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.
Highlights
The 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
Ankylosing spondylitis (AS) has a strong genetic predisposition and the lack of efficacy of monoclonal antibodies against different cytokines, highlighting the diversity of type 17 cytokines and immune cells, which is critical to the pathogenesis of spondyloarthritis and AS [3]
Inclusion criteria for this study were as follows: individuals with AS combined with femoral head necrosis were categorized into the experimental group, and those only with femoral head necrosis were categorized into the control group
Summary
The 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. The main characteristic change is sacroiliac arthritis, and the disease occurrence is inextricably linked to genetics [1, 2]. In AS, the SAA1, TUBA8 in Ankylosing Spondylitis damage to structures due to ankylosing changes and spine tonicity is irreversible [4]. A common clinical disease with a high disability rate, is caused by factors such as excessive alcohol consumption and the heavy use of short-term high-dose glucocorticoids [5]. The potential diagnostic biomarkers for AS combined with osteonecrosis of the femur, a disease that has a significant impact on the quality of life of patients, remain largely unknown
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