P0761STUDY ON THE MECHANISM OF MICROINFLAMMATION WITH UREMIA CAUSED BY LACTOBACILLUS ACTIVATION OF INTESTINAL MACROPHAGES BY MINCLE

Abstract

Abstract Background and Aims My previous studies have found that Intestinal macrophages in the uremic rats are polarized towards a proinflammatory phenotype and had dysfunction of phagocytosis leading to aggravate microinflammation and assist bacterial translocation in uremia resulting in microinflammation. However, it is still unclear what kind of mechanism of action of intestinal bacteria activates intestinal macrophages and thus participates in the occurrence and development of microinflammation in uremia. Method Male Sprague-Dawley rats were randomly divided into two groups: sham, uremia. The macrophage ultrastructure was examined by transmission electron microscopy. Immunochemistry was used to analyze the expression of macrophage-inducible C-type lectin (Mincle). RT-PCR and western blot were employed to assess the mRNA and protein expression of toll-like receptor 4 (TLR4). Results Our RCT study found that the number of Lactobacilli in the intestines of patients with end-stage diabetic nephropathy was significantly higher than that in non-diabetic patients(Figure 1). The plasma levels of endotoxin, CRP, IL-6, and TNF-a in the uremia group were greater than those in the sham group (p>0.05)(Table 1).Compared with the sham group, the uremic macrophages showed fewer cytoplasmic protrusions and pseudopodia(Figure 2) and the uremia group exhibited macrophages with higher staining intensities for Mincle and higher mRNA and protein expression of TLR4(Figure 3-5). Conclusion Studies have shown that Lactobacillus planta can directly activate Mincle. The relationship between Mincle and the activation of intestinal macrophages was verified. The solution to this scientific problem will not only clarify the molecular mechanism of intestinal bacteria in controlling the activation of intestinal macrophages, but also link the immune regulation of intestinal macrophages with the micro-inflammation of uremia so as to clarify the micro-inflammation state of uremia.