Antibacterial, Anti-Inflammatory, and Antioxidant Cotton-Based Wound Dressing Coated with Chitosan/Cyclodextrin-Quercetin Inclusion Complex Nanofibers.

Quercetin, recognized for its antioxidant, anti-inflammatory, and antibacterial properties, faces limited biomedical application due to its low solubility. Cotton, a preferred wound dressing material over synthetic ones, lacks inherent antibacterial and wound-healing attributes and can benefit from quercetin features. This study explores the potential of overcoming these challenges through the inclusion complexation of quercetin with cyclodextrins (CDs) and the development of a nanofibrous coating on a cotton nonwoven textile.

Functionalization of cotton nonwoven with cyclodextrin/lawsone inclusion complex nanofibrous coating for antibacterial wound dressing.

Functionalizing cotton to induce biological activity is a viable approach for developing wound dressing. This study explores the development of cotton-based wound dressing through coating with biologically active nanofibers. Bioactive compounds like lawsone offer dual benefits of wound healing and infection prevention, however, their limited solubility and viability hinder their applications.

Recombinant production of a diffusible signal factor inhibits invasion and animal carriage.

The complex chemical environment of the intestine is defined largely by the metabolic products of the resident microbiota. Enteric pathogens, elegantly evolved to thrive in the gut, use these chemical products as signals to recognize specific niches and to promote their survival and virulence. Our previous work has shown that a specific class of quorum-sensing molecules found within the gut, termed diffusible signal factors (DSF), signals the repression of tissue invasion, thus defining a means by which this pathogen recognizes its location and modulates virulence to optimize its survival.

Salmonella Invasion Is Controlled by Competition among Intestinal Chemical Signals.

The intestine is a complex, ever-changing environment replete with an array of signaling molecules. To colonize such a complex organ, pathogens have adapted to utilize specific cues from the local environment to intricately regulate the expression of their virulence determinants. Salmonella preferentially colonizes the distal ileum, a niche enriched in the metabolite formic acid.

Antibacterial nanofibers of pullulan/tetracycline-cyclodextrin inclusion complexes for Fast-Disintegrating oral drug delivery.

Tetracycline is a widely used antibiotic suffering from poor water solubility and low bioavailability. Here, hydroxypropyl-beta-cyclodextrin (HPβCD) was used to form inclusion complexes (IC) of tetracycline with 2:1 M ratio (CD:drug). Then, tetracycline-HPβCD-IC was mixed with pullulan- a non-toxic, water-soluble biopolymer - to form nanofibrous webs via electrospinning.

AraC-type regulators HilC and RtsA are directly controlled by an intestinal fatty acid to regulate Salmonella invasion.

Invasion of the intestinal epithelium is an essential but energetically expensive survival strategy and is, therefore, tightly regulated by using specific cues from the environment. The enteric pathogen Salmonella controls its invasion machinery through the elegant coordination of three AraC-type transcription activators, HilD, HilC, and RtsA. Most environmental signals target HilD to control invasion, whereas HilC and RtsA are known only to augment these effects on HilD.

A diffusible signal factor of the intestine dictates Salmonella invasion through its direct control of the virulence activator HilD.

Successful intestinal infection by Salmonella requires optimized invasion of the gut epithelium, a function that is energetically costly. Salmonella have therefore evolved to intricately regulate the expression of their virulence determinants by utilizing specific environmental cues. Here we show that a powerful repressor of Salmonella invasion, a cis-2 unsaturated long chain fatty acid, is present in the murine large intestine.

Salmonella invasion is controlled through the secondary structure of the hilD transcript.

Virulence functions of bacterial pathogens are often energetically costly and thus are subjected to intricate regulatory mechanisms. In Salmonella, invasion of the intestinal epithelium, an essential early step in virulence, requires the production of a multi-protein type III secretion apparatus. The pathogen mitigates the overall cost of invasion by inducing it in only a fraction of its population.

Salmonella Typhi outer membrane protein STIV is a potential candidate for vaccine development against typhoid and paratyphoid fever.

Enteric fever, caused by Salmonella enterica serovars, Typhi (S. Typhi) and Paratyphi (S. Paratyphi) is a major public health challenge for the developing nations.

Epithelial invasion by Salmonella Typhi using STIV-Met interaction.

Typhoid is a life-threatening febrile illness that affects ~24.2 million people worldwide and is caused by the intracellular bacteria Salmonella Typhi (S. Typhi).

Multivalent gold nanoparticle-peptide conjugates for targeting intracellular bacterial infections.

Although nanoparticle-tagged antimicrobal peptides have gained considerable importance in recent years, their structure-function correlation has not yet been explored. Here, we have studied the mechanism of action of a designed antimicrobial peptide, VG16KRKP (VARGWKRKCPLFGKGG), delivered via gold nanoparticle tagging against Salmonella infection by combining biological experiments with high- and low-resolution spectroscopic techniques. In comparison with the free VG16KRKP peptide or gold nanoparticle alone, the conjugated variant, Au-VG16KRKP, is non-cytotoxic to eukaryotic cells, but exhibits strong bacteriolytic activity in culture.

A recombinant protein of Salmonella Typhi induces humoral and cell-mediated immune responses including memory responses.

Gram negative enteric bacteria, Salmonella enterica serovar Typhi (S. Typhi), the etiological agent of typhoid fever is a major public health problem in developing countries. While a permanent solution to the problem would require improved sanitation, food and water hygiene, controlling the infection by vaccination is urgently required due to the emergence of multidrug resistant strains in multiple countries.

An AIL family protein promotes type three secretion system-1-independent invasion and pathogenesis of Salmonella enterica serovar Typhi.

Adhesion and invasion of Intestinal Epithelial Cells (IECs) are critical for the pathogenesis of Salmonella Typhi, the aetiological agent of human typhoid fever. While type three secretion system-1 (T3SS-1) is a major invasion apparatus of Salmonella, independent invasion mechanisms were described for non-typhoidal Salmonellae. Here, we show that T2942, an AIL-like protein of S.