Nitric oxide in upper airways inflammatory diseases

Maniscalco, Mauro; Miceli, Sofia; Pelaia, Girolamo

doi:10.1007/s00011-006-6111-1

Cited by 125 publications

(128 citation statements)

References 116 publications

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“…NO is a free radical gas molecule that intervenes in a large number of fundamental cellular processes such as vascular regulation, neurotransmission, and immunity (3,4). NO reacts in water with oxygen and its reactive intermediates to yield (i) stable anions such as NO 2 Ϫ and NO 3 Ϫ , (ii) unstable higher oxides such as N 2 O 3 , and (iii) unstable peroxides (ONOO Ϫ ).…”

Section: Discussionmentioning

confidence: 99%

“…However, in maturing DC, protein degradation by caspases was inhibited, presumably by NO (1). NO is a central messenger molecule in vascular regulation, immunity, and neurotransmission (3,4). Despite the fact that NO was produced in large amounts in lipopolysaccharide (LPS)-treated DC, it is still unclear whether NO alone can contribute directly to the initiation and induction of DC maturation and T cell proliferation, respectively, in the absence of LPS.…”

Section: Dendritic Cells (Dc)mentioning

confidence: 99%

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Nitric-oxide Synthase 2 Interacts with CD74 and Inhibits Its Cleavage by Caspase during Dendritic Cell Development

Huang

Cai

Chua

et al. 2008

Journal of Biological Chemistry

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Dendritic cells (DC) are professional antigen-presenting cells that possess specific and efficient mechanisms to initiate immune responses. Upon encounter with pathogens, immature DC will go through a maturation process that converts them to highly immunogenic mature DC. Despite the fact that nitric oxide (NO) was produced in large amounts in maturing DC, it is still unclear whether NO is the key molecule that initiates and enhances DC maturation and T cell proliferation, respectively. Here, we report that NO donor and overexpression of either nitric-oxide synthase 2 (NOS2) or nitric-oxide synthase 3 (NOS3) alone can induce surface expression of major histocompatibility complex class II (MHC II) and both the essential co-stimulatory molecules CD80 and CD86 in immature DC. Consistently, NO donor-treated immature DC were capable of enhancing T cell proliferation in vitro in the absence of lipolysaccharide. Interestingly, NOS2 interacts with CD74 (the MHC II-associated invariant chain), and the degradation of CD74 by caspases in immature DC was inhibited upon treatment with NO donor. Because the trafficking of MHC II is CD74-dependent, the increase in cell surface localization of MHC II in maturing DC is in part due to the increase in CD74 protein expression in the presence of NOS2 and NO. Dendritic cells (DC)2 are professional antigen-presenting cells that possess specific and efficient mechanisms to initiate immune responses. Major histocompatibility complex class II (MHC II) molecules bind peptides derived from internalized proteins that have entered the endocytic pathway and present them at the cell surface for the activation of CD4 ϩ T cells. Upon encounter with pathogens, immature DC go through a maturation process that converts them to highly immunogenic mature DC. Immature DC are good at capturing pathogens or foreign antigens, but most of the intracellular MHC II molecules that can bind and present antigens to T cells are localized to the late endosomes. In mature DC, MHC II molecules are free to traffic to the cell surface together with their peptides to present to T cells. Some protein molecules play essential roles in controlling the retention and trafficking of MHC II in DC. We previously showed that in the immature DC, a number of endosomal proteins were degraded by caspases (1, 2). However, in maturing DC, protein degradation by caspases was inhibited, presumably by NO (1). NO is a central messenger molecule in vascular regulation, immunity, and neurotransmission (3, 4). Despite the fact that NO was produced in large amounts in lipopolysaccharide (LPS)-treated DC, it is still unclear whether NO alone can contribute directly to the initiation and induction of DC maturation and T cell proliferation, respectively, in the absence of LPS.Here, we report that NO donor-treated immature DC were capable of enhancing T cell proliferation in vitro in the absence of LPS. In addition, the MHC II-associated invariant chain (CD74) was up-regulated in immature DC upon treatment with NO donor. CD74 is a type II integ...

