings ◽  
A Heydorn ◽  
J Schulte Esch

2005 ◽  
Vol 142 (1) ◽  
pp. 62-67 ◽  
Author(s):  
C. Routsi ◽  
E. J. Giamarellos-Bourboulis ◽  
A. Antonopoulou ◽  
S. Kollias ◽  
S. Siasiakou ◽  
...  
Keyword(s):  

2018 ◽  
Vol 114 (6) ◽  
pp. 907-918 ◽  
Author(s):  
Lucie Jolly ◽  
Kevin Carrasco ◽  
Marc Derive ◽  
Jérémie Lemarié ◽  
Amir Boufenzer ◽  
...  

2018 ◽  
Vol 24 (7) ◽  
pp. 1122-1127 ◽  
Author(s):  
Jessica Morales-Ortíz ◽  
Matthew T. Rondina ◽  
Samuel M. Brown ◽  
Colin Grissom ◽  
A. Valance Washington

We have previously demonstrated that elevated levels of soluble triggering receptor expressed on myeloid cells–like transcript 1 (sTLT-1) modulate sepsis-induced inflammation and positively correlate with disseminated intravascular coagulation (DIC). Here, we evaluate the clinical implications of plasma sTLT-1 in acute respiratory distress syndrome (ARDS), which is common in sepsis patients. Soluble TLT-1 levels in the plasma of ARDS patients (n = 20) were determined by slot blot analysis and were compared with clinical parameters to identify significant associations. For comparisons to ARDS, we also measured sTLT-1 levels in matched healthy controls (n = 20). Of the 20 plasma samples evaluated from patients with ARDS, 60% were diagnosed with sepsis and 40% were diagnosed with septic shock. The white blood cells (WBCs) of patients with ARDS were found to be significantly elevated over healthy controls with a mean of 13 k/µL over 6.2 k/µL, respectively. The mean plasma levels of sTLT-1 were 148.4 pg/mL ± 16.52 in the patient cohort and 92.45 pg/mL ± 17.12 in the control group ( P = .02). No statistically significant correlations were found between plasma levels of sTLT-1 and WBCs, sepsis, septic shock or acute physiologic, and chronic health evaluation II scores. A statistically significant inverse correlation (r2 = .25, P < .05) was found between plasma sTLT-1 and peripheral platelet counts in patients with ARDS. Increased levels of sTLT-1 in ARDS patients suggest that TLT-1 may mediate the pathobiology of ARDS. Moreover, our data are the first to demonstrate a specific platelet marker in the development of ARDS due to sepsis.


2019 ◽  
Vol 15 (3) ◽  
pp. 713-721 ◽  
Author(s):  
Monika Jedynak ◽  
Andrzej Siemiątkowski ◽  
Robert Milewski ◽  
Barbara Mroczko ◽  
Maciej Szmitkowski

Sign in / Sign up

Export Citation Format

Share Document