Time-course of sTREM (soluble triggering receptor expressed on myeloid cells)-1, procalcitonin, and C-reactive protein plasma concentrations during sepsis

Gibot, Sébastien; Cravoisy, Aurélie; Kolopp‐Sarda, Marie‐Nathalie; Béné, Marie‐Christine; Fauré, G; Bollaert, Pierre‐Édouard; Lévy, Bruno

doi:10.1097/01.ccm.0000159089.16462.4a

Cited by 212 publications

(183 citation statements)

References 23 publications

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“…Individual microbial components, such as lipopolysaccharide (LPS) and peptidoglycan, can cause up-regulation of cell surface-localized TREM-1 by monocytes, as well as release in its soluble (s)TREM-1 form (Begum et al, 2004;Gibot et al, 2004b;Gomez-Pina et al, 2007;Murakami et al, 2007;Ramanathan et al, 2005;Zeng et al, 2007). The sTREM-1 appears to be released during the course of infection, and may well be a particularly useful marker of systemic inflammation, as demonstrated in systemic sepsis, septic arthritis, pneumonia (Collins et al, 2009;Gibot et al, 2005;Gibot et al, 2004a;Gibot et al, 2004c;Knapp et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

Involvement of the TREM-1/DAP12 pathway in the innate immune responses to Porphyromonas gingivalis

Bostancı

Thurnheer

Belibasakis

2011

Molecular Immunology

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Porphyromonas gingivalis, is a Gram-negative obligate oral anaerobic bacterium highly implicated in periodontal disease, the most prevalent chronic inflammatory disease, but recent evidence also indicates a potential contribution to systemic inflammation. The Triggering Receptor Expressed on Myeloid cells 1 (TREM-1) is a cell surface receptor of the immunoglobulin superfamily, which, along with its adaptor signalling molecule DAP12, is involved in immune response to bacterial and fungal infections, particularly by amplifying the production of pro-inflammatory cytokines by the host. The aim of the present study was to investigate the effect of P. gingivalis on the expression of the TREM-1/DAP12 pathway, as well as its engagement in pro-inflammatory cytokine production, by the myelomonocytic cell line MonoMac-6. P. gingivalis enhanced TREM-1 gene expression by the cells, concomitantly to an increase of soluble TREM-1 secretion. Engagement of TREM-1, by introducing anti-TREM-1 to the experimental system, resulted in further potentiation of the pro-inflammatory responses to P. gingivalis, as evaluated by a further enhancement of interleukin (IL)-1 and IL-6 secretion. On the contrary, the synthetic TREM-1 antagonist LP17 reduced the P. gingivalis-induced IL-1 and IL-6 secretion by approximately 50%. In conclusion, the putative periodontal pathogen P. gingivalis can positively regulate the expression of the TREM-1/DAP12 pathway in monocytic cells. Moreover, engagement of TREM-1 can further potentiate the pro-inflammatory responses to P. gingivalis infection. This effect may contribute not only to the pathogenesis of inflammatory periodontal disease, but also to the enhancement of systemic inflammation.

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Section: Introductionmentioning

confidence: 99%

Involvement of the TREM-1/DAP12 pathway in the innate immune responses to Porphyromonas gingivalis

Bostancı

Thurnheer

Belibasakis

2011

Molecular Immunology

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“…[13] In addition, elevated concentrations of a soluble form of TREM-1 (sTREM-1) were detectable in fluids from patients with infections, whereas a progressive decline in plasma sTREM-1 concentrations indicates a favorable clinical evolution of septic shock, although the mechanism of generation of sTREM-1 remains unclear. [9,14,15] Therefore, TREM-1 functions as an amplifier as well as a critical mediator of inflammatory response in the context of septic shock. However, the association between genomic variations within the TREM-1 gene and septic shock remains unknown.…”

Section: Introductionmentioning

confidence: 99%

Relationships between genetic polymorphisms of triggering receptor expressed on myeloid cells-1 and septic shock in a Chinese Han population

