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1. Maladaptive Autophagy in the Pathogenesis of Autoimmune Epithelitis in Sjögren's Syndrome.

Author

Colafrancesco, Serena, Barbati, Cristiana, Priori, Roberta, Putro, Erisa, Giardina, Federico, Gattamelata, Angelica, Monosi, Benedetta, Colasanti, Tania, Celia, Alessandra Ida, Cerbelli, Bruna, Giordano, Carla, Scarpa, Susanna, Fusconi, Massimo, Cavalli, Giulio, Berardicurti, Onorina, Gandolfo, Saviana, Nayar, Saba, Barone, Francesca, Giacomelli, Roberto, and De Vita, Salvatore

Subjects
FLOW cytometry, IN vitro studies, LYSOSOMES, MONONUCLEAR leukocytes, AUTOPHAGY, APOPTOSIS, IMMUNOBLOTTING, FLUORESCENT antibody technique, IMMUNOGLOBULIN light chains, CELL adhesion molecules, HISTOLOGICAL techniques, DESCRIPTIVE statistics, SURVIVAL analysis (Biometry), SJOGREN'S syndrome, EPITHELIAL cells, SALIVARY glands, MEMBRANE proteins, CASPASES
Abstract

Objective: Salivary gland epithelial cells (SGECs) are key cellular drivers in the pathogenesis of primary Sjögren's syndrome (SS); however, the mechanisms sustaining SGEC activation in primary SS remain unclear. We undertook this study to determine the role of autophagy in the survival and activation of SGECs in primary SS. Methods: Primary SGECs isolated from the minor SGs of patients with primary SS or sicca syndrome were evaluated by flow cytometry, immunoblotting, and immunofluorescence to assess autophagy (autophagic flux, light chain 3 IIB [LC3‐IIB], p62, LC3‐IIB+/lysosome‐associated membrane protein 1 [LAMP‐1] staining), apoptosis (annexin V/propidium iodide [PI], caspase 3), and activation (intercellular adhesion molecule, vascular cell adhesion molecule). Focus score and germinal center presence were assessed in the SGs from the same patients to assess correlation with histologic severity. Human SG (HSG) cells were stimulated in vitro with peripheral blood mononuclear cells (PBMCs) and serum from primary SS patients in the presence or absence of autophagy inhibitors to determine changes in autophagy and epithelial cell activation. Results: SGECs from primary SS patients (n = 24) exhibited increased autophagy (autophagic flux [P = 0.001]; LC3‐IIB [P = 0.02]; p62 [P = 0.064]; and as indicated by LC3‐IIB/LAMP‐1+ staining), increased expression of antiapoptotic molecules (Bcl‐2 [P = 0.006]), and reduced apoptosis (annexin V/PI [P = 0.002]; caspase 3 [P = 0.057]), compared to samples from patients with sicca syndrome (n = 16). Autophagy correlated with histologic disease severity. In vitro experiments on HSG cells stimulated with serum and PBMCs from primary SS patients confirmed activation of autophagy and expression of adhesion molecules, which was reverted upon pharmacologic inhibition of autophagy. Conclusion: In primary SS SGECs, inflammation induces autophagy and prosurvival mechanisms, which promote SGEC activation and mirror histologic severity. These findings indicate that autophagy is a central contributor to the pathogenesis of primary SS and a new therapeutic target. [ABSTRACT FROM AUTHOR]

Published
2022
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2. Maladaptive autophagy in the pathogenesis of autoimmune epithelitis in Sjögren's syndrome

Author

Angelica Gattamelata, Massimo Fusconi, Serena Colafrancesco, Bruna Cerbelli, B Monosi, Tania Colasanti, F. Giardina, Francesca Barone, Giulio Cavalli, Saba Nayar, Alessandra Ida Celia, Roberta Priori, Cristiana Barbati, S. De Vita, S. Gandolfo, Cesare Alessandri, Cesare Giordano, Roberto Giacomelli, Fabrizio Conti, S Scarpa, Onorina Berardicurti, E. Putro, Colafrancesco, Serena, Barbati, Cristiana, Priori, Roberta, Putro, Erisa, Giardina, Federico, Gattamelata, Angelica, Monosi, Benedetta, Colasanti, Tania, Celia, Alessandra Ida, Cerbelli, Bruna, Giordano, Carla, Scarpa, Susanna, Fusconi, Massimo, Cavalli, Giulio, Berardicurti, Onorina, Gandolfo, Saviana, Nayar, Saba, Barone, Francesca, Giacomelli, Roberto, De Vita, Salvatore, Alessandri, Cristiano, and Conti, Fabrizio

Subjects
autophagy, sjögren's syndrome, epithelium, salivary gland epithelial cells (SGECs), Immunology, Inflammation, Pathogenesis, stomatognathic system, Rheumatology, Annexin, Sicca syndrome, medicine, Humans, Immunology and Allergy, Annexin A5, Caspase 3, business.industry, Cell adhesion molecule, Autophagy, Germinal center, stomatognathic diseases, Sjogren's Syndrome, Apoptosis, Leukocytes, Mononuclear, Cancer research, medicine.symptom, business, Cell Adhesion Molecules, Transcription Factors
Abstract

Objective: Salivary gland epithelial cells (SGECs) are key cellular drivers in the pathogenesis of primary Sjögren's syndrome (SS); however, the mechanisms sustaining SGEC activation in primary SS remain unclear. We undertook this study to determine the role of autophagy in the survival and activation of SGECs in primary SS. Methods: Primary SGECs isolated from the minor SGs of patients with primary SS or sicca syndrome were evaluated by flow cytometry, immunoblotting, and immunofluorescence to assess autophagy (autophagic flux, light chain 3 IIB [LC3-IIB], p62, LC3-IIB+/lysosome-associated membrane protein 1 [LAMP-1] staining), apoptosis (annexin V/propidium iodide [PI], caspase 3), and activation (intercellular adhesion molecule, vascular cell adhesion molecule). Focus score and germinal center presence were assessed in the SGs from the same patients to assess correlation with histologic severity. Human SG (HSG) cells were stimulated in vitro with peripheral blood mononuclear cells (PBMCs) and serum from primary SS patients in the presence or absence of autophagy inhibitors to determine changes in autophagy and epithelial cell activation. Results: SGECs from primary SS patients (n=24) exhibited increased autophagy (autophagic flux [P=0.001]; LC3-IIB [P=0.02]; p62 [P=0.064]; and as indicated by LC3-IIB/LAMP-1+ staining), increased expression of antiapoptotic molecules (Bcl-2 [P=0.006]), and reduced apoptosis (annexin V/PI [P=0.002]; caspase 3 [P=0.057]), compared to samples from patients with sicca syndrome (n=16). Autophagy correlated with histologic disease severity. In vitro experiments on HSG cells stimulated with serum and PBMCs from primary SS patients confirmed activation of autophagy and expression of adhesion molecules, which was reverted upon pharmacologic inhibition of autophagy. Conclusion: In primary SS SGECs, inflammation induces autophagy and prosurvival mechanisms, which promote SGEC activation and mirror histologic severity. These findings indicate that autophagy is a central contributor to the pathogenesis of primary SS and a new therapeutic target.

Published
2021

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