Soluble Triggering Receptor Expressed on Myeloid Cell-1 Is Increased in Patients With Ventilator-Associated Pneumonia

Horonenko, Grigory; Hoyt, Jeffrey C.; Robbins, Richard; Singarajah, Clement; Umar, Anam; Pattengill, Jenny; Hayden, John M.

doi:10.1378/chest.06-2731

Cited by 62 publications

(49 citation statements)

References 23 publications

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“…Determann et al [41] measured s-TREM in adult patients with VAP and controls and did not find differences in plasma levels; however, levels in BAL were higher in patients with VAP. These results differed from those published by Horoneko et al [42], who did not find differences in s-TREM concentrations between patients with VAP and controls. Srinivasan et al [43] evaluated the role of s-TREM and plasminogen activation inhibitor-1 (PLA-1) in the diagnosis of VAP in a PICU.…”

Section: Diagnostic Biomarkerscontrasting

confidence: 99%

Ventilator-Associated Pneumonia in Neonatal Patients: An Update

et al. 2013

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Ventilator-associated pneumonia (VAP) is a serious complication related to mechanical ventilation in the neonatal period. However, lack of a specific definition and difficulties obtaining noncontaminated samples of the lower respiratory airway render microbiological diagnosis and etiological treatment extremely difficult. Thus far, only few studies have approached VAP using accepted Centers for Disease Control and Prevention criteria and reliable sampling techniques. In recent years, however, the blind-protected bronchoalveolar lavage technique with protected specimen brush and the development of validated biomarkers have attempted to overcome the diagnostic difficulties and assess the response to therapy. This updated review on neonatal VAP aims to stimulate neonatologists' interest in this subtle but serious complication of mechanical ventilation.

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Section: Diagnostic Biomarkerscontrasting

confidence: 99%

Ventilator-Associated Pneumonia in Neonatal Patients: An Update

et al. 2013

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“…Patients with VAP had higher BAL interleukin 1β (IL-1β), IL-8, granulocyte colony-stimulating factor (G-CSF) and macrophage inflammatory protein-1α (MIP-1α) than the non-VAP ventilated group and healthy controls. Interestingly, unlike in the previous study,7 18 sTREM concentrations did not differ between the VAP and non-VAP groups.…”

contrasting

confidence: 99%

Novel pulmonary biomarkers in the diagnosis of VAP

Johnston

McAuley

O'Kane

2010

Thorax

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“…This soluble form has been found at high concentrations only in fluids from patients with microbial infections (2,9,12). Further, increased sTREM-1 levels have been observed in patients with ventilator-associated pneumonia (13). Other studies also suggest an up-regulation of soluble TREM-1 in plasma from patients who suffer from sepsis vs those undergoing a systemic inflammatory response syndrome (14).…”

mentioning

confidence: 99%

Metalloproteinases Shed TREM-1 Ectodomain from Lipopolysaccharide-Stimulated Human Monocytes

Gómez-Piña

Soares‐Schanoski

Rodríguez‐Rojas

et al. 2007

The Journal of Immunology

178

155

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Triggering receptors expressed on myeloid cell (TREM) proteins are a family of cell surface receptors that participate in diverse cellular processes such as inflammation, coagulation, and bone homeostasis. TREM-1, in particular, is expressed on neutrophils and monocytes and is a potent amplifier of inflammatory responses. LPS and other microbial products induce up-regulation of cell surface-localized TREM-1 and the release of its soluble form, sTREM-1. Two hypotheses have been advanced to explain the origin of sTREM-1: alternative splicing of TREM-1 mRNA and proteolytic cleavage(s) of mature, membrane-anchored TREM-1. In this report, we present conclusive evidence in favor of the proteolytic mechanism of sTREM-1 generation. No alternative splicing forms of TREM-1 were detected in monocytes/macrophages. Besides, metalloproteinase inhibitors increased the stability of TREM-1 at the cell surface while significantly reducing sTREM-1 release in cultures of LPS-challenged human monocytes and neutrophils. We conclude that metalloproteinases are responsible for shedding of the TREM-1 ectodomain through proteolytic cleavage of its long juxtamembrane linker.

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Soluble Triggering Receptor Expressed on Myeloid Cell-1 Is Increased in Patients With Ventilator-Associated Pneumonia

Cited by 62 publications

References 23 publications

Ventilator-Associated Pneumonia in Neonatal Patients: An Update

Ventilator-Associated Pneumonia in Neonatal Patients: An Update

Novel pulmonary biomarkers in the diagnosis of VAP

Metalloproteinases Shed TREM-1 Ectodomain from Lipopolysaccharide-Stimulated Human Monocytes

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