Effects of lipopolysaccharide on changes in red blood cells in a mice endotoxemia model

Abstract

The aim of this study was to evaluate changes in RBC aggregation and deformability over 24 hr and suggest specific shear stress values for detecting RBC deformability in a mouse endotoxemia model using lipopolysaccharide (LPS).Six-week-old male BALB/c mice received LPS (20 mg/kg) intraperitoneally. Aggregation indices (AIs) and T1/2 were measured to assess RBC aggregation, and elongation indices (EIs) were used to assess RBC deformability at shear stress values of 0.3, 0.5, 1, 3, 7, 10, 15 and 20 Pascals (Pa) 0, 30 min, 1, 2, 4, 6, 9, 12, 18 and 24 hours after the LPS injection.No significant differences were detected in the AIs during the study period, however, T1/2 shortened significantly 2, 6, 12, 18, and 24 hr after the LPS injection. The EIs increased significantly 24 hr after LPS injection at 0.5 and 1 Pa shear stress, whereas it decreased significantly at 10 Pa of shear stress 24 hr after the LPS injection.Altered RBC deformability was detectable 24 hr after the LPS injection and T1/2 may be a sensitive marker for detecting changes in RBC aggregation. The EIs should be measured at 1 Pa to detect changes in RBC deformability in LPS-induced septic mice.

Protective potentials of polymyxin B and honey against bacterial lipopolysaccharide-induced endotoxemia in mice

“…LPS binds three times more to the RBC membrane and activates WBCs, accelerates oxygen-free radical formation, and activates the Toll-like receptor (TLR-4), causing complement-mediated hemolysis and reducing erythrocytes, potentially inhibiting hematopoiesis [ 16 ]. LPS binds more to RBC membranes due to biochemical alterations caused by free radicals and cytokines.…”

“…LPS binds more to RBC membranes due to biochemical alterations caused by free radicals and cytokines. That decreases membrane elasticity and deformability and may lead to a loss of normal membrane flexibility [ 16 ]. Alongside RBCs, the Hb concentration and PCV are also reduced.…”

O-GlcNAcylation of RIPK1 rescues red blood cells from necroptosis

“…Several studies have indicated that the administration of TMG or NButGT (27), an OGA inhibitor, improves the survival of LPS-injected mice (28,29) and has a protective effect on cardiovascular function or lung-tissue damage, which suggests that O-GlcNAcylation is deeply engaged in LPS-induced pathophysiological changes (30,31). However, the role of O-GlcNAcylation in the functional disruption of erythrocytes induced by LPS-induced endotoxemia (32,33) should be further investigated. Using erythrocytes isolated from the whole blood of LPS i.p.…”