Respiratory Research

  1465-993X

 

 

Cơ quản chủ quản:  BioMed Central Ltd. , BMC

Lĩnh vực:
Pulmonary and Respiratory Medicine

Các bài báo tiêu biểu

Role of TNFα in pulmonary pathophysiology
Tập 7 Số 1 - 2006
Srirupa Mukhopadhyay, John R. Hoidal, Tapan K. Mukherjee
Abstract

Tumor necrosis factor alpha (TNFα) is the most widely studied pleiotropic cytokine of the TNF superfamily. In pathophysiological conditions, generation of TNFα at high levels leads to the development of inflammatory responses that are hallmarks of many diseases. Of the various pulmonary diseases, TNFα is implicated in asthma, chronic bronchitis (CB), chronic obstructive pulmonary disease (COPD), acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). In addition to its underlying role in the inflammatory events, there is increasing evidence for involvement of TNFα in the cytotoxicity. Thus, pharmacological agents that can either suppress the production of TNFα or block its biological actions may have potential therapeutic value against a wide variety of diseases. Despite some immunological side effects, anti-TNFα therapeutic strategies represent an important breakthrough in the treatment of inflammatory diseases and may have a role in pulmonary diseases characterized by inflammation and cell death.

Idiopathic pulmonary fibrosis: pathogenesis and management
Tập 19 Số 1 - 2018
Giacomo Sgalla, Bruno Iovene, Mariarosaria Calvello, Margherita Ori, Francesco Varone, Luca Richeldi
Muscarinic receptor signaling in the pathophysiology of asthma and COPD
Tập 7 Số 1 - 2006
Reinoud Gosens, Johan Zaagsma, Herman Meurs, Andrew J. Halayko
The lung as a route for systemic delivery of therapeutic proteins and peptides
Remigius U. Agu, Michael Ikechukwu Ugwoke, Michoel Armand, Renaat Kinget, Norbert Verbeke
Macrophages: friend or foe in idiopathic pulmonary fibrosis?
Tập 19 Số 1 - 2018
Lei Zhang, Yi Wang, Guorao Wu, Weining Xiong, Weikuan Gu, Cong Yi Wang
Role of matrix metalloproteinases in the pathogenesis of idiopathic pulmonary fibrosis
- 2016
Annie Pardo, Sandra Cabrera, Mabel Maldonado, Moisés Selman
Regulation of alveolar macrophage death in acute lung inflammation
Tập 19 Số 1 - 2018
Erica Fan, Jie Fan
Wnt signalling in lung development and diseases
- 2006
Judit E. Pongrácz, Robert A. Stockley
Abstract

There are several signalling pathways involved in lung organogenesis including Notch, TGFβ /BMP, Sonic hedgehog (Shh), FGF, EGF, and Wnt. Despite the widely acknowledged significance of Wnt signalling in embryonic lung development, the role of different Wnt pathways in lung pathologies has been slow to emerge.

In this review, we will present a synopsis of current Wnt research with particular attention paid to the role of Wnt signals in lung development and in pulmonary diseases.

Performance of a new hand-held device for exhaled nitric oxide measurement in adults and children
Tập 7 Số 1 - 2006
Kjell Alving, Christer Janson, Lennart Nordvall
AbstractBackground

Exhaled nitric oxide (NO) measurement has been shown to be a valuable tool in the management of patients with asthma. Up to now, most measurements have been done with stationary, chemiluminescence-based NO analysers, which are not suitable for the primary health care setting. A hand-held NO analyser which simplifies the measurement would be of value both in specialized and primary health care. In this study, the performance of a new electrochemical hand-held device for exhaled NO measurements (NIOX MINO) was compared with a standard stationary chemiluminescence unit (NIOX).

Methods

A total of 71 subjects (6–60 years; 36 males), both healthy controls and atopic patients with and without asthma were included. The mean of three approved exhalations (50 ml/s) in each device, and the first approved measurement in the hand-held device, were compared with regard to NO readings (Bland-Altman plots), measurement feasibility (success rate with 6 attempts) and repeatability (intrasubject SD).

Results

Success rate was high (≥ 84%) in both devices for both adults and children. The subjects represented a FENOrange of 8–147 parts per billion (ppb). When comparing the mean of three measurements (n = 61), the median of the intrasubject difference in exhaled NO for the two devices was -1.2 ppb; thus generally the hand-held device gave slightly higher readings. The Bland-Altman plot shows that the 95% limits of agreement were -9.8 and 8.0 ppb. The intrasubject median difference between the NIOX and the first approved measurement in the NIOX MINO was -2.0 ppb, and limits of agreement were -13.2 and 10.2 ppb. The median repeatability for NIOX and NIOX MINO were 1.1 and 1.2 ppb, respectively.

Conclusion

The hand-held device (NIOX MINO) and the stationary system (NIOX) are in clinically acceptable agreement both when the mean of three measurements and the first approved measurement (NIOX MINO) is used. The hand-held device shows good repeatability, and it can be used successfully on adults and most children. The new hand-held device will enable the introduction of exhaled NO measurements into the primary health care.

Effects of different mesenchymal stromal cell sources and delivery routes in experimental emphysema
Tập 15 - Trang 1-14 - 2014
Mariana A Antunes, Soraia C Abreu, Fernanda F Cruz, Ana Clara Teixeira, Miquéias Lopes-Pacheco, Elga Bandeira, Priscilla C Olsen, Bruno L Diaz, Christina M Takyia, Isalira PRG Freitas, Nazareth N Rocha, Vera L Capelozzi, Débora G Xisto, Daniel J Weiss, Marcelo M Morales, Patricia RM Rocco
We sought to assess whether the effects of mesenchymal stromal cells (MSC) on lung inflammation and remodeling in experimental emphysema would differ according to MSC source and administration route. Emphysema was induced in C57BL/6 mice by intratracheal (IT) administration of porcine pancreatic elastase (0.1 UI) weekly for 1 month. After the last elastase instillation, saline or MSCs (1-105), isolated from either mouse bone marrow (BM), adipose tissue (AD) or lung tissue (L), were administered intravenously (IV) or IT. After 1 week, mice were euthanized. Regardless of administration route, MSCs from each source yielded: 1) decreased mean linear intercept, neutrophil infiltration, and cell apoptosis; 2) increased elastic fiber content; 3) reduced alveolar epithelial and endothelial cell damage; and 4) decreased keratinocyte-derived chemokine (KC, a mouse analog of interleukin-8) and transforming growth factor-β levels in lung tissue. In contrast with IV, IT MSC administration further reduced alveolar hyperinflation (BM-MSC) and collagen fiber content (BM-MSC and L-MSC). Intravenous administration of BM- and AD-MSCs reduced the number of M1 macrophages and pulmonary hypertension on echocardiography, while increasing vascular endothelial growth factor. Only BM-MSCs (IV > IT) increased the number of M2 macrophages. In conclusion, different MSC sources and administration routes variably reduced elastase-induced lung damage, but IV administration of BM-MSCs resulted in better cardiovascular function and change of the macrophage phenotype from M1 to M2.