Puthia M
Bioactive Suture with Added Innate Defense Functionality for the Reduction of Bacterial Infection and Inflammation.
Of more than 300 million surgical procedures performed worldwide annually,[1] almost 10% develop surgical site infections (SSIs).[2] SSIs account for a substantial clinical and economic burden.[3] Although many factors contribute to SSIs, preventive measures before, during, and after surgery can lower the SSI incidence.[4] Causes of SSIs vary depending on anatomy, surgical procedure, and exogenous in addition to endogenous, patient-derived factors. Bacterial contamination is one cause that can be controlled.[4, 5] In hospitals, preventive measures such as hygiene routines are implemented but even under sterile surgical conditions, infections may occur due to the spread of bacteria from the patient's own bacterial flora.[6] It has also been reported that up to 60% of the bacteria recovered from infected surgical wounds developed antibiotic resistance.[7]
ReadTargeting Toll-like receptor-driven systemic inflammation by engineering an innate structural fold into drugs.
There is a clinical need for conceptually new treatments that target the excessive activation of inflammatory pathways during systemic infection.
ReadObservation of multiple protein temperature transitions dependent upon the chemical environment
Surgical site infections (SSI) are a clinical and economic burden. Suture-associated SSI may develop when bacteria colonize the suture surface and form biofilms that are resistant to antibiotics.
ReadSARS-CoV-2 spike protein as a bacterial lipopolysaccharide delivery system in an overzealous inflammatory cascade
Keywords: COVID-19, SARS-CoV-2, spike protein, lipopolysaccharide, TLR4, hyperinflammation
ReadSARS-CoV-2 spike protein as a bacterial lipopolysaccharide delivery system in an overzealous inflammatory cascade
Pulmonary and systemic hyperinflammation are some of the prominent hallmarks of severe COVID-19 disease.
ReadAntibacterial and Anti-Inflammatory Effects of Apolipoprotein E
Keywords: apolipoprotein E; antimicrobial peptides; Gram-negative bacteria; host defense; innate immunity; aggregation
ReadSARS-CoV-2 Spike protein binds to bacterial lipopolysaccharide and boosts proinflammatory activity
There is a link between high lipopolysaccharide (LPS) levels in the blood and the metabolic syndrome, and metabolic syndrome predisposes patients to severe COVID-19. Here, we define an interaction between SARS-CoV-2 spike (S) protein and LPS, leading to aggravated inflammation *in vitro* and *in vivo*. Native gel electrophoresis demonstrated that SARS-CoV-2 S protein binds to LPS.
ReadThrombin-derived C-terminal fragments aggregate and scavenge bacteria and their proinflammatory products.
Thrombin-derived C-terminal peptides (TCPs), including a major 11-kDa fragment (TCP96), are produced through cleavage by human neutrophil elastase and aggregate lipopolysaccharide (LPS) and the Gram-negative bacterium Escherichia coli However, the physiological roles of TCP96 in controlling bacterial infections and reducing LPS-induced inflammation are unclear. Here, using various biophysical methods, in silico molecular modeling, microbiological and cellular assays, and animal models, we examined the structural features and functional roles of recombinant TCP96 (rTCP96) in the aggregation of multiple bacteria and the Toll-like receptor (TLR) agonists they produce.
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