Peng¹,

Li²,

Zhou³

et al. 2015

World Journal of Emergency Medicine

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BACKGROUND: Triggering receptor expressed on myeloid cells-1 (TREM-1) is a cell surface receptor expressed on neutrophils and monocytes. TREM-1 acts to amplify infl ammation and serves as a critical mediator of infl ammatory response in the context of sepsis. To date, the predisposition of TREM-1 gene polymorphisms to septic shock has not been reported. This study was designed to investigate whether TREM-1 genomic variations are associated with the development of septic shock. METHODS:We genotyped two TREM-1 single nucleotide polymorphisms (SNPs, rs2234237 and rs2234246) and evaluated the relationships between these SNPs and septic shock on susceptibility and prognosis.RESULTS: TREM-1 rs2234246 A allele in the promoter region was signifi cantly associated with the susceptibility of septic shock in recessive model (AA, OR=3.10, 95%CI 1.15 to 8.32, P=0.02), and in codominant model (AG, OR=0.72, 95%CI 0.43-1.19, P=0.02; AA, OR=2.71, 95%CI 1.00-7.42; P=0.03). However, in three inherited models (dominant model, recessive model, and codominant model), none of the assayed loci was signifi cantly associated with the prognosis of septic shock. The nonsurvivor group demonstrated higher plasma IL-6 levels (99.7±34.7 pg/mL vs. 61.2±26.5 pg/mL, P<0.01) than the survivor group. Plasma concentrations of IL-6 among the three genotypes of rs2234246 were AA 99.4±48.9 pg/mL, AG 85.4±43 pg/mL, and GG 65.3±30.7 pg/mL (P<0.01). The plasma concentrations of IL-6 in patients with AA genotypes were signifi cantly higher than those in patients with GG genotypes (P<0.01).CONCLUSION: TREM-1 genetic polymorphisms rs2234246 may be significantly correlated only with susceptibility to septic shock in the Chinese Han population.

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“…TREM-1 and its soluble form are therefore potential diagnostic markers for infectious and chronic inflammatory diseases and also potential future targets for therapeutic manipulation. 15,16 In order for sTREM-1 to be a reliable marker of disease, a greater understanding of the cells relevant to its release and mechanisms of its cleavage are required. Furthermore, the long term impact of reducing TREM-1 cleavage into the soluble form is currently unknown.…”

Section: Introductionmentioning

confidence: 99%

Reversal of TREM-1 ectodomain shedding and improved bacterial clearance by intranasal metalloproteinase inhibitors

et al. 2017

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Triggering receptor expressed on myeloid cells-1 (TREM-1) is expressed on neutrophils and monocyte/macrophages and amplifies Toll-like receptor-mediated inflammation during infection. TREM-1 also exists in an antagonistic soluble form (sTREM-1) that has been used as a peripheral biomarker in sepsis, though the mechanisms of its release are not entirely clear. The requirement of TREM-1 in single microbial infections is controversial, with some studies showing a protective role and others a contribution to immunopathology. Furthermore, the role of membrane-bound and sTREM-1 in polygenic infections is currently unknown. In a mouse co-infection model where preceding viral infection greatly enhances bacteria co-infection, we now determine a mechanisms for the striking increase in sTREM-1 and the loss of TREM-1 on surface of neutrophils. We identified a matrix metalloproteinase (MMP)-9 cleavage site in TREM-1 and that the increase of MMP-9 in bronchoalveolar lavage fluid mirrors sTREM-1 release. In vitro studies with neutrophils and MMP-9 and the reduction of sTREM-1 in vivo after MMP-9 inhibition verifies that this enzyme cleaves TREM-1. Intriguingly, MMP-9 inhibition significantly reduces bacterial load and ensuing immunopathology in a co-infection model. This highlights MMP-9 inhibition as a potential therapeutic via blocking cleavage of TREM-1.

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Time-course of sTREM (soluble triggering receptor expressed on myeloid cells)-1, procalcitonin, and C-reactive protein plasma concentrations during sepsis

Abstract: A progressive decline of plasma sTREM-1 concentration indicates a favorable clinical evolution during the recovery phase of sepsis. In addition, baseline sTREM-1 level may prove useful in predicting outcome of septic patients.

Cited by 212 publications

References 23 publications

Involvement of the TREM-1/DAP12 pathway in the innate immune responses to Porphyromonas gingivalis

Involvement of the TREM-1/DAP12 pathway in the innate immune responses to Porphyromonas gingivalis

Relationships between genetic polymorphisms of triggering receptor expressed on myeloid cells-1 and septic shock in a Chinese Han population

Reversal of TREM-1 ectodomain shedding and improved bacterial clearance by intranasal metalloproteinase inhibitors

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