Neutrophil Priming by Cigarette Smoke Condensate and a Tobacco Anti-Idiotypic Antibody

Koethe, Susan M.; Kuhnmuench, John R.; Becker, Carl G.

doi:10.1016/s0002-9440(10)64810-9

Cited by 46 publications

(31 citation statements)

References 32 publications

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“…Inflammation is common to the pathogenesis of these diseases. It has been reported that nicotine is chemotactic for neutrophils (41) and cigarette smoke primes neutrophils (42). The present study suggests that nicotine present in tobacco smoke may further enhance tissue and DNA damage through HOCl-mediated chlorination by myeloperoxidase secreted from neutrophils, contributing to lung carcinogenesis and other smoking-related diseases.…”

Section: Table I Effect Of Ferrous and Ferric Ions On Hocl-mediated Fsupporting

confidence: 52%

Chlorination of Guanosine and Other Nucleosides by Hypochlorous Acid and Myeloperoxidase of Activated Human Neutrophils

Masuda¹,

Suzuki²,

Friesen³

et al. 2001

Journal of Biological Chemistry

133

119

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Activated human neutrophils secrete myeloperoxidase, which generates HOCl from H 2 O 2 and Cl ؊ . We have found that various (2-deoxy)nucleosides react with HOCl to form chlorinated (2-deoxy)nucleosides, including novel 8-chloro(2-deoxy)guanosine, 5-chloro(2-deoxy)cytidine, and 8-chloro(2-deoxy)adenosine formed in yields of 1.6, 1.6, and 0.2%, respectively, when 0.5 mM nucleoside reacted with 0.5 mM HOCl at pH 7.4. The relative chlorination, oxidation, and nitration activities of HOCl, myeloperoxidase, and activated human neutrophils in the presence and absence of nitrite were studied by analyzing 8-chloro-, 8-oxo-7,8-dihydro-, and 8-nitroguanosine, respectively, using guanosine as a probe. 8-Chloroguanosine was always more easily formed than 8-oxo-7,8-dihydro-or 8-nitro-guanosine. Using electrospray ionization tandem mass spectrometry, we show that several chlorinated nucleosides including 8-chloro(2-deoxy)guanosine are formed following exposure of isolated DNA or RNA to HOCl. Micromolar concentrations of tertiary amines such as nicotine and trimethylamine dramatically enhanced chlorination of free (2-deoxy)nucleosides and nucleosides in RNA by HOCl. As the G؊463A polymorphism of the MPO gene, which strongly reduces myeloproxidase mRNA expression, is associated with a reduced risk of lung cancer, chlorination damage of DNA /RNA and nucleosides by myeloperoxidase and its enhancement by nicotine may be important in the pathophysiology of human diseases associated with tobacco habits.

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Section: Table I Effect Of Ferrous and Ferric Ions On Hocl-mediated Fsupporting

confidence: 52%

Chlorination of Guanosine and Other Nucleosides by Hypochlorous Acid and Myeloperoxidase of Activated Human Neutrophils

Masuda¹,

Suzuki²,

Friesen³

et al. 2001

Journal of Biological Chemistry

133

119

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“…The idea of autoimmunity as a mechanism for the chronic inflammatory and emphysematous damage [55,56] is also supported by the detection of circulating autoantibodies directed against proteins that could have been damaged following chronic cigarette smoke exposure, such as antielastin antibodies [50], anti-epithelial antibodies [57] and tobacco anti-idiotypic antibodies [58], in smoking patients with COPD. The anti-epithelial antibodies were particularly avid against pulmonary epithelium and endothelium, and mediated antibody-directed cytotoxicity, making them potentially pathogenic.…”

Section: Dendritic Cellsmentioning

confidence: 99%

Multifaceted mechanisms in COPD: inflammation, immunity, and tissue repair and destruction

