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An Antibody Against Triggering Receptor Expressed on Myeloid Cells 1 (TREM-1) Dampens Proinflammatory Cytokine Secretion by Lamina Propria Cells from Patients with IBD.

Artikel i vetenskaplig tidskrift
Författare Siggeir Fannar Brynjólfsson
Maria K Magnusson
Philip L Kong
Teis Jensen
Joseph L Kuijper
Katarina Håkansson
Christine B Read
Vibeke W Stennicke
Henrik Sjövall
Mary Jo Wick
Publicerad i Inflammatory bowel diseases
Volym 22
Nummer/häfte 8
Sidor 1803-11
ISSN 1536-4844
Publiceringsår 2016
Publicerad vid Institutionen för biomedicin, avdelningen för mikrobiologi och immunologi
Institutionen för medicin, avdelningen för invärtesmedicin och klinisk nutrition
Sidor 1803-11
Språk en
Länkar dx.doi.org/10.1097/MIB.000000000000...
www.ncbi.nlm.nih.gov/entrez/query.f...
https://gup.ub.gu.se/file/206785
Ämnesord TREM-1, PGLYRP-1, inflammation, ulcerative colitis, Crohn's disease, inflammatory-bowel-disease, dendritic cells, intestinal macrophages, crohns-disease, septic shock, cutting edge, monocytes, homeostasis, responses, immunity, Gastroenterology & Hepatology
Ämneskategorier Gastroenterologi

Sammanfattning

Triggering receptor expressed on myeloid cells 1 (TREM-1) is a potent amplifier of inflammation. Recently, the antimicrobial peptide PGLYRP-1 was shown to be the ligand of TREM-1. Here, the ability of an anti-TREM-1 antibody to dampen the release of proinflammatory cytokines by colon lamina propria cells (LPCs) from patients with IBD was investigated and correlated with PGLYRP-1 levels.Biopsies from patients with ulcerative colitis (UC, n = 45) or Crohn's disease (CD, n = 26) were compared with those from individuals undergoing colonoscopy for other reasons (n = 17). TREM-1 expression was analyzed on myeloid cells by flow cytometry. Cell culture experiments with LPCs were used to analyze PGLYRP-1 and inflammatory cytokine levels and assess the effect of anti-TREM-1 on cytokine secretion.The frequency of TREM-1-expressing neutrophils and recruited macrophages was higher in inflamed than in noninflamed biopsies. The PGLYRP-1 level in inflamed tissue was higher than in noninflamed tissue; it was produced primarily by neutrophils, and its level correlated with the secretion of proinflammatory cytokines. Secretion of myeloperoxidase, tumor necrosis factor-α, interleukin-1β, and interleukin-8 by LPCs stimulated with the potent TREM-1 agonist consisting of PGLYRP-1 complexed with peptidoglycan was reduced in the presence of anti-TREM-1. Moreover, a blocking effect of anti-TREM-1 was apparent when LPCs from a subset of inflamed individuals with elevated PGLYRP-1 were stimulated with killed bacteria.An anti-TREM-1 antibody can dampen secretion of proinflammatory cytokines in inflamed patients with elevated PGLYRP-1. Moreover, PGLYRP-1 + myeloperoxidase is a potential biomarker for predicting the effect of anti-TREM-1 therapy.

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