Association of endotoxaemia with low grade inflammation, metabolic syndrome and distinct response to lipopolysaccharide in type 1 diabetes

Abstract Mechanisms of endotoxaemia as a source of low grade inflammation in type 1 diabetes (T1D) are not clear enough. We investigated the levels of lipopolysaccharide (LPS), lipopolysaccharide binding protein (LBP), endogenous anti-endotoxin core antibodies (EndoCAb IgG and IgM) and high sensitivity C reactive protein (hsCRP) in T1D. 74 patients with T1D and 33 control subjects were included. Higher levels of hsCRP and EndoCAb IgG were observed in T1D compared to control (p = 0.002 and p = 0.091, respectively). LBP (\(\beta\) = 0.29 (0.08; 0.50), p = 0.007), EndoCAb IgG (\(\beta\) = 0.25 (0.04; 0.46), p = 0.019) and LPS were significantly associated with hsCRP in T1D. In contrast to the situation in the control group, LPS did not correlate with LBP, EndoCAb, leukocytes and HDL in T1D. Within T1D group, patients with metabolic syndrome (MS) had higher level of LPS compared to patients without MS (MS 0.42 (0.35–0.56), no MS 0.34 (0.3–0.4), p = 0.009) and MS was associated with LPS (OR = 3.3 (1.6; 6.8), p = 0.001) and EndoCAb IgM (OR = 0.43 (0.20; 0.91), p = 0.027). To conclude, endotoxaemia is associated with low grade inflammation, MS and distinct response to LPS in T1D.