Rabbit Anti-Human TREM1 Polyclonal antibody

An acidic arabinogalactan (AGP-2) isolated from green gram Hemicellulose-B was purified using Sephacryl S-400 and its molecular weight was found to be similar to 1200 kDa. Characterization of the AGP-2 by various structural methods indicated 1,3- beta- D- Galactan backbone substituted, at O-6 with 1, 5 linked arabinofuranosyl side chains, which were further substituted either with mono/di/tri substituted arabinofuranosyl residues resulting in highly branched structure. Glucuronic acid residues are present as non reducing end terminals. AGP-2 enhanced the release of NO, TNF- alpha, IL-6 and IL- 1 beta and phagocytic capability of macrophages whereas carboxyl reduced AGP-2 failed to show the similar result indicating the importance of carboxyl groups in macrophage activation. Pretreatment of macrophages with antibodies specific to extracellular domains of TLR2, TLR4 and TREM1 significantly reduced the AGP-2 induced release of NO and TNF-alpha indicating the interaction of AGP-2 with TLRs to activate macrophages.

Triggering receptor expressed on myeloid cells-1 (TREM-1) is a potent amplifier of pro-inflammatory innate immune responses, but its significance in non-infectious diseases remains unclear. Here, we demonstrate that TREM-1 promotes cardiovascular disease by exacerbating atherosclerosis. TREM-1 is expressed in advanced human atheromas and is highly upregulated under dyslipidemic conditions on circulating and on lesion-infiltrating myeloid cells in the Apoe(-/-) mouse model. TREM-1 strongly contributes to high-fat, high-cholesterol diet (HFCD)-induced monocytosis and synergizes with HFCD serum-derived factors to promote pro-inflammatory cytokine responses and foam cell formation of human monocyte/macrophages. Trem1(-/-) Apoe(-/-) mice exhibit substantially attenuated diet-induced atherogenesis. In particular, our results identify skewed monocyte differentiation and enhanced lipid accumulation as novel mechanisms through which TREM-1 can promote atherosclerosis. Collectively, our findings illustrate that dyslipidemia induces TREM-1 surface expression on myeloid cells and subsequently synergizes with TREM-1 to enhance monopoiesis, pro-atherogenic cytokine production and foam cell formation.