title: Evaluation of TREM1 gene expression in circulating polymorphonuclear leukocytes and its inverse correlation with the severity of pathophysiological conditions in patients with acute bacterial infections.
abstract: During bacterial infection, activated polymorphonuclear leukocytes (PMNs) often cause  inflammation and organ dysfunction in severely ill patients. Gene expression was analyzed in circulating PMNs  isolated from these patients to determine the distinct expression profile. We focused on immunomodulatory genes,  such as those for pattern recognition receptors, inflammatory cytokines, PMN surface antigens, and myeloid cell  receptors in PMNs. Gene expression in 23 patients (12 with pneumonia and 11 with sepsis) were analyzed using  quantitative real-time polymerase chain reaction. The mRNA levels of TLR2 (20/23 cases) and CD14 (18/23 cases)  were upregulated in the PMNs of patients when compared with healthy subjects. The mRNA expression levels of TLR4  (16/23 cases) and IL6 (16/23 cases) were downregulated in patients' PMNs, and of TNFA (16/23 cases) were  upregulated in these cells. Although mRNA levels of IL8RA (15/23 cases) were downregulated in PMNs, MAC-1 mRNA  levels (14/23 cases) were upregulated in the same cells. Copies of the TREM1 transcript were 0.7- to 2.1-fold  higher in patients with moderate pneumonia than in the healthy subjects; the average fold change was 1.1. The  mRNA levels were 0.3-fold lower in the patients with severe pneumonia and sepsis than in the healthy subjects.  In conclusion, the downregulation of TREM1 expression in PMNs is associated with the severity of the  pathophysiological conditions and may be used as a surrogate marker of acute bacterial infections.
authors.affiliation: Department of Microbiology & Immunology, Teikyo University School of Medicine, Tokyo, Japan. ubat@med.teikyo-u.ac.jp
authors.forename: Tsuneyuki
authors.initials: T
authors.lastname: Ubagai
authors.forename: Shigeru
authors.initials: S
authors.lastname: Tansho
authors.forename: Ryuji
authors.initials: R
authors.lastname: Ieki
authors.forename: Yasuo
authors.initials: Y
authors.lastname: Ono
mesh_terms: D000208:Acute Disease; D000368:Aged; D016470:Bacteremia / Q000097:blood* / Q000235:genetics; D016022:Case-Control Studies; D016207:Cytokines / Q000096:biosynthesis / Q000097:blood / Q000235:genetics; D015536:Down-Regulation; D005260:Female; D015870:Gene Expression; D020869:Gene Expression Profiling; D054884:Host-Pathogen Interactions; D006801:Humans; D008297:Male; D008562:Membrane Glycoproteins / Q000096:biosynthesis / Q000097:blood* / Q000235:genetics; D008875:Middle Aged; D009504:Neutrophils / Q000378:metabolism*; D018410:Pneumonia, Bacterial / Q000097:blood* / Q000235:genetics; D012333:RNA, Messenger / Q000097:blood; D060888:Real-Time Polymerase Chain Reaction; D011971:Receptors, Immunologic / Q000096:biosynthesis / Q000097:blood* / Q000235:genetics; D000073871:Triggering Receptor Expressed on Myeloid Cells-1
chemical_list: D016207:Cytokines; D008562:Membrane Glycoproteins; D012333:RNA, Messenger; D011971:Receptors, Immunologic; C408842:TREM1 protein, human; D000073871:Triggering Receptor Expressed on Myeloid Cells-1