Hyperoxia increases leptin production: a mechanism mediated through endogenous elevation of corticosterone

2001 ◽  
Vol 281 (5) ◽  
pp. L1150-L1156 ◽  
Author(s):  
Constance Barazzone-Argiroffo ◽  
Patrick Muzzin ◽  
Yves R. Donati ◽  
Chen-Da Kan ◽  
Michel L. Aubert ◽  
...  
Keyword(s):  
Weight Loss ◽  
Lung Damage ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Oxygen Breathing ◽  
Factor Α ◽  
Deficient Mice ◽  
Necrosis Factor ◽  
Alveolar Edema

Leptin, a cytokine involved in the regulation of food intake, has been reported to be decreased in lung diseases such as chronic obstructive pulmonary disease and cystic fibrosis and increased in critically ill patients with sepsis. We investigated the role of leptin during hyperoxia in mice, which results in alveolar edema, severe weight loss, and death within 3–4 days. In oxygen-breathing mice, serum leptin was increased six- to sevenfold and its mRNA was upregulated in white adipose tissue. Leptin elevation could not be attributed to changes in circulating tumor necrosis factor-α but was completely dependent on endogenous corticosterone elevation because adrenalectomized mice did not exhibit any increase in leptin levels. Using leptin-deficient mice and wild-type mice treated with anti-leptin antibody, we demonstrate that weight loss was leptin independent. Lung damage was moderately attenuated in leptin-deficient mice but was not modified by anti-leptin antibody or leptin administration, suggesting that leptin does not play an essential role in the direct and short-term effects of oxygen-induced injury.

scholarly journals Exacerbated Imiquimod-Induced Psoriasis-Like Skin Inflammation in IRF5-Deficient Mice

2020 ◽  
Vol 21 (10) ◽  
pp. 3681
Author(s):  
Momoko Nakao ◽  
Tomomitsu Miyagaki ◽  
Makoto Sugaya ◽  
Shinichi Sato
Keyword(s):  
Critical Role ◽  
Skin Inflammation ◽  
Interferon Α ◽  
Toll Like Receptor ◽  
Adaptive Immune ◽  
Th17 Cytokines ◽  
Factor Α ◽  
Deficient Mice ◽  
Necrosis Factor

Interferon regulatory factors (IRFs) play diverse roles in the regulation of the innate and adaptive immune responses in various diseases. In psoriasis, IRF2 is known to be involved in pathogenesis, while studies on other IRFs are limited. In this study, we investigated the role of IRF5 in psoriasis using imiquimod-induced psoriasis-like dermatitis. Although IRF5 is known to play a critical role in the induction of proinflammatory cytokines by immune cells, such as dendritic cells (DCs), macrophages, and monocytes, IRF5 deficiency unexpectedly exacerbated psoriasiform skin inflammation. The interferon-α and tumor necrosis factor-α mRNA expression levels were decreased, while levels of Th17 cytokines including IL-17, IL-22, and IL-23 were increased in IRF5-deficient mice. Furthermore, IL-23 expression in DCs from IRF5-deficient mice was upregulated both in steady state and after toll-like receptor 7/8 agonist stimulation. Importantly, the expression of IRF4, which is also important for the IL-23 production in DCs, was augmented in DCs from IRF5-deficient mice. Taken together, our results suggest that IRF5 deficiency induces the upregulation of IRF4 in DCs followed by augmented IL-23 production, resulting in the amplification of Th17 responses and the exacerbation of imiquimod-induced psoriasis-like skin inflammation. The regulation of IRF4 or IRF5 expression may be a novel therapeutic approach to psoriasis.

scholarly journals Smoking and interstitial lung diseases

2015 ◽  
Vol 24 (137) ◽  
pp. 428-435 ◽  
Author(s):  
George A. Margaritopoulos ◽  
Eirini Vasarmidi ◽  
Joseph Jacob ◽  
Athol U. Wells ◽  
Katerina M. Antoniou
Keyword(s):  
Lung Cancer ◽  
Chronic Obstructive Pulmonary Disease ◽  
Langerhans Cell Histiocytosis ◽  
Lung Diseases ◽  
Interstitial Lung Diseases ◽  
Lung Damage ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Pulmonary Langerhans Cell Histiocytosis

