TY - JOUR
T1 - An inflammatory Signature of Glucose Impairment in Cystic Fibrosis
AU - Montemari, Anna Lisa
AU - Manco, Melania
AU - Fiocchi, Alessandro Giovanni
AU - Bartoli, Manuela
AU - Facchiano, Francesco
AU - Tabolacci, Claudio
AU - Scatigna, Maria
AU - Ciciriello, Fabiana
AU - Alghisi, Federico
AU - Montemitro, Enza
AU - Carsetti, Rita
AU - Lucidi, Vincenzina
AU - Fiscarelli, Ersilia Vita
N1 - Funding Information:
We are grateful to Dr Cinzia Leuter, Medicine and Surgery, Campus Bio-Medico, University of Rome, Italy for her advice. Claudio Tabolacci was supported by Fondazione Umberto Veronesi that is gratefully acknowledged. The technological support from the “Complex Protein Mixture (CPM) Analysis” Facility at the Dept. OMM, Istituto Superiore di Sanità, is kindly acknowledged. The authors acknowledge the patients for their enthusiastic participation and dedicate this work to Barbara Bartoli and all deceased patients of our CF center.
Funding Information:
This study was funded through RC 201802P004364.
Publisher Copyright:
© 2022 Montemari et al. This wterms.php and incorporate the Cr.
PY - 2022
Y1 - 2022
N2 - Objective and Design: Cystic fibrosis-related diabetes (CFRD) is a severe complication associated with increased morbidity and mortality in cystic fibrosis (CF) patients. Extensive inflammatory state in CF leads to pancreas damage and insulin resistance with consequent altered glucose tolerance and CFRD development. The aim of the present study was to identify circulating levels of inflammatory markers specifically associated with impaired glucose tolerance (IGT) and overt CFRD in a sample of young adults with CF. Materials and Methods: Sixty-four CF outpatients, without evident active pulmonary exacerbation, infectious and autoimmune diseases, were enrolled in the study and the levels of 45 inflammatory serum mediators were measured through x magnetic bead panel multiplex technology. Results: Serum levels of PDGF-AA, CCL20/MIP3α, IFNα, CCL11/eotaxin, CXCL1/GROα, GMCSF, B7H1/PDL1, IL13, IL7, VEGF, and TGFα were all significantly (p<0.05) elevated in patients according to glycemic status and directly correlated with glycated hemoglobin and C-reactive protein levels. Conclusion: Our findings suggest that increased levels of specific circulating inflammatory mediators are directly associated with impaired glucose tolerance in CF patients, thus, potentially implicating them in CFRD pathogenesis and warranting larger longitudinal studies to validate their monitoring as predictor of CFRD onset.
AB - Objective and Design: Cystic fibrosis-related diabetes (CFRD) is a severe complication associated with increased morbidity and mortality in cystic fibrosis (CF) patients. Extensive inflammatory state in CF leads to pancreas damage and insulin resistance with consequent altered glucose tolerance and CFRD development. The aim of the present study was to identify circulating levels of inflammatory markers specifically associated with impaired glucose tolerance (IGT) and overt CFRD in a sample of young adults with CF. Materials and Methods: Sixty-four CF outpatients, without evident active pulmonary exacerbation, infectious and autoimmune diseases, were enrolled in the study and the levels of 45 inflammatory serum mediators were measured through x magnetic bead panel multiplex technology. Results: Serum levels of PDGF-AA, CCL20/MIP3α, IFNα, CCL11/eotaxin, CXCL1/GROα, GMCSF, B7H1/PDL1, IL13, IL7, VEGF, and TGFα were all significantly (p<0.05) elevated in patients according to glycemic status and directly correlated with glycated hemoglobin and C-reactive protein levels. Conclusion: Our findings suggest that increased levels of specific circulating inflammatory mediators are directly associated with impaired glucose tolerance in CF patients, thus, potentially implicating them in CFRD pathogenesis and warranting larger longitudinal studies to validate their monitoring as predictor of CFRD onset.
KW - cystic fibrosis-related diabetes
KW - cytokines
KW - growth factors
KW - immune mediators
KW - impaired glucose tolerance
KW - inflammation
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U2 - 10.2147/JIR.S365772
DO - 10.2147/JIR.S365772
M3 - Article
AN - SCOPUS:85139484287
SN - 1178-7031
VL - 15
SP - 5677
EP - 5685
JO - Journal of Inflammation Research
JF - Journal of Inflammation Research
ER -