Chung¹,

Adcock²

2008

Eur Respir J

517

425

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Chronic obstructive pulmonary disease is a leading global cause of morbidity and mortality that is characterised by inexorable deterioration of small airways obstruction with emphysema associated with cellular inflammation and structural remodelling. Other features include apoptosis as well as proliferation of cells, and both tissue repair and lack of tissue repair.Metalloprotease release, together with that of apoptotic factors, may underlie the emphysema, and, conversely, fibrosis of the small airways may be accounted for by the effects of growth factor activation. In advanced disease, influential factors include the development of autoimmunity, with activation of dendritic cells and T-helper cells of both type 1 and 2, and the senescence response.An inability of macrophages to ingest apoptosed cells and bacteria may exacerbate inflammatory responses. Systemic inflammation with concomitant cardiovascular disease and metabolic syndrome may reflect the effect of cigarette smoke on nonpulmonary cells. Corticosteroid resistance may be secondary to oxidative stress mechanisms, such as inactivation of histone deacetylases.The mechanisms of chronic obstructive pulmonary disease may be heterogeneous, according to severity, and clinical phenotypes need to be correlated with cellular and pathological processes. Treatments may be targeted to patients with specific mechanisms.

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“…This increased expression of adhesion molecules is correlated with an increased respiratory burst. Studies concerning the effects of cigarette smoke on neutrophils show additional effects on priming of the peripheral blood neutrophils [83,84]. An increase of the expression of MAC-1 (CD11b/CD18) and formyl-methionylleucyl-phenylalanine (fMLP) receptors on neutrophils was demonstrated after stimulation of peripheral blood neutrophils with cigarette smoke condensate [82].…”

Section: Neutrophils Are Important Effector Cells In Copd and Can Medmentioning

confidence: 99%

Systemic inflammation in chronic obstructive pulmonary disease

Oudijk

Lammers²,

Koenderman³

2003

Eur Respir J

169

110

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Chronic obstructive pulmonary disease (COPD) is characterised by a chronic inflammation in the pulmonary tissue. The disease is associated with a switch from a self-limiting inflammatory response, mainly initiated by smoke inhalation, to a chronic persistent inflammatory response after prolonged interaction with cigarette smoke. The extent of the inflammatory reaction is correlated with the severity of the disease.Chronic inflammation in the pulmonary tissue is also associated with systemic effects. These effects range from cytokine-induced priming of peripheral leukocytes, to muscle wasting induced by cytokines such as tumour necrosis factor-a. Despite a general consensus that chronic inflammation is a characteristic phenomenon of the disease, surprisingly little is known regarding the underlying pathogenetic mechanisms.A clear communication is present between the disease mechanisms in the pulmonary compartment and peripheral tissues, leading to the concept of COPD as a systemic inflammatory disease. This communication can be mediated by: 1) leakage of reactive oxygen species and stress-induced cytokines directly into the peripheral blood, 2) (pre)activation of peripheral blood leukocytes that can result in aberrant homing and activation of inflammatory cells in distant tissues, and 3) the liberation of proinflammatory mediators by leukocytes and/or stromal cells present in the pulmonary tissues during progression of the disease.The current authors hypothesise that the occurrence of a chronic inflammatory response after prolonged interaction of the pulmonary tissue with cigarette smoke causes aberrant homing of leukocytes to the tissue and delayed apoptosis. This leads to the autonomous characteristic of the inflammatory response in patients with chronic obstructive pulmonary disease. Eur Respir J 2003; 22: Suppl. 46, 5s-13s.

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Neutrophil Priming by Cigarette Smoke Condensate and a Tobacco Anti-Idiotypic Antibody

Cited by 46 publications

References 32 publications

Chlorination of Guanosine and Other Nucleosides by Hypochlorous Acid and Myeloperoxidase of Activated Human Neutrophils

Chlorination of Guanosine and Other Nucleosides by Hypochlorous Acid and Myeloperoxidase of Activated Human Neutrophils

Multifaceted mechanisms in COPD: inflammation, immunity, and tissue repair and destruction

Systemic inflammation in chronic obstructive pulmonary disease

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