Dysregulation of SAA1, TUBA8 and Monocytes Are Key Factors in Ankylosing Spondylitis With Femoral Head Necrosis

Abstract

IntroductionThe mechanism of ankylosing spondylitis with femoral head necrosis is unknown, and our study aimed investigate the effects of genetic and immune cell dysregulation on ankylosing spondylitis.Materials and MethodsThe protein expression of all ligaments in ankylosing spondylitis with femoral head necrosis was obtained using label-free quantification protein park analysis of six pairs of specimens. The possible pathogenesis was explored using differential protein analysis, weighted gene co-expression network analysis, recording intersections with hypoxia-related genes, immune cell correlation analysis, and drug sensitivity analysis. Finally, routine blood test data from 502 AS and 162 healthy controls were collected to examine immune cell differential analysis.ResultsSAA1 and TUBA8 were significantly expressed differentially in these two groups and correlated quite strongly with macrophage M0 and resting mast cells (P < 0.05). Routine blood data showed that monocytes were significantly more expressed in AS than in healthy controls (P < 0.05). SAA1 and TUBA8 were closely related to the sensitivity of various drugs, which might lead to altered drug sensitivity.ConclusionDysregulation of SAA1, TUBA8 and monocytes are key factors in ankylosing spondylitis with femoral head necrosis.