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HLA-B27 does not affect invasion of arthritogenic bacteria into human cells

O Ortiz-Alvarez1, D T Yu, R E Petty

  • 1Department of Pediatrics, University of British Columbia, Vancouver, Canada.

The Journal of Rheumatology
|September 11, 1998
PubMed
Abstract

Insights

Human leukocyte antigen B27 (HLA-B27) expression does not affect the invasion of Salmonella typhimurium or Yersinia enterocolitica into human cells. This finding suggests HLA-B27 is not involved in reactive arthritis pathogenesis related to these bacteria.

Area of Science:

  • Immunogenetics
  • Microbiology
  • Cell Biology

Background:

  • Human leukocyte antigen B27 (HLA-B27) is associated with autoimmune diseases like reactive arthritis.
  • Reactive arthritis can be triggered by bacterial infections, including Salmonella and Yersinia.

Purpose of the Study:

  • To determine if HLA-B27 expression influences the entry of Salmonella typhimurium and Yersinia enterocolitica into human cells.
  • To investigate the role of HLA-B27 in the pathogenesis of reactive arthritis.

Main Methods:

  • Standard bacterial invasion assays were conducted using various human cell lines (HeLa, U937, C1R, Jurkat) and their HLA-B27 transfectants.
  • Invasion assays were also performed on peripheral blood cells (T lymphocytes, monocytes, B lymphocytes/dendritic cells) from healthy donors and patients with ankylosing spondylitis.
  • The percentage of internalized bacteria was quantified and compared between HLA-B27 positive and negative cells.

Main Results:

  • No statistically significant difference in the percentage of intracellular Salmonella typhimurium and Yersinia enterocolitica was observed between HLA-B27 positive and negative cells in cultured cell lines.
  • Similarly, bacterial internalization rates did not differ significantly between HLA-B27 positive and negative peripheral blood derived cells.

Conclusions:

  • The presence of HLA-B27 on human cells does not alter bacterial invasion.
  • HLA-B27 expression is unlikely to be a significant factor in the pathogenesis of reactive arthritis caused by Salmonella and Yersinia infections.

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