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Insights into the pathogenesis of axial spondyloarthropathy based on gene expression profiles
Arthritis Research & Therapy, 11/10/09

Sharma MS et al. – Our observations are the first to implicate SPARC, SLPI, and NLRP2, a component of the innate immune system, in the pathogenesis of SpA. Our results also indicate a possible role for IL-1 and its receptors in SpA. In accord with the bone pathology component of SpA, we also found that expression levels of transcripts reflecting bone remodeling factors are also distinguishable in peripheral blood from patients with SpA versus controls. These results confirm some previously identified biomarkers implicated in the pathogenesis of SpA and also point to novel mediators in this disease.

Methods

High-density, human GeneChip(R) probe arrays (HG-U133 plus 2.0, Affymetrix, Inc.) used to profile mRNA of peripheral blood cells from 18 subjects with SpA
25 normal individuals
Samples processed as 2 separate sets at different times (11 SpA + 12 control subjects in primary set (Set 1); 7 SpA+ 13 control subjects in the validation set (Set 2))
Blood samples taken at time when patients not receiving systemic immunomodulatory therapy
Differential expression defined as a 1.5-fold change with q value < 5%
Gene ontology and pathway information also studied

Results

Signals from 134 probe sets (representing 95 known and 12 unknown gene transcripts) consistently different from controls in both Sets 1 and 2
Included among these were transcripts for group of 20 genes, such as interleukin-1 (IL-1) receptors 1 and 2, Nod-like receptor family, pyrin domain containing 2 (NLRP2), secretory leukocyte peptidase inhibitor (SLPI), secreted protein acidic and rich in cysteine (SPARC), and triggering receptor expressed on myeloid cells 1 (TREM-1) that are clearly related to immune or inflammatory response and group of 4 transcripts that have strong role in bone remodeling

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