Florin-Dan Popescu

Prof. Dr. Florin-Dan Popescu

orcid

Research Focus & Metrics

Academic Career Length

24Years (2003-Present)

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

Representative Publications

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1 January 2015 in World Journal of Methodology
Verified
Journal Article
Open access
FPFlorin-Dan Popescu
Florin-Dan Popescu
Cross-reactivity between aeroallergens and food allergens

Verified
Journal Article
Open access
PDF file
Sylwia Smolinska-WilczynskaSylwia Smolinska-Wilczynska
Sylwia Smolinska-Wilczynska
FPFlorin-Dan Popescu
Florin-Dan Popescu
Magdalena Zemelka-WiacekMagdalena Zemelka-Wiacek
Magdalena Zemelka-Wiacek
Objective: This review aims to comprehensively evaluate the current evidence on the role of prebiotics, probiotics, synbiotics, and postbiotics—collectively referred to as “biotics”—in modulating the human gut microbiota and enhancing intestinal epithelial integrity. Findings: Biotics exert their beneficial effects through several mechanisms, including by promoting the growth of beneficial microbes, producing short-chain fatty acids (SCFAs), strengthening the gut barrier, and regulating immune responses. Prebiotics selectively stimulate beneficial bacteria, probiotics introduce live microorganisms with therapeutic functions, synbiotics combine the strengths of both, and postbiotics offer non-viable microbial components and metabolites that mimic probiotic benefits with enhanced safety profiles. Each type of biotic demonstrates unique and complementary effects across a range of conditions, such as inflammatory bowel disease, irritable bowel syndrome, obesity, constipation, and antibiotic-associated diarrhea. Implications: As disruptions in the gut microbiota and intestinal barrier are increasingly linked to chronic and immune-mediated diseases, leveraging biotics offers promising avenues for personalized nutrition, preventive healthcare, and adjunct therapies. The integration of biotics into clinical and dietary strategies may significantly contribute to improving gastrointestinal and systemic health.

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Journal Article
Open access
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Sylwia Smolinska-WilczynskaSylwia Smolinska-Wilczynska
Sylwia Smolinska-Wilczynska
DADarío Antolín-Amérigo2
Darío Antolín-Amérigo2
FPFlorin-Dan Popescu
Florin-Dan Popescu
Marek JutelMarek Jutel
Marek Jutel
Thymic stromal lymphopoietin (TSLP) is a pleiotropic cytokine that has emerged as a critical player in the development and progression of allergy and asthma. It is primarily produced by epithelial cells and functions as a potent immune system activator. TSLP acts through interaction with its receptor complex, composed of the TSLP receptor (TSLPR) and interleukin-7 receptor alpha chain (IL-7Rα), activating downstream complex signalling pathways. The TSLP major isoform, known as long-form TSLP (lfTSLP), is upregulated in the airway epithelium of patients with allergic diseases. More research is warranted to explore the precise mechanisms by which short-form TSLP (sfTSLP) regulates immune responses. Understanding the dynamic interplay between TSLP and the dysfunctional epithelium provides insights into the mechanisms underlying allergy and asthma pathogenesis. Targeting TSLP represents an important therapeutic strategy, as it may upstream disrupt the inflammatory cascade and alleviate symptoms associated with allergic inflammation.

29 November 2018 in World Journal of Methodology
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Journal Article
Open access
FPFlorin-Dan Popescu
Florin-Dan Popescu
MVMariana Vieru
Mariana Vieru
Precision medicine allergy immunoassay methods for assessing immunoglobulin E sensitization to aeroallergen molecules

1 October 2005 in Journal of Cellular and Molecular Medicine
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FPFlorin-Dan Popescu
Florin-Dan Popescu

Verified
Journal Article
Open access
PDF file
Sylwia Smolinska-WilczynskaSylwia Smolinska-Wilczynska
Sylwia Smolinska-Wilczynska
DADarío Antolín-Amérigo2
Darío Antolín-Amérigo2
FPFlorin-Dan Popescu
Florin-Dan Popescu
Bradykinin (BK) metabolism and its receptors play a central role in drug-induced angioedema (AE) without urticaria through increased vascular permeability. Many cardiovascular and diabetic drugs may cause BK-mediated AE. Angiotensin-converting enzyme inhibitors (ACEIs) and neprilysin inhibitors impair BK catabolism. Dipeptidyl peptidase-IV (DPP-IV) inhibitors reduce the breakdown of BK and substance P (SP). Moreover, angiotensin receptor blockers, thrombolytic agents, and statins may also induce BK-mediated AE. Understanding pathophysiological mechanisms is crucial for preventing and treating drug-induced AE.