Cytokine-Ion Channel Interactions in Pulmonary Inflammation

Hamacher, Juerg and Hadizamani, Yalda and Borgmann, Michele and Mohaupt, Markus and Maennel, Daniela Narcissa and Moehrlen, Ueli and Lucas, Rudolf and Stammberger, Uz (2018) Cytokine-Ion Channel Interactions in Pulmonary Inflammation. FRONTIERS IN IMMUNOLOGY, 8: 1644. ISSN 1664-3224

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Abstract

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 reabsorption, be it postnatally, or in case of hydrostatic or permeability edema. Whereas a wealth of literature exists on the physiological basis of fluid and solute reabsorption 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 acute respiratory distress syndrome, and in the pulmonary reimplantation 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-signaling, 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 unraveling of unmet needs in future research.

Item Type: Article
Uncontrolled Keywords: TUMOR-NECROSIS-FACTOR; EPITHELIAL SODIUM-CHANNEL; ALVEOLAR FLUID CLEARANCE; ACUTE LUNG INJURY; KERATINOCYTE GROWTH-FACTOR; RESPIRATORY-DISTRESS-SYNDROME; LECTIN-LIKE DOMAIN; PROTEIN-KINASE-C; PRIMARY GRAFT DYSFUNCTION; BETA-ADRENERGIC AGONIST; epithelial sodium channel; Na+/K+-ATPase; tumor necrosis factor; TNF tip peptide; pneumonia; acute respiratory distress syndrome; lung transplantation; ischemia-reperfusion injury
Subjects: 600 Technology > 610 Medical sciences Medicine
Divisions: Medicine > Lehrstuhl für Immunologie
Depositing User: Petra Gürster
Date Deposited: 25 Jun 2020 08:39
Last Modified: 25 Jun 2020 08:39
URI: https://pred.uni-regensburg.de/id/eprint/15219

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