Bilateral, chronic, bacterial conjunctivitis in giant fornix syndrome

Giant fornix syndrome (GFS) results in chronic, relapsing conjunctivitis in elderly patients with enophthalmos and enlarged fornices, in which infectious material collects and perpetuates inflammation. A 98-year-old woman presented with persistent, bilateral, purulent conjunctivitis; corneal epithelial defects and progressive blepharospasm that did not respond to artificial tears, topical antibiotics and steroids and amniotic membrane grafts. Additional findings of deep-set orbits with enlarged upper fornices were diagnostic of GFS. Over the next 2 months, she responded to a combination of topical and systemic antibiotics, autologous serum eye drops, povidone-iodine forniceal rinses, and hypochlorous acid treatment of the eyelashes. GFS is an important diagnostic consideration in elderly patients with chronic conjunctivitis and deep-set orbits.

Fluorescent probe for the detection of hypochlorous acid in water samples and cell models

A new fluorescence probe was successfully applied to test strips and imaging analysis of exogenous and endogenous hypochlorite in living cells.

Antimicrobial Activity of Neutrophils Against Mycobacteria

The mycobacterium genus contains a broad range of species, including the human pathogens M. tuberculosis and M. leprae. These bacteria are best known for their residence inside host cells. Neutrophils are frequently observed at sites of mycobacterial infection, but their role in clearance is not well understood. In this review, we discuss how neutrophils attempt to control mycobacterial infections, either through the ingestion of bacteria into intracellular phagosomes, or the release of neutrophil extracellular traps (NETs). Despite their powerful antimicrobial activity, including the production of reactive oxidants such as hypochlorous acid, neutrophils appear ineffective in killing pathogenic mycobacteria. We explore mycobacterial resistance mechanisms, and how thwarting neutrophil action exacerbates disease pathology. A better understanding of how mycobacteria protect themselves from neutrophils will aid the development of novel strategies that facilitate bacterial clearance and limit host tissue damage.

Hypochlorite-Modified LDL Induces Arrhythmia and Contractile Dysfunction in Cardiomyocytes

Neutrophil-derived myeloperoxidase (MPO) and its potent oxidant, hypochlorous acid (HOCl), gained attention as important oxidative mediators in cardiac damage and dysfunction. As cardiomyocytes generate low-density lipoprotein (LDL)-like particles, we aimed to identify the footprints of proatherogenic HOCl-LDL, which adversely affects cellular signalling cascades in various cell types, in the human infarcted myocardium. We performed immunohistochemistry for MPO and HOCl-LDL in human myocardial tissue, investigated the impact of HOCl-LDL on electrophysiology and contractility in primary cardiomyocytes, and explored underlying mechanisms in HL-1 cardiomyocytes and human atrial appendages using immunoblot analysis, qPCR, and silencing experiments. HOCl-LDL reduced ICa,L and IK1, and increased INaL, leading to altered action potential characteristics and arrhythmic events including early- and delayed-afterdepolarizations. HOCl-LDL altered the expression and function of CaV1.2, RyR2, NCX1, and SERCA2a, resulting in impaired contractility and Ca2+ homeostasis. Elevated superoxide anion levels and oxidation of CaMKII were mediated via LOX-1 signaling in HL-1 cardiomyocytes. Furthermore, HOCl-LDL-mediated alterations of cardiac contractility and electrophysiology, including arrhythmic events, were ameliorated by the CaMKII inhibitor KN93 and the INaL blocker, ranolazine. This study provides an explanatory framework for the detrimental effects of HOCl-LDL compared to native LDL and cardiac remodeling in patients with high MPO levels during the progression of cardiovascular disease.

