TY - JOUR
T1 - Triggering receptor expressed on myeloid cells (TREM-1) is regulated post-transcriptionally and its ligand is present in the sera of some septic patients
AU - Wong-Baeza, I.
AU - González-Roldán, N.
AU - Ferat-Osorio, E.
AU - Esquivel-Callejas, N.
AU - Aduna-Vicente, R.
AU - Arriaga-Pizano, L.
AU - Astudillo-De La Vega, H.
AU - Villasis-Keever, M. A.
AU - Torres-González, R.
AU - Estrada-García, I.
AU - López-Macías, C.
AU - Isibasi, A.
PY - 2006/9
Y1 - 2006/9
N2 - Inflammation is necessary for survival, but it is also an important cause of human morbidity and mortality, as exemplified by sepsis. During inflammation, cells of the innate immune system are recruited and activated in response to infection, trauma or injury. These cells are activated through receptors, such as Toll-like receptors (TLRs), which recognize microbial ligands such as lipopolysaccharide (LPS). Triggering receptor expressed on myeloid cells (TREM)-1 amplifies the inflammatory response initiated by TLRs, and its expression on the surface of monocytes increases in the presence of TLR ligands. Here we have shown that in monocytes TREM-1 mRNA levels, measured by reverse transcription-polymerase chain reaction (RT-PCR), remained unchanged and TREM-1 protein levels, measured by flow cytometry, increased, indicating that LPS increases TREM-1 expression by a post-transcriptional mechanism. 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. We describe a mechanism for the regulation of TREM-1 expression on monocytes and the possible presence of its ligand in serum; these findings help to explain the contribution of TREM-1 during systemic inflammation.
AB - Inflammation is necessary for survival, but it is also an important cause of human morbidity and mortality, as exemplified by sepsis. During inflammation, cells of the innate immune system are recruited and activated in response to infection, trauma or injury. These cells are activated through receptors, such as Toll-like receptors (TLRs), which recognize microbial ligands such as lipopolysaccharide (LPS). Triggering receptor expressed on myeloid cells (TREM)-1 amplifies the inflammatory response initiated by TLRs, and its expression on the surface of monocytes increases in the presence of TLR ligands. Here we have shown that in monocytes TREM-1 mRNA levels, measured by reverse transcription-polymerase chain reaction (RT-PCR), remained unchanged and TREM-1 protein levels, measured by flow cytometry, increased, indicating that LPS increases TREM-1 expression by a post-transcriptional mechanism. 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. We describe a mechanism for the regulation of TREM-1 expression on monocytes and the possible presence of its ligand in serum; these findings help to explain the contribution of TREM-1 during systemic inflammation.
KW - DAP12
KW - Inflammation
KW - Sepsis
KW - TREM-1
UR - http://www.scopus.com/inward/record.url?scp=33747446927&partnerID=8YFLogxK
U2 - 10.1111/j.1365-2249.2006.03158.x
DO - 10.1111/j.1365-2249.2006.03158.x
M3 - Artículo
C2 - 16907912
SN - 0009-9104
VL - 145
SP - 448
EP - 455
JO - Clinical and Experimental Immunology
JF - Clinical and Experimental Immunology
IS - 3
ER -