The Increased Expression of TREM-1 on Monocytes Is Associated With Infectious and Noninfectious Inflammatory Processes

Ferat‐Osorio, Eduardo; Esquivel-Callejas, Noemí; Wong‐Baeza, Isabel; Aduna-Vicente, Rosalía; Arriaga-Pizano, Lourdes; Sánchez-Fernández, Patricio; Torres-González, R; López-Macías, Constantino; Isibasí, Armando

doi:10.1016/j.jss.2007.12.805

Cited by 32 publications

(27 citation statements)

References 32 publications

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“…In addition when monocytic cell line THP-1 was exposed to hypoxia, TLR4 expression was significantly decreased in hypoxic cells as compare to normoxic cells. 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 [17,18] and strongly elevated after bacterial infection [19]. TREM-1 activation also enhances the production of TNF-a, IL-6, and MIP-2, as well as PMN infiltration [7].…”

Section: Discussionmentioning

confidence: 95%

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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Section: Discussionmentioning

confidence: 95%

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

et al. 2013

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“…Previously published researchers showed that sTREM‐1 levels are centrally involved in acute microbial inflammation and are a crucial mediator of septic shock; only 19% of healthy controls had detectable sTREM‐1 9, 10. However, the role of sTREM‐1 is subject to intensive research in various noninfectious diseases, such as heart surgery, cardiac arrest, anti–neutrophil cytoplasmic antibody–associated vasculitis, and rheumatoid arthritis 30, 31, 32, 33, 34, 35. Therefore, it is reasonable to propose that elevated sTREM‐1 in the serum could be derived from activated monocytes/macrophages in atherosclerotic plaque or neutrophils accumulated in the injured myocardium after AMI.…”

Section: Discussionmentioning

confidence: 99%

Prognostic Utility of Soluble TREM‐1 in Predicting Mortality and Cardiovascular Events in Patients With Acute Myocardial Infarction

Wang

Tang

Shen

et al. 2018

JAHA

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BackgroundTriggering receptor expressed on myeloid cells‐1 (TREM‐1) is thought to be critical for inflammatory signal amplification and involved in the development of atherosclerosis. TREM‐1 is significantly increased in patients with myocardial infarction. The aim of this study was to investigate the association between soluble TREM‐1 (sTREM‐1) and mortality and cardiovascular events in patients with acute myocardial infarction.Methods and ResultsWe included 838 consecutive patients with acute myocardial infarction from October 7, 2012 to December 5, 2014. Blood samples were collected from patients with acute myocardial infarction immediately after diagnosis. During follow‐up, 88 patients died, and 180 patients reached the combined end points of major adverse cardiovascular event (MACE). Patients with high sTREM‐1 (higher than the median) had increased risk of all‐cause mortality and MACE compared with those with low sTREM‐1 (log‐rank test, P<0.001). After adjustment for confounding risk factors by Cox regression analysis, high sTREM‐1 remained an independent predictor of all‐cause mortality (hazard ratio, 1.978; 95% confidence interval, 1.462–2.675; P<0.001) and MACE (hazard ratio, 2.413; 95% confidence interval, 2.022–2.879; P<0.001). After the addition of sTREM‐1 to the reference model, the C‐statistic for all‐cause mortality increased from 0.86 to 0.89, and the difference was 0.023 (95% confidence interval, 0.0009–0.0477), and the C‐statistic for MACE increased from 0.71 to 0.80, and the difference was 0.087 (95% confidence interval, 0.053–0.122). sTREM‐1 levels were consistently positively associated with risks of all‐cause mortality and MACE in various subpopulations, and there was no significant interaction among prespecified subgroups.Conclusions sTREM‐1 was significantly associated with all‐cause mortality and MACE, independent of established conventional risk factors in patients with acute myocardial infarction.

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“…Expression of TREM-1 is detected on a variety of immune cells, such as PMNs, macrophages, and monocytes (4,11,33), and strongly elevated after bacterial infection (5,28). Studies have demonstrated that activation of TREM-1 alters the dynamics of pulmonary IRAK-M expression and improves the host defense during pneumococcal pneumonia (25).…”

Section: Discussionmentioning

confidence: 99%

TREM-1 Amplifies Corneal Inflammation after Pseudomonas aeruginosa Infection by Modulating Toll-Like Receptor Signaling and Th1/Th2-Type Immune Responses

Peng

Sun

et al. 2011

Infect Immun

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As a novel family of cell surface receptors, triggering receptors expressed on myeloid cells (TREMs) play an important role in inflammatory responses. However, the role of TREMs in the ocular immune system remains unknown. In this study, we examined the expression and function of TREM-1 in Pseudomonas aeruginosa keratitis, one of the most common sight-threatening ocular diseases. TREM-1 was significantly increased in human corneas after P. aeruginosa infection. Consistent with TREM-1 expression at the human ocular surface, TREM-1 levels (mRNA and protein) were also elevated in the infected corneas of C57BL/6 (B6) mice at 1, 3, and 5 days postinfection. To determine whether TREM-1 dictates the outcome of P. aeruginosa keratitis in susceptible mice, TREM-1 signaling in B6 mice was blocked with a soluble mTREM-1/Fc fusion protein. The results indicated that blockade of TREM-1 reduced the severity of corneal disease, polymorphonuclear neutrophil infiltration, Th1/proinflammatory cytokine expression and Toll-like receptor (TLR) activation but enhanced the production of Th2 cytokines, murine ␤-defensin 2 (mBD2), single Ig interleukin-1R-related molecule (SIGIRR), and ST2. Furthermore, we also used agonistic anti-mTREM-1 antibody to activate TREM-1 signaling in B6 mice and found that TREM-1 activation resulted in worsened disease and earlier corneal perforation in infected B6 mouse corneas and elevated production of proinflammatory cytokines and TLR signaling molecules but reduced expression of mBD2, SIGIRR, and ST2. To the best of our knowledge, this study provides the first evidence that TREM-1 functions as an inflammatory amplifier in P. aeruginosa keratitis by modulating TLR signaling and Th1/Th2 responses.

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The Increased Expression of TREM-1 on Monocytes Is Associated With Infectious and Noninfectious Inflammatory Processes

Cited by 32 publications

References 32 publications

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

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

Prognostic Utility of Soluble TREM‐1 in Predicting Mortality and Cardiovascular Events in Patients With Acute Myocardial Infarction

TREM-1 Amplifies Corneal Inflammation after Pseudomonas aeruginosa Infection by Modulating Toll-Like Receptor Signaling and Th1/Th2-Type Immune Responses

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