Soluble Form of the Triggering Receptor Expressed on Myeloid Cells-1 as a Marker of Microbial Infection

Gibot, Sébastien; Cravoisy, Aurélie

doi:10.3121/cmr.2.3.181

Cited by 118 publications

(125 citation statements)

References 26 publications

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“…It demonstrates that the putative oral pathogen P. gingivalis can stimulate the expression of the TREM-1 / DAP12 pathway in monocytic cells, associated with an increased release of sTREM-1, which may constitute a marker of systemic inflammation (Gibot and Cravoisy, 2004). Moreover, TREM-1 engagement can further potentiate the pro-inflammatory responses of monocytes to P. gingivalis infection, whereas its inhibition can conversely reduce this.…”

Section: Discussionmentioning

confidence: 94%

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: Discussionmentioning

confidence: 94%

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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“…TREM-1 is a recently identified immunoglobulin-like cell surface receptor mainly expressed on neutrophils and a subset of CD14 high monocytes [7]. Activation of TREM-1 by the crosslinking antibody leads to the production of multiple pro-inflammatory cytokines and chemokines, and this response can synergize with innate immune stimuli to amplify inflammatory responses [8][9][10][11]. Hypoxic stress also triggers unfolded protein response pathway due to accumulation of misfolded proteins in the endoplasmic reticulum (ER).…”

Section: Introductionmentioning

confidence: 99%

Hypoxic Stress Induced TREM-1 and Inflammatory Chemokines in Human Peripheral Blood Mononuclear Cells

et al. 2013

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Hypoxia is a condition of low pO 2 , which creates a unique microenvironment affecting cell phenotype and subsequent immune response generation. Little is known about the impact of hypoxia on the phenotypic expression of NK cell, TREM-1, TLR-4 and inflammatory chemokines. In the present study we have determined the frequency of peripheral blood populations of CD16/CD56 (NK Cells) expressing cells, presence of activation marker CD354 (TREM-1), Toll like receptor (CD 284) on the cell surface and chemokines IL-8 and RANTES in the cellular supernatant of normoxia and hypoxia exposed cells by flow cytometry. GRP-78 expression was determined by reverse transcriptase polymerase chain reaction. The blood was collected from healthy individuals and exposed to normoxic and hypoxic (0.5 %) environment for 24 h. The percentage of NK cells (CD 16/56) was marginally up regulated while TLR-4 expression was diminished in hypoxia exposed cells as compare to the normoxic cells. TREM-1 expression was significantly up-regulated (p \ 0.05) in hypoxia as compared to the normoxic control. In addition when monocytic cell line THP-1 was exposed to 0.5 % hypoxia for 24 h, TLR4 expression was significantly decreased in hypoxic cells as compared to normoxic cells. Furthermore, GRP-78 mRNA expression was also upregulated by hypoxia or LPS exposure. These events are paralleled by strengthening up-regulation of the chemokines IL-8 and RANTES an otherwise necessary event for the chemotaxis of the neutrophils and macrophages to the inflammatory site. In conclusion, this study provides a novel insight into the mechanism linking low oxygen tension to the regulation of immune and inflammatory responses, leading to new perspectives of the role of hypoxia in programming immune cell functions.

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“…As a member of the immunoglobulin superfamily, the triggering receptor expressed on myeloid cells-1 (TREM-1) is strongly expressed on activated phagocytes [65,66] . A soluble form is released during bacterial or fungal infections and can be detected as biomarker in distinct body fluids [67] .…”

Section: Soluble Triggering Receptor Expresses On Myeloid Cells-1mentioning

confidence: 99%

Are there new approaches for diagnosis, therapy guidance and outcome prediction of sepsis?

Kojic

Siegler

Uhle

et al. 2015

WJEM

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Beside many efforts to improve outcome, sepsis is still one of the most frequent causes of death in critically ill patients. It is the most common condition with high mortality in intensive care units. The complexity of the septic syndrome comprises immunological aspects -i.e. , sepsis induced immunosuppression -but is not restricted to this fact in modern concepts. So far, exact mechanisms and variables determining outcome and mortality stay unclear. Since there is no typical risk profile, early diagnosis and risk stratification remain difficult, which hinders rapid and effective treatment initiation. Due to the heterogeneous nature of sepsis, potential therapy options should be adapted to the individual. Biomarkers like C-reactive protein and procalcitonin are routinely used as complementary tools in clinical decision-making. Beyond the acute phase proteins, a wide bunch of promising substances and non-laboratory tools with potential diagnostic and prognostic value is under intensive investigation. So far, clinical decision just based on biomarker assessment is not yet feasible. However, biomarkers should be considered as a complementary approach. Core tip: Sepsis is a complex continuum of disturbed systems. Despite the presence of clinical consensus criteria, the early diagnosis especially in the perioperative setting is challenging. A magnitude of potential new biomarkers is tested for this purpose, but evidence is mounting that due to the complex nature of the syndrome, biomarkers are rather complementary tools for clinical decision making than "magic bullets". Moreover, biomarkers are also evaluated for therapy guidance, linking diagnostic results to an individual therapeutic regime. This review summarizes the developments in the biomarker field, aiming to provide an overview about current targets and their limitations.

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Soluble Form of the Triggering Receptor Expressed on Myeloid Cells-1 as a Marker of Microbial Infection

Cited by 118 publications

References 26 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

Hypoxic Stress Induced TREM-1 and Inflammatory Chemokines in Human Peripheral Blood Mononuclear Cells

Are there new approaches for diagnosis, therapy guidance and outcome prediction of sepsis?

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