Lidia La Barbera

Dr. Lidia La Barbera


Research Focus & Metrics

Academic Career Length

5Years (2022-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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28 January 2022 in Cells
Verified
Journal Article
Open access
PDF file
Bartolo TamburiniBartolo Tamburini
Bartolo Tamburini
MMMarco Pio La Manna
Marco Pio La Manna
LBLidia La Barbera
Lidia La Barbera
Leila MohammadnezhadLeila Mohammadnezhad
Leila Mohammadnezhad
GBGiusto Davide Badami
Giusto Davide Badami
NCNadia Caccamo
Nadia Caccamo
Inflammatory bowel disease (IBD) is an increasingly urgent medical problem that strongly impairs quality of life for patients. A global rise in incidence has been observed over the last few decades, with the highest incidence rates recorded in North America and Europe. Still, an increased incidence has been reported in the last ten years in newly industrialized countries in Asia, including China and India, both with more than one billion inhabitants. These data underline that IBD is an urgent global health problem. In addition, it is estimated that between 20% and 30% of IBD patients will develop colorectal cancer (CRC) within their lifetime and CRC mortality is approximately 50% amongst IBD patients. Although the exact etiology of IBD is still being defined, it is thought to be due to a complex interaction between many factors, including defects in the innate and adaptive immune system; microbial dysbiosis, i.e., abnormal levels of, or abnormal response to, the gastrointestinal microbiome; a genetic predisposition; and several environmental factors. At present, however, it is not fully understood which of these factors are the initiators of inflammation and which are compounders. The purpose of this review is to analyze the complex balance that exists between these elements to maintain intestinal homeostasis and prevent IBD or limit adverse effects on people’s health.

31 January 2025 in Antioxidants
Verified
Journal Article
Open access
PDF file
Bartolo TamburiniBartolo Tamburini
Bartolo Tamburini
Diana Di LibertoDiana Di Liberto
Diana Di Liberto
Giovanni PratelliGiovanni Pratelli
Giovanni Pratelli
CRChiara Rizzo
Chiara Rizzo
LBLidia La Barbera
Lidia La Barbera
Giuliana GugginoGiuliana Guggino
Giuliana Guggino
Rheumatoid arthritis (RA) is a long-term systemic autoimmune disorder that causes joint inflammation, swelling, pain, bone erosion, and deformities. Recent findings emphasize the anti-inflammatory and antioxidant properties of bioactive natural compounds, such as polyphenols extracted from plants and fruits, and their possible synergistic effect when used in combination with current therapies to improve the prognosis and symptoms of inflammatory rheumatic diseases. Here, we report that Sicilian extra virgin olive oil polyphenol-enriched extracts (PE-EVOOs) reduce intracellular reactive oxygen species (ROS) and pro-inflammatory cytokines, such as tumor necrosis factor-α (TNF-α) and interleukin-1 β (IL-1β), in peripheral mononuclear cells (PBMCs) obtained from both RA patients and healthy subjects (HSs) treated with lipopolysaccharides (LPS) as a control. HPLC-ESI-MS analysis highlighted that PE-EVOOs are rich in different polyphenolic compounds responsible for many of the observed biological effects. At molecular levels, Western blotting analyses revealed that PE-EVOO treatment is associated with the downregulation of the phosphorylated and active form of the inflammatory transcription factor NF-κB and the pro-inflammatory enzyme cyclooxygenase 2 (COX2). In addition, PE-EVOOs upregulated the transcription factor Nrf2 and its target antioxidant enzyme catalase and manganese superoxide dismutase (MnSOD). Collectively, these results suggest a possible use of PE-EVOOs as potential adjuvants for the treatment of RA.

8 October 2025 in Nutrients
Verified
Journal Article
Open access
PDF file
ASAurelio Seidita
Aurelio Seidita
PMPasquale Mansueto
Pasquale Mansueto
MSMaurizio Soresi
Maurizio Soresi
Diana Di LibertoDiana Di Liberto
Diana Di Liberto
GCGabriele De Carlo
Gabriele De Carlo
ACAntonio Carroccio
Antonio Carroccio
Background: Wheat or cow’s milk intake might influence the primary Sjögren’s Syndrome (pSS) clinical manifestations. A high prevalence (20–30%) of autoimmune diseases, including pSS, has been reported in non-celiac wheat sensitivity (NCWS). This study aimed to identify the prevalence of self-reported NCWS and sensitivity/intolerance to other foods in patients with pSS, and to establish the specific clinical and immunological features of this subgroup of patients. Methods: 82 prospectively enrolled pSS patients were compared to 161 type 2 diabetes controls without rheumatological disease. The presence of a self-reported NCWS, and/or self-reported milk intolerance (SRMI), and/or multiple food sensitivity (MFS) was assessed by a validated questionnaire. Clinical and immunological features of pSS subjects, stratified according to the presence/absence of self-reported NCWS, were analyzed. Results: pSS patients had a higher frequency of self-reported NCWS (47.6% vs. 18.6%, p < 0.0001), SRMI (29.3% vs. 5.6%, p < 0.0001) and MFS (30.5% vs. 9.3% p < 0.0003) compared to controls. After the intake of wheat-containing products, 18 (21.9%) pSS patients reported the worsening of disease-specific symptoms, whereas 11 (13.4%) reported a significative clinical improvement after wheat-free diet (WFD) introduction. Moreover, 47.6% of pSS subjects complained of wheat-related gastrointestinal/extraintestinal disorders. No clinical/immunological feature differentiates pSS patients with and without self-reported NCWS, excluding a higher frequency of SRMI (39.5% vs. 11.9%, p = 0.01) and MFS (65.7% vs. 23.8%; p = 0.0004) in the former. Conclusions: This study shows a clear association between pSS and NCWS, confirming that wheat intake could be a common trigger of symptoms of both these conditions. WFD adoption seems to reduce both gastrointestinal/extraintestinal and pSS-specific symptoms in a subgroup of pSS patients, opening new possibilities for their clinical management.