Interleukin 6 gene polymorphism in patients with degenerative lumbar scoliosis: a cohort study

Purpose

Low bone mass and a female gender increase susceptibility to the development of degenerative lumbar scoliosis (DLS), which suggests the potential involvement of an osteoporosis-related gene in the pathogenesis of DLS. In the present study, the authors studied the relations between polymorphisms of interleukin 6 (IL-6) gene and DLS in a patient cohort.

Methods

In 184 patients with a diagnosis of DLS, the authors determined the presence of the -597 G/A, -572 G/C, and -174 G/C polymorphisms, measured bone mineral densities at the lumbar spine (LSBMD) and femoral neck (FNBMD), assessed radiological findings including lumbar scoliosis and lateral listhesis, investigated biochemical markers of bone turnover, and compared these results obtained with those of 220 healthy normal controls.

Results

Genotype frequencies in the DLS patients and controls revealed a significant difference for the IL6-572 G/C polymorphism (P = 0.0168). Mean LSBMD was lower in DLS patients than in controls, but no significant difference was found between these two groups with respect to FNBMD, biochemical markers, or radiological findings. A significant association was found between the IL6-572 G/C polymorphism and LSBMD. LSBMD in DLS with the CC genotype was found to be significantly higher than in DLS with the GC (P < 0.05) or GG (P < 0.05) genotypes.

Conclusion

The results of this study suggest that the IL6-572 G/C polymorphism influences LSBMD in Korean DLS patients and the prevalence of the disease.

     

Obesity and dysregulated central and peripheral macrophage–neuron cross‐talk

The involvement of macrophages in the pathogenesis of obesity has been recognized since 2003. Early studies mostly focused on the role of macrophages in adipose tissue (AT) and in obesity‐associated chronic low‐grade inflammation. Lately, AT macrophages were shown to undergo intrinsic metabolic changes that affect their immune function (i.e., immunometabolism), corresponding to their unique properties along the range of pro‐ versus anti‐inflammatory activity. In parallel, recent studies in mice revealed critical neuronal–macrophage interactions, both in the CNS and in peripheral tissues, including in white and brown AT. These intercellular activities impinge on energy and metabolic homeostasis, partially by also engaging adipocytes in a neuronal–macrophage–adipocyte ménage à trois. Finally, neuropeptides (NP), such as NPY and appetite‐reducing NPFF, may prove as mediators in such intercellular network. In this concise review, we highlight some of these recent insights on adipose macrophage immunometabolism, as well as central and peripheral neuronal–macrophage interactions with emphasis on their impact on adipocyte biology and whole‐body metabolism. We also discuss the expanding view on the role of the NP, NPY and NPFF, in obesity.