The expression of signal regulatory protein alpha (SIRPα) in periodontal cells and tissue

TL;DR

This study shows that SIRPα is expressed in periodontal cells and tissues, and its expression increases under inflammatory conditions in some cell types.

Contribution

The first demonstration of SIRPα expression in periodontal cells and tissues, including its regulation by inflammation.

Findings

SIRPα is expressed in periodontal cells including fibroblasts, osteoblasts, and keratinocytes.

Inflammatory cytokines increased SIRPα expression in fibroblasts and osteoblasts but not in keratinocytes or periodontal ligament cells.

SIRPα was detected in periodontitis tissues, particularly in infiltrating leukocytes.

Abstract

Signal regulatory protein alpha (SIRPα) is mainly expressed by cells of myeloid origin. This membrane glycoprotein is shown to be involved in regulation of different inflammatory conditions, such as colitis and arthritis. However, SIRPα has not been investigated in relationship to periodontitis, an inflammatory condition affecting the tooth supporting tissues. We aim to investigate if resident cells in the periodontium express SIRPα and whether a possible expression is affected by inflammatory conditions. Primary human keratinocytes, fibroblasts, periodontal ligament cells, and osteoblasts were cultured with or without the pro-inflammatory cytokines tumor necrosis factor alpha (TNF-α) or interleukin-1-beta (IL-1β). All different periodontal cell types showed a basal mRNA expression of SIRPα. Pro-inflammatory cytokines induced a 2–3-fold significant increase in SIRPα expression in both cultured human gingival fibroblasts and osteoblasts but neither in keratinocytes nor in periodontal ligament cells. Tissue sections from human gingival tissue biopsies were histochemically stained for SIRPα. Epithelial keratinocytes and gingival fibroblasts stained positive in sections from periodontally healthy as well as in sections from periodontitis. In periodontitis sections, infiltrating leukocytes stained positive for SIRPα. We highlight our finding that oral keratinocytes, gingival fibroblasts, and periodontal ligament cells do express SIRPα, as this has not been presented before. The fact that inflammatory stimulation of gingival fibroblasts increased the expression of SIRPα, while an increased expression by gingival fibroblasts in periodontitis tissue in situ could not be detected, is indeed contradictory.

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