| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 3355463 | Immunology Letters | 2014 | 6 Pages |
•Evaluation of surface and soluble TREM-1 levels in DENV-infected patients was made.•A significant reduction of TREM-1 expression was observed in neutrophils.•Sera from DENV-infected patients exhibited significantly higher of soluble TREM-1 levels during the first 5 days after the symptoms onset.•The increment of sTREM-1 could be a compensatory mechanism to counteract the inflammatory process elicited by DENV infection.•These data are the first to show the involvement of TREM-1 during DENV infection.
Uncontrolled and intricate production of inflammatory factors is the characteristic feature of dengue infection. The triggering receptor expressed in myeloid cells-1 (TREM-1), expressed on the surface of monocytes and neutrophils, is capable of enhancing and regulating the inflammatory response via the production of different mediators in bacterial and viral infections. Here, both the expression of TREM-1 on human monocytes and neutrophils from peripheral blood of dengue infected individuals, as well as the levels of the soluble form of TREM-1 (sTREM-1) in the sera of these patients were compared against healthy controls. A significant reduction of TREM-1 expression was observed in neutrophils during the first days of infection, followed by a gradual recovery throughout the course of infection. Also, sera from DENV-infected patients exhibited significantly higher sTREM-1 levels than healthy individuals. The difference was more pronounced during the first 5 days after the onset of symptoms. These findings highlight the dynamic process of TREM-1 expression during DENV infection. We hypothesized that increment of free sTREM-1 could be a compensatory mechanism aiming to counteract the inflammatory process elicited during DENV infection.
