Inhibition of LPS-Induced Inflammatory Response of Oral Mesenchymal Stem Cells in the Presence of Galectin-3
Alessia Paganelli,
Francesca Diomede,
Guya Diletta Marconi,
Jacopo Pizzicannella,
Thangavelu Soundara Rajan,
Oriana Trubiani,
Roberto Paganelli
Affiliations
Alessia Paganelli
PhD Course in Clinical and Experimental Medicine, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, 41124 Modena, Italy
Francesca Diomede
Department of Innovative Technologies in Medicine and Dentistry, University “G. d’Annunzio” Chieti-Pescara, 66100 Chieti, Italy
Guya Diletta Marconi
Department of Innovative Technologies in Medicine and Dentistry, University “G. d’Annunzio” Chieti-Pescara, 66100 Chieti, Italy
Jacopo Pizzicannella
Department of Engineering and Geology, University “G. d’Annunzio” Chieti-Pescara, Viale Pindaro, 42, 65127 Pescara, Italy
Thangavelu Soundara Rajan
Research and Development Unit, Theertha Biopharma Private Limited, KIADB, Industrial Area, Bommasandra, Jigani Link Road, Bangalore 560105, India
Oriana Trubiani
Department of Innovative Technologies in Medicine and Dentistry, University “G. d’Annunzio” Chieti-Pescara, 66100 Chieti, Italy
Roberto Paganelli
Saint Camillus International University of Health and Medical Sciences (UniCamillus), 00131 Rome, Italy
Galectin-3 (GAL-3) is a beta-galactoside binding lectin produced by mesenchymal stem cells (MSCs) and other cell sources under inflammatory conditions. Several studies have reported that GAL-3 exerts an anti-inflammatory action, regulated by its natural ligand GAL-3 BP. In the present study, we aimed to assess the GAL-3 mediated regulation of the MSC function in an LPS-induced inflammation setting. Human gingival mesenchymal stem cells (hGMSCs) were stimulated in vitro with LPSs; the expression of TLR4, NFκB p65, MyD88 and NALP3 were assessed in the hGMSCs via immunofluorescence imaging using confocal microscopy, Western blot assay, and RT-PCR before and after the addition of GAL-3, both alone and with the addition of its inhibitors. LPSs stimulated the expression of TLR4, NFκB p65, MyD88 and NALP3 in hGMSCs, which was inhibited by GAL-3. The addition of either GAL3-BP or the antibody to GAL-3 were able to revert the GAL-3-mediated effects, restoring the expression of TLR4, NFκB p65, MyD88 and NALP3. GAL-3 induces the downregulation of the LPS-induced inflammatory program in MSCs.
