(Q46856479)

English

Differential protease, innate immunity, and NF-kappaB induction profiles during lung inflammation induced by subchronic cigarette smoke exposure in mice.

scientific article published on 16 December 2005

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scholarly article

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Europe PubMed Central

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10 January 2020

Differential protease, innate immunity, and NF-kappaB induction profiles during lung inflammation induced by subchronic cigarette smoke exposure in mice (English)

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Europe PubMed Central

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10 January 2020

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based on heuristic

inferred from title

Steven Bozinovski

2

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10 January 2020

Michelle J. Hansen

7

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10 January 2020

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Vlahos R

1

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10 January 2020

Jones JE

3

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10 January 2020

Powell J

4

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10 January 2020

Gras J

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10 January 2020

Lilja A

6

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10 January 2020

Gualano RC

8

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10 January 2020

Irving L

9

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10 January 2020

Anderson GP

10

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10 January 2020

publication date

16 December 2005

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10 January 2020

American Journal of Physiology - Lung Cellular and Molecular Physiology

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10 January 2020

290

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10 January 2020

5

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10 January 2020

L931-45

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10 January 2020

Nuclear factor-kappaB: a pivotal transcription factor in chronic inflammatory diseases

1 reference

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Granulocyte/macrophage-colony-stimulating factor (GM-CSF) regulates lung innate immunity to lipopolysaccharide through Akt/Erk activation of NFkappa B and AP-1 in vivo.

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Nuclear localisation of p65 in sputum macrophages but not in sputum neutrophils during COPD exacerbations.

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Respiratory health effects of exposure to environmental tobacco smoke

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Tumor necrosis factor-alpha is central to acute cigarette smoke-induced inflammation and connective tissue breakdown

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Acute cigarette smoke-induced connective tissue breakdown requires both neutrophils and macrophage metalloelastase in mice

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Selective accumulation of differentiated CD8+ T cells specific for respiratory viruses in the human lung.

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Increased expression of nuclear factor-kappaB in bronchial biopsies from smokers and patients with COPD.

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Impact of cigarette smoke on clearance and inflammation after Pseudomonas aeruginosa infection

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Constitutive activation of the SRC family kinase Hck results in spontaneous pulmonary inflammation and an enhanced innate immune response

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TLR4 signaling induces TLR2 expression in endothelial cells via neutrophil NADPH oxidase

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Bacterial lipopolysaccharide and IFN-gamma induce Toll-like receptor 2 and Toll-like receptor 4 expression in human endothelial cells: role of NF-kappa B activation

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Virus-specific CD8+ T cells in primary and secondary influenza pneumonia

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21 January 2018

The development of emphysema in cigarette smoke-exposed mice is strain dependent

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21 January 2018

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Transcription factor Nrf2 plays a pivotal role in protection against elastase-induced pulmonary inflammation and emphysema

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Macrophages are necessary for maximal nuclear factor-kappa B activation in response to endotoxin

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Characterization of the interstitial lung and peripheral blood T cell receptor repertoire in cigarette smokers.

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Cigarette smoke inhibits lipopolysaccharide-induced production of inflammatory cytokines by suppressing the activation of activator protein-1 in bronchial epithelial cells.

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Interleukin-1beta causes pulmonary inflammation, emphysema, and airway remodeling in the adult murine lung

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The transcription factor EGR-1 suppresses transformation of human fibrosarcoma HT1080 cells by coordinated induction of transforming growth factor-beta1, fibronectin, and plasminogen activator inhibitor-1.

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The global burden of disease, 1990–2020

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The effect of cigarette smoking on neutrophil kinetics in human lungs

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Role of resident alveolar macrophages in leukocyte traffic into the alveolar air space of intact mice

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Monocytes are potent facilitators of alveolar neutrophil emigration during lung inflammation: role of the CCL2-CCR2 axis

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Differential regulation of neutrophil-activating chemokines by IL-6 and its soluble receptor isoforms

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Short-term cigarette smoke exposure enhances allergic airway inflammation in mice

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Increase in macrophage elastase (MMP-12) in lungs from patients with chronic obstructive pulmonary disease

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