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:Supramolecular self-assembly (SA) is a naturally occurring and free energy-driven process of molecules to produce nanostructured systems depending on the assembling environment. SA molecules have captivated the research attention since they possess singular physicochemical properties that are potentially useful to make the nanostructures quite suitable for biomedical applications, such as diagnostics, drug delivery, tissue engineering, and regenerative medicine. Due to their high biological activity and low toxicity, the self-assembly properties of peptides bid certain advantages as drugs and drug delivery platforms. Among the discovered self-assembling bioactive peptides (SAPs), antimicrobial peptides (AMPs) are widely distributed through plant and animal kingdoms and play a key role as an alternative strategy to fight infections bypassing conventional antimicrobial drugs, susceptible to antimicrobial resistance. Based on this evidence, in this review, we summarized the mechanism of the self-assembling of peptides, the main forces responsible for the SAPs formation, and the studies regarding their possible implication in infectious diseases as well as wound dressing materials.

2024-04-01·Letters in Drug Design & Discovery

Aptamers-based Strategies for the Treatment of Microbial Infections

作者: Marinelli, Lisa ; Cacciatore, Ivana ; Vicaretti, Giuseppina ; Di Stefano, Antonio ; Di Rienzo, Annalisa

Background:Nowadays, infectious diseases caused by bacteria are one of the major risks for the human population worldwide. Antimicrobial resistance determined the necessity to develop both, new drugs and therapeutic approaches as alternatives to antibiotics and novel methods to detect bacteria. Aptamers have revealed their potential in combating antimicrobial infections. Aptamers are small singlestranded DNA or RNA oligonucleotides obtained through an in vitro process able to bind several targets with high affinity and specificity.Objective:The aim of this review is to provide an overview of the state of the art of aptamer-based antimicrobial therapeutic strategies, new methods of detection of bacteria, and their potential use as delivery systems.Conclusion:Recent applications on research about aptamers suggest their important potential in discovering novel pharmacological tools for the treatment of microbial infections.

2023-09-01·Biomedicine & Pharmacotherapy

The immune activity of selective estrogen receptor modulators is gene and macrophage subtype-specific yet converges on Il1b downregulation

Article

作者: Allegretti, Marcello ; Locati, Massimo ; Cesta, Candida Maria ; Sfogliarini, Chiara ; Pepe, Giovanna ; Vegeto, Elisabetta

Raloxifene belongs to the family of Selective Estrogen Receptor Modulators (SERMs), which are drugs widely prescribed for Estrogen Receptor alpha (ERα)-related pathologies. Recently, SERMs are being tested in repurposing strategies for ERα-independent clinical indications, including a wide range of microbial infections. Macrophages are central in the fight against pathogen invasion. Despite estrogens have been shown to regulate macrophage phenotype, SERMs activity in these cells is still poorly defined. We investigated the activity of Raloxifene in comparison with another widely used SERM, Tamoxifen, on immune gene expression in macrophages obtained from mouse and human tissues, including mouse peritoneal macrophages, bone marrow-derived macrophages, microglia or human blood-derived macrophages, assaying for the involvement of the ERα, PI3K and NRF2 pathways also under inflammatory conditions. Our data demonstrate that Raloxifene acts by a dual mechanism, which entails ERα antagonism and off-target mediators. Moreover, micromolar concentrations of Raloxifene increase the expression of immune metabolic genes, such as Vegfa and Hmox1, through PI3K and NRF2 activation selectively in peritoneal macrophages. Conversely, Il1b mRNA down-regulation by SERMs is consistently observed in all macrophage subtypes and unrelated to the PI3K/NRF2 system. Importantly, the production of the inflammatory cytokine TNFα induced by the bacterial endotoxin, LPS, is potentiated by SERMs and paralleled by the cell subtype-specific increase in IL1β secretion. This work extends our knowledge on the biological and molecular mechanisms of SERMs immune activity and indicate macrophages as a pharmacological target for the exploitation of the antimicrobial potential of these drugs.

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