Downregulation of Secretory Leukocyte Proteinase Inhibitor in Chronic Obstructive Lung Disease: The Role Of TGF-β/Smads Signaling Pathways

Luo, Bailing; Niu, Ruichao; Feng, Juntao; Xie, Xiaoyun; Ma, Lijuan

doi:10.1016/j.arcmed.2008.02.002

Cited by 21 publications

(18 citation statements)

References 28 publications

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“…increased production of lysozyme and lactoferrin has been observed in bronchoalveolar lavage (BAL) fluid of patients with COPD [130]. Whereas a reduction of SLPI in BAL has been shown in experimental COPD [131], no change in SLPI was observed in BAL from patients with asthma or COPD [132]. In contrast, lipoxinA4 was reduced in induced sputum from patients with asthma [133,134], possibly contributing to the persistence of inflammation in severe disease [135].…”

Section: Altered Chemical Barriermentioning

confidence: 99%

Chronic inflammatory airway diseases: the central role of the epithelium revisited

Gohy

Hupin

Pilette

et al. 2016

Clin Experimental Allergy

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The respiratory epithelium plays a critical role for the maintenance of airway integrity and defense against inhaled particles. Physical barrier provided by apical junctions and mucociliary clearance clears inhaled pathogens, allergens or toxics, to prevent continuous stimulation of adaptive immune responses. The "chemical barrier", consisting of several anti-microbial factors such as lysozyme and lactoferrin, constitutes another protective mechanism of the mucosae against external aggressions before adaptive immune response starts. The reconstruction of damaged respiratory epithelium is crucial to restore this barrier. This review examines the role of the airway epithelium through recent advances in health and chronic inflammatory diseases in the lower conducting airways (in asthma and chronic obstructive pulmonary disease). Better understanding of normal and altered epithelial functions continuously provides new insights into the physiopathology of chronic airway diseases and should help to identify new epithelial-targeted therapies.

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Section: Altered Chemical Barriermentioning

confidence: 99%

Chronic inflammatory airway diseases: the central role of the epithelium revisited

Gohy

Hupin

Pilette

et al. 2016

Clin Experimental Allergy

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“…Bronchial epithelial cells can also produce TGF- β either constitutively or upon stimulation such as by cigarette smoke [15, 16], whereas IFN- γ inhibits epithelial TGF- β release whilst promoting pIgR/SC expression. Intriguingly, it was shown that TGF- β expression is increased in small airway epithelium from smokers and patients with COPD [17, 18], and was suggested as a factor downregulating SLPI expression in these patients [19]. A reduction in SLPI secretion can also be induced by elastase, as recently reported [20].…”

Section: Discussionmentioning

confidence: 87%

Dual Effect of Neutrophils on pIgR/Secretory Component in Human Bronchial Epithelial Cells: Role of TGF-

Ratajczak

Guisset

Detry

et al. 2010

Journal of Biomedicine and Biotechnology

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Neutrophils have a dual affect on epithelial pIgR/SC, the critical receptor for transcellular routing of mucosal IgA, but mechanisms of pIgR/SC upregulation remain elusive. Requirements of cytokine, redox, and signalling pathways for pIgR/SC production were assessed in human bronchial epithelial (Calu-3) cells cocultured with increasing numbers of blood neutrophils. Increased SC production was observed after incubation for 48 hrs with intermediate neutrophil numbers (1.25 to 2.5 × 106), was favoured by the elastase inhibitor SLPI, and correlated with increased TGF-β production. Exogenous TGF-β stimulated SC production with a maximal effect at 48 hrs and both TGF-β- and neutrophil-driven SC upregulation were dependent on redox balance and p38 MAP-kinase activation. This paper shows that activated neutrophils could upregulate epithelial pIgR/SC production through TGF-β-mediated activation of a redox-sensitive and p38 MAPK-dependent pathway. An imbalance between the two neutrophil-driven opposite mechanisms (SC upregulation and SC degradation) could lead to downregulation of pIgR/SC, as observed in severe COPD.

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“…The doses of rolipram and dexamethasone were used in the present study based on our preliminary results and previous studies [14,15]. CS and LPS treatment was performed as follows: rats were confined in a container made of plexiglass (85 cm× 85 cm× 45 cm), and pump CS from 12 standard cigarettes into the container, and rats were exposed to the smoking for 20 min, twice a day with an interval of 15 min and 6 days per week, LPS was administrated intratracheally every 4 weeks at a dose of 1 mg/kg, it took 12 weeks to establish a rat COPD-like animal model [16][17][18][19]. Zl-n-91, rolipram and dexamethasone were diluted in 60% Polyethylene glycol and administrated intraperitoneally for 8 weeks from the fifth week.…”

Section: Methodsmentioning

confidence: 99%

Zl-n-91, a selective phosphodiesterase 4 inhibitor, suppresses inflammatory response in a COPD-like rat model

Wang

Jiang

Tang

et al. 2010

International Immunopharmacology

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Downregulation of Secretory Leukocyte Proteinase Inhibitor in Chronic Obstructive Lung Disease: The Role Of TGF-β/Smads Signaling Pathways

Cited by 21 publications

References 28 publications

Chronic inflammatory airway diseases: the central role of the epithelium revisited

Chronic inflammatory airway diseases: the central role of the epithelium revisited

Dual Effect of Neutrophils on pIgR/Secretory Component in Human Bronchial Epithelial Cells: Role of TGF-

Zl-n-91, a selective phosphodiesterase 4 inhibitor, suppresses inflammatory response in a COPD-like rat model

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