For many years has been well known that smoking could cause lung damage. Chronic obstructive pulmonary disease and lung cancer have been the two most common smoking-related lung diseases. In the recent years, attention has also focused on the role of smoking in the development of interstitial lung diseases (ILDs). Indeed, there are three diseases, namely respiratory bronchiolitis-associated ILD, desquamative interstitial pneumonia and pulmonary Langerhans cell histiocytosis, that are currently considered aetiologically linked to smoking and a few others which are more likely to develop in smokers. Here, we aim to focus on the most recent findings regarding the role of smoking in the pathogenesis and clinical behaviour of ILDs.

scholarly journals TLR7 promotes smoke-induced lung damage through the activity of mast cell tryptase

2020 ◽  
Author(s):  
Tatt Jhong Haw ◽  
Malcolm Starkey ◽  
Stelios Pavlidis ◽  
Sheena Tam ◽  
Prema M. Nair ◽  
...  
Keyword(s):  
Mast Cell ◽  
Cell Activity ◽  
Lung Damage ◽  
Chronic Obstructive ◽  
Toll Like Receptor ◽  
Mast Cell Tryptase ◽  
Obstructive Pulmonary Disease ◽  
Mast Cell Stabilizer ◽  
Tlr7 Agonist ◽  
Deficient Mice

Abstract Toll-like receptor (TLR)7 is known for eliciting immunity against single-stranded RNA viruses. TLR7 was increased in both human and cigarette smoke (CS)-induced experimental chronic obstructive pulmonary disease (COPD). Severity of CS-induced emphysema and COPD was reduced in TLR7-deficient mice whilst inhalation of imiquimod (TLR7-agonist) induced emphysema in naïve mice. Imiquimod-induced emphysema was reduced in mice treated with mast cell stabilizer cromolyn or deficient in mast cell protease-6. Therapeutic treatment with anti-TLR7 monoclonal antibody suppressed CS-induced emphysema, experimental COPD and accumulation of pulmonary mast cells. We demonstrate an unexpected role for TLR7 in mediating emphysema and COPD through mast cell activity.

scholarly journals Detection of Erythropoietin in Exhaled Breath Condensate of Nonhypoxic Subjects Using a Multiplex Bead Array

2006 ◽  
Vol 2006 ◽  
pp. 1-5 ◽  
Author(s):  
Christian Schumann ◽  
Kathy Triantafilou ◽  
Stefan Krueger ◽  
Vinzenz Hombach ◽  
Martha Triantafilou ◽  
...  
Keyword(s):  
Exhaled Breath Condensate ◽  
Sleep Apnoea ◽  
Chronic Obstructive ◽  
Exhaled Breath ◽  
Obstructive Pulmonary Disease ◽  
Obstructive Sleep ◽  
Breath Condensate ◽  
Necrosis Factor ◽  
Multiplex Bead

As a noninvasive method, exhaled breath condensate (EBC) has gained importance to improve monitoring of lung diseases and to detect biomarkers. The aim of the study was to investigate, whether erythropoietin (EPO) is detectable in EBC. EBC was collected from 22 consecutive patients as well as from healthy individuals. Using a multiplex fluorescent bead immunoassay, we detected EPO in EBC, as well as tumour necrosis factor-α(TNF-α) in 13 out of 22 patients simultaneously (EPO 0.21±0.03 in U/mL and TNF-α34.6±4.2 in pg/mL, mean±SEM). No significant differences for EPO levels or correlation between EPO and TNF-αwere found but TNF-αwas significantly higher in patients with chronic obstructive pulmonary disease (COPD) than in non-COPD (obstructive sleep apnoea, OSA, and lung healthy patients). This is the first report of detection of EPO in EBC. Due to the small study size more data is needed to clarify the role of EPO in EBC.

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