Antimicrobial properties of nitric oxide and its application in antimicrobial formulations and medical devices

Jones, Mitchell L.; Ganopolsky, Jorge G.; Labbé, Alain; Wahl, Christopher J.; Prakash, Satya

doi:10.1007/s00253-010-2733-x

Cited by 172 publications

(133 citation statements)

References 42 publications

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“…Surprisingly, TCC-treated ms, instead of switching to a glycolytic pathway for energy demand, consumed more oxygen and exhibited heightened oxidative metabolism at 3 h pi and then produced higher levels of ·NO than SYL-infected ms. These results suggest that ·NO may contribute to T. cruzi killing as multiple reactive nitrogen species (RNS) (40). High oxygen consumption has been described to correlate with increased ROS levels in neutrophils and PBMCs activated with diverse stimuli (41,42) and with L-arginine supplementation for endothelial NOS activity (43).…”

Section: Discussionmentioning

confidence: 94%

Macrophages Promote Oxidative Metabolism To Drive Nitric Oxide Generation in Response to Trypanosoma cruzi

et al. 2016

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dTrypanosoma cruzi is the causative agent of chronic chagasic cardiomyopathy. Why macrophages (ms), the early responders to infection, fail to achieve parasite clearance is not known. Mouse (RAW 264.7) and human (THP-1 and primary) ms were infected for 3 h and 18 h with T. cruzi TcI isolates, SylvioX10/4 (SYL, virulent) and TCC (nonpathogenic), which represent m stimulation and infection states, respectively. Ms incubated with lipopolysaccharide and gamma interferon (LPS/IFN-␥) and with interleukin-4 (IL-4) were used as controls. We monitored the cytokine profile (using enzyme-linked immunosorbent assay [ELISA]), reactive oxygen species (ROS; fluorescent probes), nitric oxide (·NO; Griess assay), and metabolic state using a customdesigned mitoxosome array and Seahorse XF24 Analyzer. LPS/IFN-␥ treatment of ms elicited a potent increase in production of tumor necrosis alpha (TNF-␣) at 3 h and of ROS and ·NO by 18 h. Upon SYL infection, murine ms elicited an inflammatory cytokine profile (TNF-␣ > > TGF-␤ ؉ IL-10) and low levels of ·NO and ROS production. LPS/IFN-␥ treatment resulted in the inhibition of oxidative metabolism at the gene expression and functional levels and a switch to the glycolytic pathway in ms, while IL-4-treated ms utilized oxidative metabolism to meet energy demands. SYL infection resulted in an intermediate functional metabolic state with increased mitoxosome gene expression and glycolysis, and IFN-␥ addition shut down the oxidative metabolism in SYL-infected ms. Further, TCC-and SYL-stimulated ms exhibited similar levels of cell proliferation and production of TNF-␣ and ROS, while TCC-stimulated ms exhibited up to 2-fold-higher levels of oxidative metabolism and ·NO production than SYL-infected ms. Inhibiting ATP-coupled O 2 consumption suppressed the ·NO generation in SYL-infected ms. Mitochondrial oxygen consumption constitutes a mechanism for stimulating ·NO production in ms during T. cruzi infection. Enhancing the oxidative metabolism provides an opportunity for increased ·NO production and pathogen clearance by ms to limit disease progression. Chagas cardiomyopathy is a neglected debilitating disease caused by the blood-borne parasite Trypanosoma cruzi. T. cruzi isolates are classified within six genetic groups (TcI to TcVI) which give insight into the evolution of the parasite (1). The virulent T. cruzi strain SylvioX10/4 (SYL) (2) and the nonpathogenic T. cruzi isolate (TCC) (3) are both of the TcI lineage which is considered to be the most common cause of disease in the Southern zone countries of South America, Central America, and Mexico. In mice and rats, SYL elicits acute parasitemia and persistent inflammatory infiltrate and injury in the myocardium and skeletal muscle during the chronic disease phase (4), while infection with the TCC isolate results in no detectable parasitemia or tissue injury (5).Macrophages (ms) serve as the first responders to T. cruzi infection, and their inflammatory activation exerts cytotoxic effects via NADPH oxidase (NOX)-mediated superoxide (O 2 · Ϫ ) ...