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Section: Discussionmentioning

confidence: 99%

Section: Dendritic Cells (Dc)mentioning

confidence: 99%

Nitric-oxide Synthase 2 Interacts with CD74 and Inhibits Its Cleavage by Caspase during Dendritic Cell Development

Huang

Cai

Chua

et al. 2008

Journal of Biological Chemistry

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“…To date, nNO has been reported to be very low, almost exclusively among subjects with PCD, and to separate convincingly between the presence and absence of PCD [3][4][5][6][7][8]. However, overlap in nNO values have been reported between PCD and other pulmonary diseases with symptoms mimicking PCD [9][10][11]. Hence, the true discriminative power of nNO in less selected, mixed population of patients referred for diagnostic testing of PCD will need to be settled before the role of nNO in the diagnosis of PCD can be fully appreciated.…”

mentioning

confidence: 99%

Choice of nasal nitric oxide technique as first-line test for primary ciliary dyskinesia

Marthin¹,

Nielsen²

2010

European Respiratory Journal

100

140

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Nasal nitric oxide (nNO) has a well-known potential as an indirect discriminative marker between patients with primary ciliary dyskinesia (PCD) and healthy subjects, but real-life experience and usefulness in young children is sparsely reported. Three nNO sampling methods were examined and compared as first-line tests for PCD.Healthy subjects, confirmed PCDs, consecutive referrals with PCD-like symptoms and patients with cystic fibrosis (CF) had nNO sampled during breath hold (BH-nNO), oral exhalation against resistance (OE-R-nNO) and tidal breathing (TB-nNO) aiming to expand age range into infancy.282 subjects, 117 consecutive referrals, 59 PCDs, 49 CF patients and 57 healthy subjects, were included. All methods separated significantly between PCD and non-PCD, including CF with reliability, in ranking order BH-nNO.OE-R-nNO.TB-nNO. Acceptability in children ranked in reverse order. A problematic high fraction (39%) of false positive TB-nNO was found in young children. An unexpected large fraction (6.8%) of PCDs had nNO values above cut-off.nNO is a helpful first-line tool in real-life PCD work-up in all age groups if the sampling method is chosen according to age. nNO can be misleading in a few patients with true PCD. Further studies are strongly needed in young children.

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“…In 1998, Robert F. Furchgott, Ferid Murad and Louis J. Ignarro were awarded the Nobel Prize in Physiology or Medicine for their discoveries concerning NO as a signaling molecule in the cardiovascular system. Since 1991, when Gustafsson et al [5] discovered that NO is present in exhaled breath of humans – and 2 years later, when Alving et al [6] showed that exhaled NO is increased in patients with asthma – several aspects of exhaled and nasal NO have been studied [19]. Actually, the molecule NO was named ‘molecule of the year’ in 1992 by the journal Science .…”

Section: Introductionmentioning

confidence: 99%

Nitric Oxide: A Promising Methodological Approach in Airway Diseases

Şahin

Klimek

Mullol

et al. 2011

Int Arch Allergy Immunol

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Nitric oxide (NO) is a potent biological mediator, and has a regulatory role in a wide variety of cellular and tissue functions. In the upper and lower airways, NO has been suggested to be involved in different functions with regulatory, protective, defensive or damaging effects. It is obvious that NO plays an important role in host defense, and is liberated in the nose and the paranasal sinuses. This review aims to highlight some aspects of the origin and function of NO in airway diseases, such as allergic rhinitis, chronic rhinosinusitis with and without nasal polyps, primary ciliary dyskinesia, and cystic fibrosis. In conclusion, NO measurement may be a promising noninvasive diagnostic marker for airway pathologies.

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Nitric oxide in upper airways inflammatory diseases

Cited by 125 publications

References 116 publications

Nitric-oxide Synthase 2 Interacts with CD74 and Inhibits Its Cleavage by Caspase during Dendritic Cell Development

Nitric-oxide Synthase 2 Interacts with CD74 and Inhibits Its Cleavage by Caspase during Dendritic Cell Development

Choice of nasal nitric oxide technique as first-line test for primary ciliary dyskinesia

Nitric Oxide: A Promising Methodological Approach in Airway Diseases

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