RESUMEN
Physical forces affect both the function and phenotype of cells in the lung. Bronchial, alveolar, and other parenchymal cells, as well as fibroblasts and macrophages, are normally subjected to a variety of passive and active mechanical forces associated with lung inflation and vascular perfusion as a result of the dynamic nature of lung function. These forces include changes in stress (force per unit area) or strain (any forced change in length in relation to the initial length) and shear stress (the stress component parallel to a given surface). The responses of cells to mechanical forces are the result of the cell's ability to sense and transduce these stimuli into intracellular signaling pathways able to communicate the information to its interior. This review will focus on the modulation of intracellular pathways by lung mechanical forces and the intercellular signaling. A better understanding of the mechanisms by which lung cells transduce physical forces into biochemical and biological signals is of key importance for identifying targets for the treatment and prevention of physical force-related disorders.
Asunto(s)
Humanos , Pulmón/fisiología , Mecanorreceptores/fisiología , Mecanotransducción Celular/fisiología , Matriz Extracelular/fisiología , Uniones Intercelulares/fisiología , Membranas Intracelulares/fisiología , Pulmón/citología , Estrés MecánicoRESUMEN
Objetivo: El estrés oxidativo forma parte esencial de la cadena de acontecimientos que conducen al estado inflamatorio de la vía aérea tras la agresión bacteriana. El objetivo del presente trabajo ha sido investigar si el análisis del condensado del vapor exhalado (CER) de pacientes con infección pulmonar grave refleja las alteraciones del estado oxidativo de la interfase aérea. Pacientes y métodos: Se ha estudiado a un total de 48 pacientes divididos en 4 grupos: sujetos sin enfermedad respiratoria (n = 14), pacientes con neumonía multilobular (n = 13), con enfermedad pulmonar obstructiva crónica sobreinfectados (n = 14) y con neumonía grave ventilados mecánicamente (n = 7). Se obtuvo una muestra de CER en las primeras 72 h tras el ingreso y se determinó la concentración de nitrito, nitrato, 8-isoprostano y mieloperoxidasa (MPO). Resultados: Se apreciaron variaciones significativas de la concentración de nitrito, 8-isoprostano y MPO en los pacientes respecto del grupo control, pero no entre los diferentes grupos de pacientes. La concentración de MPO se relacionó con las concentraciones de 8-isoprostano y nitrato normalizadas para el valor de nitrito. Conclusiones: El análisis de la concentración de 8-isoprostano y MPO en el CER permite apreciar el estrés oxidativo en la interfase aérea de los pacientes con infección pulmonar grave
Objective: Oxidative stress is an intrinsic part of the chain of events leading to inflammation of the airways caused by bacterial infection. The aim of this study was to determine whether analysis of exhaled breath condensate from patients with severe lung infections reveals changes in the redox state at the airway surface. Patients and methods: The study included a total of 48 subjects divided into 4 groups: individuals without respiratory disease (n=14), patients with multilobar pneumonia (n=13), patients who had chronic obstructive pulmonary disease with superinfection (n=14), and mechanically ventilated patients with severe pneumonia (n=7). A sample of exhaled breath condensate was obtained within the first 72 hours of hospital admission and the concentrations of nitrite, nitrate, 8-isoprostane, and myeloperoxidase (MPO) were determined. Results: Significant differences in the concentrations of nitrite, 8-isoprostane, and MPO were observed between patients and individuals without respiratory disease but no differences were found between the 3 patient groups. The concentration of MPO was correlated with the concentrations of 8-isoprostane and nitrate, which were normalized to the nitrite concentration. Conclusions: Analysis of the concentrations of 8-isoprostane and MPO in exhaled breath condensate allows assessment of oxidative stress in the airways of patients with severe lung infections