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

Front Immunol. 2022 Jan 18:12:814278. doi: 10.3389/fimmu.2021.814278. eCollection 2021.

Abstract

Introduction: 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.

Materials and methods: The 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.

Results: SAA1 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.

Conclusion: Dysregulation of SAA1, TUBA8 and monocytes are key factors in ankylosing spondylitis with femoral head necrosis.

Keywords: ankylosing spondylitis; drug sensitivity analysis; femoral head necrosis; immune cell composition analysis; immune cell infiltration; protein park analysis; routine blood tests; weighted gene co-expression network analysis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Computational Biology / methods
  • Disease Susceptibility
  • Femur Head Necrosis / diagnosis
  • Femur Head Necrosis / etiology*
  • Femur Head Necrosis / metabolism*
  • Gene Expression Profiling
  • Gene Expression Regulation
  • Gene Regulatory Networks
  • Humans
  • Monocytes / immunology*
  • Monocytes / metabolism*
  • Protein Interaction Mapping
  • Protein Interaction Maps
  • Serum Amyloid A Protein / genetics*
  • Spondylitis, Ankylosing / complications*
  • Spondylitis, Ankylosing / diagnosis
  • Spondylitis, Ankylosing / etiology*
  • Tubulin / genetics*

Substances

  • SAA1 protein, human
  • Serum Amyloid A Protein
  • TUBA8 protein, human
  • Tubulin