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.
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.
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.