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Section: Discussionmentioning

confidence: 94%

Macrophages Promote Oxidative Metabolism To Drive Nitric Oxide Generation in Response to Trypanosoma cruzi

et al. 2016

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“…It is well known that NO reacts with oxygen and superoxide to form highly reactive intermediates that facilitate bacterial killing through oxidative and nitrosative stresses (19,49). As oxygen plays an integral role in the antibacterial action of NO, anaerobic environments may reduce the biocidal efficacy of NO (20,50).…”

Section: Discussionmentioning

confidence: 99%

Antibacterial Action of Nitric Oxide-Releasing Chitosan Oligosaccharides against Pseudomonas aeruginosa under Aerobic and Anaerobic Conditions

Reighard

2015

Antimicrob Agents Chemother

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Chitosan oligosaccharides were modified with N-diazeniumdiolates to yield biocompatible nitric oxide (NO) donor scaffolds. The minimum bactericidal concentrations and MICs of the NO donors against Pseudomonas aeruginosa were compared under aerobic and anaerobic conditions. Differential antibacterial activities were primarily the result of NO scavenging by oxygen under aerobic environments and not changes in bacterial physiology. Bacterial killing was also tested against nonmucoid and mucoid biofilms and compared to that of tobramycin. Smaller NO payloads were required to eradicate P. aeruginosa biofilms under anaerobic versus aerobic conditions. Under oxygen-free environments, the NO treatment was 10-fold more effective at killing biofilms than tobramycin. These results demonstrate the potential utility of NO-releasing chitosan oligosaccharides under both aerobic and anaerobic environments. Pseudomonas aeruginosa is an opportunistic human pathogen that frequently colonizes people with compromised immune systems, such as those with cystic fibrosis (CF) or severe burn wounds (1). The success of P. aeruginosa as a pathogen is related to its multitude of virulence factors, which increase adherence to the host cells, induce inflammation, and disrupt the host immune response (1). Furthermore, P. aeruginosa is intrinsically resistant to many antibiotics due to low membrane permeability and increased expression of ␤-lactamases and efflux pumps (2-4). In addition to this native resistance, P. aeruginosa readily adapts to antibiotic challenge by acquiring resistance genes (3, 5) and forming protective, cooperative communities known as biofilms (6, 7).While all antibiotic resistance mechanisms are not fully understood, at least three main factors reduce antibiotic efficacy against bacterial biofilms compared to planktonic cells. First, P. aeruginosa in biofilms secretes a protective layer of exopolysaccharides that prevent the diffusion of antibiotics (7). In the context of cystic fibrosis, biofilm-bound P. aeruginosa exists predominantly as the mucoid phenotype, characterized by a secreted alginate matrix that provides a physical barrier against the host immune response and antibiotics (8). This exopolysaccharide matrix also prevents the diffusion of oxygen into biofilms, causing P. aeruginosa to switch from aerobic to anaerobic respiration (9). The reduced metabolic activity of P. aeruginosa undergoing anaerobic respiration protects the bacterium against traditional antibiotics that are most effective against rapidly dividing cells, including aminoglycosides and ␤-lactams (10, 11). Finally, biofilms produce persister cells (i.e., dormant bacteria that are highly resistant to chemical disinfectants and exhibit multidrug tolerance) much more frequently than planktonic bacterial cultures (3, 7).The failure of conventional antibiotics to treat P. aeruginosa biofilms and infections necessitates the development of new antibacterial agents. Nitric oxide (NO), an endogenously produced free radical that can disperse (12, 13) and ...

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“…Paradoxically, it is not uncommon for tumor cells to constitutively express NO, aiding in tumor growth by increasing neovascularization and upregulating the production of DNA dependent protein kinases (DNA-PKcs), which are required for DNA repair [5,26,27]. In addition to antitumor effects, NO has been shown to display significant antimicrobial properties and its expression by immune and epithelial cells has been shown to decrease replication and kill infectious agents [5,28].…”

Section: Introductionmentioning

confidence: 99%

Nitric Oxide Sensors for Biological Applications

2018

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Nitric oxide (NO) is an essential signaling molecule within biological systems and is believed to be involved in numerous diseases. As a result of NO's high reaction rate, the detection of the concentration of NO, let alone the presence or absence of the molecule, is extremely difficult. Researchers have developed multiple assays and probes in an attempt to quantify NO within biological solutions, each of which has advantages and disadvantages. This review highlights many of the current NO sensors, from those that are commercially available to the newest sensors being optimized in research labs, to assist in the understanding and utilization of NO sensors in biological fields.

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Antimicrobial properties of nitric oxide and its application in antimicrobial formulations and medical devices

Cited by 172 publications

References 42 publications

Macrophages Promote Oxidative Metabolism To Drive Nitric Oxide Generation in Response to Trypanosoma cruzi

Macrophages Promote Oxidative Metabolism To Drive Nitric Oxide Generation in Response to Trypanosoma cruzi

Antibacterial Action of Nitric Oxide-Releasing Chitosan Oligosaccharides against Pseudomonas aeruginosa under Aerobic and Anaerobic Conditions

Nitric Oxide Sensors for Biological Applications

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