Oral L-arginine supplementation in cystic fibrosis patients: a placebo-controlled study

Grasemann, Hartmut; Grasemann, Corinna; Kurtz, Fionn; Tietze-Schillings, G.; Vester, Udo; Ratjen, Félix

doi:10.1183/09031936.04.00086104

Cited by 56 publications

(35 citation statements)

References 30 publications

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“…We also showed that the statistical significance of the relationship was lost in patients receiving inhaled corticosteroids. Our results suggest that NO deficiency in conducting airways may participate in bronchial obstruction since GRASEMANN et al [24] have shown that nebulised L-arginine not only significantly increased exhaled NO concentration but also resulted in a sustained improvement of FEV1 in patients with CF. Interestingly, in this latter study, oxygen saturation also increased significantly after the inhalation of L-arginine, which suggests an effect of NO on V9/Q9 matching (we found a relationship between Pa,O 2 and J'aw,NO) [24].…”

Section: Cystic Fibrosis and Non-cystic Fibrosis Bronchiectasis D Humentioning

confidence: 60%

Exhaled nitric oxide in cystic fibrosis: relationships with airway and lung vascular impairments

Hubert

Aubourg²,

Fauroux³

et al. 2009

European Respiratory Journal

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A reduction of exhaled nitric oxide (NO) fraction and endothelial-mediated dysfunction have been reported in cystic fibrosis (CF). The aims of the present study were to search for relationships between flow-independent NO exchange parameters (bronchial NO flux (J9aw,NO) and alveolar NO concentration (CA,NO)) and lung function tests characterising airflow limitation and pulmonary vascular bed (capillary blood volume and physiological dead space/tidal volume (VD/VT) ratio on exercise).In total, 34 patients (16 children, 18 adults) with CF, without resting pulmonary hypertension, underwent spirometry, exhaled NO measurement (multiple constant flow analytical method), gas transfer assessment (carbon monoxide and NO, allowing the calculation of capillary volume and membrane conductance) and a graded exercise test with oxygen uptake (V9O 2 ), carbon dioxide production (V9CO 2 ) and arterial blood gas evaluations.Both J9aw,NO and CA,NO correlated positively with airflow limitation. CA,NO correlated positively with capillary/alveolar volume. During exercise, criteria of mild pulmonary vascular disease were evidenced in some patients that participated in exercise limitation (negative correlation between physiological VD/VT and peak V9O 2 ). CA,NO at rest correlated positively with these parameters of wasted ventilation during exercise (physiological VD/VT, minute ventilation (V9E)/V9CO 2 at ventilatory threshold and V9E/V9CO 2 slope).Flow-independent exhaled NO parameters are linked to airway and early vascular diseases in patients with CF.

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Section: Cystic Fibrosis and Non-cystic Fibrosis Bronchiectasis D Humentioning

confidence: 60%

Exhaled nitric oxide in cystic fibrosis: relationships with airway and lung vascular impairments

Hubert

Aubourg²,

Fauroux³

et al. 2009

European Respiratory Journal

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“…Addition of acidified nitrite, which can generate NO either spontaneously or from NIR activity, was found to effectively control P. aeruginosa, S. aureus and Burkholderia cepacia biofilms [124,125], although in these cases high concentrations of nitrite (15 mM) were used and NO acted via a toxic, killing effect on biofilms. In preliminary clinical studies, treatments with nebulized L-arginine in CF patients infected with P. aeruginosa resulted in sustained improvement in lung function associated with significantly increased NOS activity within lung tissues, suggesting that the NO augmentation could potentially reduce the bacterial infection [126,127]. However in these studies, the effect of increased L-arginine on P. aeruginosa growth was not investigated and will need to be confirmed in subsequent trials.…”

Section: Stimulation Of Endogenous No Productionmentioning

confidence: 97%

Nitric Oxide: A Key Mediator of Biofilm Dispersal with Applications in Infectious Diseases

Barraud¹,

Kelso²,

Rice

et al. 2014

CPD

215

196

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Studies of the biofilm life cycle can identify novel targets and strategies for improving biofilm control measures. Of particular interest are dispersal events, where a subpopulation of cells is released from the biofilm community to search out and colonize new surfaces. Recently, the simple gas and ubiquitous biological signaling molecule nitric oxide (NO) was identified as a key mediator of biofilm dispersal conserved across microbial species. Here, we review the role and mechanisms of NO mediating dispersal in bacterial biofilms, and its potential for novel therapeutics. In contrast to previous attempts using high dose NO aimed at killing pathogens, the use of low, non-toxic NO signals (picomolar to nanomolar range) to disperse biofilms represents an innovative and highly favourable approach to improve infectious disease treatments. Further, several NO-based technologies have been developed that offer a versatile range of solutions to control biofilms, including: (i) NO-generating compounds with short or long half-lives and safe or inert residues, (ii) novel compounds for the targeted delivery of NO to infectious biofilms during systemic treatments, and (iii) novel NO-releasing materials and surface coatings for the prevention and dispersal of biofilms. Overall the use of low levels of NO exploiting its signaling properties to induce dispersal represents an unprecedented and promising strategy for the control of biofilms in clinical and industrial contexts. AbstractStudies of the biofilm life cycle can identify novel targets and strategies for improving biofilm control measures. Of particular interest are dispersal events, where a subpopulation of cells is released from the biofilm community to search out and colonize new surfaces. Recently, the simple gas and ubiquitous biological signaling molecule nitric oxide (NO) was identified as a key mediator of biofilm dispersal conserved across microbial species. Here, we review the role and mechanisms of NO mediating dispersal in bacterial biofilms, and its potential for novel therapeutics. In contrast to previous attempts using high dose NO aimed at killing pathogens, the use of low, non-toxic NO signals (picomolar to nanomolar range) to disperse biofilms represents an innovative and highly favourable approach to improve infectious disease treatments. Further, several NO-based technologies have been developed that offer a versatile range of solutions to control biofilms, including: (i) NO-generating compounds with short or long half-lives and safe or inert residues, (ii) novel compounds for the targeted delivery of NO to infectious biofilms during systemic treatments, and (iii) novel NO-releasing materials and surface coatings for the prevention and dispersal of biofilms. Overall the use of low levels of NO exploiting its signaling properties to induce dispersal represents an unprecedented and promising strategy for the control of biofilms in clinical and industrial contexts. 3 Increased antimicrobial tolerance in biofilms is the basis for chronic infecti...

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“…In a rodent model, L-arginine was associated with reduced tissue damage, decreased neutrophil recruitment, and reduced IL-1b (Hopkins et al 2006). A small study of L-arginine in CF was associated with increased eNO (Grasemann et al 2005b). L-Arginine has potential, but large prospective clinical trials have not been performed.…”

Section: Modulators Of Intracellular Signalingmentioning

confidence: 99%

Antibiotic and Anti-Inflammatory Therapies for Cystic Fibrosis

Chmiel

Konstan

Elborn

2013

Cold Spring Harbor Perspectives in Medicine

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Oral L-arginine supplementation in cystic fibrosis patients: a placebo-controlled study

Cited by 56 publications

References 30 publications

Exhaled nitric oxide in cystic fibrosis: relationships with airway and lung vascular impairments

Exhaled nitric oxide in cystic fibrosis: relationships with airway and lung vascular impairments

Nitric Oxide: A Key Mediator of Biofilm Dispersal with Applications in Infectious Diseases

Antibiotic and Anti-Inflammatory Therapies for Cystic Fibrosis

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