Cytokine-ion channel interactions in pulmonary inflammation
- 1Internal Medicine and Pneumology, Lindenhofspital, Switzerland
- 2Medizinische Fakultät, Universität des Saarlandes, Germany
- 3Lungen- und Atmungsstiftung Bern, Switzerland
- 4Internal Medicine, Lindenhofspital, Switzerland
- 5Institute of Immunology, Faculty of Medicine, University of Regensburg, Germany
- 6Paediatric Visceral Surgery, Universitäts-Kinderspital Zürich, Switzerland
- 7Vascular Biology Center, Medical College of Georgia, United States
- 8Novartis Institutes for Biomedical Research, Novartis (Switzerland), Switzerland
The lungs conceptually represent a sponge that is interposed in series in the bodies’ systemic circulation to take up oxygen and eliminate carbon dioxide. As such, it matches the huge surface areas of the alveolar epithelium to the pulmonary blood capillaries. The lung’s constant exposure to the exterior necessitates a competent immune system, as evidenced by the association of clinical immunodeficiencies with pulmonary infections. From the in utero- to the postnatal and adult situation there is an inherent vital need to manage alveolar fluid re-absorption, be it postnatally, or in case of hydrostatic or permeability oedema.
Whereas a wealth of literature exists on the physiological basis of fluid and solute re-absorption by ion channels and water pores, only sparse knowledge is available so far on pathological situations, such as in microbial infection, acute lung injury or ARDS, and in the pulmonary re-implantation response in transplanted lungs. The aim of this review is to discuss alveolar liquid clearance in a selection of lung injury models, thereby especially focusing on cytokines and mediators that modulate ion channels. Inflammation is characterized by complex and probably time-dependent co-signalling, interactions between the involved cell types, as well as by cell demise and barrier dysfunction, which may not uniquely determine a clinical picture. This review therefore aims to give integrative thoughts and wants to foster the unravelling of unmet needs in future research.
Keywords: cytokine, ion channel, ENaC, Na-K-ATPase, TNF, TGF-beta, TIP peptide, AP 301, AP 318, pulmonary inflammation, Pneumonia, viral pneumonia, Acute Lung Injury, ARDS, Lung Transplantation, ischemia reperfusion injury, pulmonary reimplantation response, High altitude pulmonary oedema, exacerbation of idiopathic pulmonary fibrosis
Received: 09 Aug 2017;
Accepted: 10 Nov 2017.
Edited by:Niccolo Terrando, Duke University, United States
Reviewed by:Michael Wilson, Imperial College London, United Kingdom
Gene T. Yocum, Columbia University, United States
Copyright: © 2017 Hamacher, Hadizamani, Borgmann, Mohaupt, Maennel, Moehrlen, Lucas and Stammberger. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: MD. Juerg Hamacher, Lindenhofspital, Internal Medicine and Pneumology, Bremgartenstrasse 119, CH-3012, Bern, Switzerland, email@example.com