Comparisons of Non-thermal Decontamination Methods to Improve the Safety for Raw Beef Consumption

The object of this study was to examine non-thermal treatments to reduce foodborne pathogens in raw beef. Foodborne-illness pathogens were inoculated in the raw beef. Death rates of foodborne illness pathogens were evaluated by non-thermal decontamination methods(high pressure processing at 500MPa[HPP] for 2min, 5min, and 7min; UV LED radiation at 405nm[UV LED] for 2h, 6h, and 24h; hypochlorous acid water at 100ppm[HAW] for 1min, 3min, and 5min; 2.5% lactic acid[LA] for 1min, 3min, and 5min; modified atmosphere that replaced O2 to CO2 [MAP] for 24h and 48​​h; bio-gel[BG] application for 24h and 48h. Quality characteristics were measured after applying the practical non-thermal decontamination methods. After the treatment of HPP for 7min, inactivity rates were 4.4-6.7Log CFU/g for E. coli, Salmonella, and L. monocytogenes and 1.7Log CFU/g for S. aureus (p <0.05). After the treatment with UV LED for 24h, the reduced cell counts were 0.5, 0.7, and 0.3Log CFU/g for E. coli , Salmonella , and S. aureus, respectively(p <0.05), but no significant reduction for L. monocytogenes. When the beef was treated with HAW was treated for 5min, 0.6Log CFU/g of E. coli, 0.5Log CFU/g of Salmonella, 0.4Log CFU/g of S. aureus , and 0.5Log CFU/g of L. monocytogenes were inactivated. After the beef was treated with LA for 5min, 1.8Log CFU/g of E. coli, 3.0Log CFU/g of Salmonella, 1.3Log CFU/g of S. aureus, and 1.9Log CFU/g of L. monocytogenes were inactivated. MAP for 48h caused the inactivation of 0.3Log CFU/g of E. coli, 0.1Log CFU/g of Salmonella. After treatment of BG for 48h, 0.3Log CFU/g of E. coli and 0.4Log CFU/g of Salmonella were significantly decreased(p <0.05). HPP cooked the beef after 2min of treatment. HAW and BG changed the surface color of the beef, LA reduced the pH of beef (p<0.05). However, UV LED did not cause any changes in the beef quality properties. These results indicates that UV LED can improve the food safety of raw beef.

Chlorine and its importance in the inactivation of bacteria, can it inactivate viruses?

Sodium hypochlorite (NaClO) and its active ingredient, hypochlorous acid (HClO), are the most widely used chlorine-based disinfectants. HClO is a fast-acting antimicrobial that interacts with many biomolecules, including amino acids, lipids, nucleic acids, and sulfur containing membrane components, causing cell damage. In this review, we present examples of the effectiveness of chlorine in general disinfection procedures to inactivate bacteria and, under some conditions, bacteria in biofilms and viruses.

HprSR is a Reactive Chlorine Species-Sensing, Two-Component System in Escherichia coli

Two-component systems (TCS) are signalling pathways that allow bacterial cells to sense, respond and adapt to fluctuating environments. Among the classical TCS of Escherichia coli , HprSR has recently been shown to be involved in the regulation of msrPQ , which encodes the periplasmic methionine sulfoxide reductase system. In this study, we demonstrate that hypochlorous acid (HOCl) induces the expression of msrPQ in an HprSR-dependant manner, whereas H 2 O 2 , NO and paraquat (a superoxide generator) do not. Therefore, HprS appears to be an HOCl-sensing histidine kinase. Using a directed mutagenesis approach, we show that Met residues located in the periplasmic loop of HprS are important for its activity: as HOCl preferentially oxidizes Met residues, we provide evidence that HprS could be activated via the reversible oxidation of its methionine residues, meaning that MsrPQ plays a role in switching HprSR off. We propose that the activation of HprS by HOCl could occur through a Met redox switch. HprSR appears to be the first characterized TCS able to detect reactive chlorine species (RCS) in E. coli . This study represents an important step towards understanding the mechanisms of RCS resistance in prokaryotes. IMPORTANCE Understanding how bacteria respond to oxidative stress at the molecular level is crucial in the fight against pathogens. HOCl is one of the most potent industrial and physiological microbiocidal oxidants. Therefore bacteria have developed counterstrategies to survive HOCl-induced stress. Over the last decade, important insights into these bacterial protection factors have been obtained. Our work establishes HprSR as a reactive chlorine species-sensing, two-component system in Escherichia coli MG1655, which regulates the expression of MsrPQ, a repair system for HOCl-oxidized proteins. Moreover we provide evidence suggesting that HOCl could activate HprS through a methionine redox switch.