title: Triggering receptor expressed on myeloid cells (TREM-1) is regulated post-transcriptionally and its ligand is present in the sera of some septic patients.
abstract: 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.
authors.affiliation: Unidad de Investigación Médica en Inmunoquímica, Hospital de Especialidades, Mexico DF, Mexico.
authors.forename: I
authors.initials: I
authors.lastname: Wong-Baeza
authors.forename: N
authors.initials: N
authors.lastname: González-Roldán
authors.forename: E
authors.initials: E
authors.lastname: Ferat-Osorio
authors.forename: N
authors.initials: N
authors.lastname: Esquivel-Callejas
authors.forename: R
authors.initials: R
authors.lastname: Aduna-Vicente
authors.forename: L
authors.initials: L
authors.lastname: Arriaga-Pizano
authors.forename: H
authors.initials: H
authors.lastname: Astudillo-de la Vega
authors.forename: M A
authors.initials: MA
authors.lastname: Villasis-Keever
authors.forename: R
authors.initials: R
authors.lastname: Torres-González
authors.forename: I
authors.initials: I
authors.lastname: Estrada-García
authors.forename: C
authors.initials: C
authors.lastname: López-Macías
authors.forename: A
authors.initials: A
authors.lastname: Isibasi
mesh_terms: D000328:Adult; D018929:Cell Culture Techniques; D016009:Chi-Square Distribution; D005260:Female; D005434:Flow Cytometry / Q000379:methods; D006801:Humans; D016753:Interleukin-10 / Q000276:immunology; D008070:Lipopolysaccharides / Q000494:pharmacology; D008213:Lymphocyte Activation; D008297:Male; D008562:Membrane Glycoproteins / Q000032:analysis* / Q000097:blood* / Q000235:genetics; D008875:Middle Aged; D009000:Monocytes / Q000378:metabolism*; D012323:RNA Processing, Post-Transcriptional; D012333:RNA, Messenger / Q000032:analysis; D011971:Receptors, Immunologic / Q000032:analysis* / Q000097:blood* / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D018805:Sepsis / Q000097:blood / Q000276:immunology*; D018709:Statistics, Nonparametric; D000073871:Triggering Receptor Expressed on Myeloid Cells-1; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology
chemical_list: D008070:Lipopolysaccharides; D008562:Membrane Glycoproteins; D012333:RNA, Messenger; D011971:Receptors, Immunologic; C408842:TREM1 protein, human; D000073871:Triggering Receptor Expressed on Myeloid Cells-1; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10