Adenosine generated via CD73 decreases IL-1β-induced CXCL8 in gingival fibroblasts

Dallin Montierth, niversity of the Pacific Arthur A. Dugoni School of Dentistry
McKay Blatter, niversity of the Pacific Arthur A. Dugoni School of Dentistry
Ana Carolina Morandini, University of the Pacific Arthur A. Dugoni School of Dentistry
Erivan S. Ramos-Junior, University of the Pacific Arthur A. Dugoni School of Dentistry

This work was supported by Research Enhancement Award to ACM [Award 03-Activity 117] from the Arthur A. Dugoni School of Dentistry.

Introduction/Context/Diagnosis

BACKGROUND: IL-8 is a chemokine that is produced by most immune cells and is encoded by the CXCL8 gene in humans. It is an important mediator of inflammation being chemotactic for neutrophils. Adenosine tri-phosphate (ATP) is also strongly involved in inflammation not only by acting on cells of the immune system but also by exerting its activity on stromal cells of the gingival microenvironment. During inflammation stressed cells can release ATP to the extracellular medium which can be hydrolyzed to adenosine by the action of CD39 and CD73. Here, we show the effects of IL-1β stimulation on CXCL-8 secretion by primary gingival fibroblasts and the involvement of CD73-generated adenosine in this process.

 

Adenosine generated via CD73 decreases IL-1β-induced CXCL8 in gingival fibroblasts

BACKGROUND: IL-8 is a chemokine that is produced by most immune cells and is encoded by the CXCL8 gene in humans. It is an important mediator of inflammation being chemotactic for neutrophils. Adenosine tri-phosphate (ATP) is also strongly involved in inflammation not only by acting on cells of the immune system but also by exerting its activity on stromal cells of the gingival microenvironment. During inflammation stressed cells can release ATP to the extracellular medium which can be hydrolyzed to adenosine by the action of CD39 and CD73. Here, we show the effects of IL-1β stimulation on CXCL-8 secretion by primary gingival fibroblasts and the involvement of CD73-generated adenosine in this process.