In this article, we review the abundant literature evaluating the usefulness of soluble triggering receptor expressed on myeloid cells-1 for the diagnosis and the prognosis evaluation of sepsis or localized infections.
Because TREM-1 participates in septic shock and in amplifying the inflammatory response to bacterial and fungal infections, we believe it could be an immunohistochemical marker for postmortem diagnosis of sepsis.
<b>Results:</b> Our analysis revealed that several markers could be useful for sepsis diagnosis, such as CD45RA, CD45RO, or CD71 on T cells; HLA-DR on NKT or classic monocytes, and TREM-1 on non-classic monocytes or neutrophils.
Importantly, extracellular actin showed co-localization with TREM-1 in lung tissue sections from septic mice, which suggested that TREM-1 recognized actin during activation in sepsis.
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.
Triggering receptor expressed on myeloid cells 1 (TREM-1), which amplifies the inflammation elicited by the Toll-like receptor pathway, was originally implicated in sepsis and bacterial infection.
TREM-1 up-regulation resulted in a grave outcome in animal models, and in patients with sepsis and rheumatoid arthritis, while its soluble form (sTREM-1) exerted anti-inflammatory effects.
Triggering receptor expressed on myeloid cells-1 (TREM-1) can amplify the proinflammatory response and may contribute to the pathogenesis of inflammatory disease such as sepsis.
Of the three tested TREM-1 SNPs (rs144672509, rs2234237, and rs2234246), only rs2234237 (Ser25Thr) was significantly associated with sepsis prognosis in three inheritance models (p < 0.05).
Thus far, TREM-1 is primarily associated with unwanted signs of overwhelming inflammation, rendering it an attractive target for conditions such as sepsis.
TREM-1 is up-regulated in PBMC of AC patients, and has higher sensitivity and specificity than other clinical inflammation markers, suggesting its importance in AC-induced sepsis.
Our results shed new light on our understanding of TREM-1 and its role in the innate inflammatory response in infections and might contribute to the development of future concepts to treat sepsis.
We also showed that TREM-1/Fc fusion protein decreased the ability of the sera of some patients with sepsis to activate monocytes, indicating that the TREM-1 ligand, whose identity is unknown, may be present in the sera of some of these patients.
Notably, blockade of TREM-1 protects mice against LPS-induced shock, as well as microbial sepsis caused by live Escherichia coli or caecal ligation and puncture.