Abstract
Respiratory diseases and lower respiratory tract infections are among the leading cause of death worldwide and, especially given the recent severe acute respiratory syndrome coronavirus‐2 pandemic, are of high and prevalent socio‐economic importance. In vitro models, which accurately represent the lung microenvironment, are of increasing significance given the ethical concerns around animal work and the lack of translation to human disease, as well as the lengthy time to market and the attrition rates associated with clinical trials. This review gives an overview of the biological and immunological components involved in regulating the respiratory epithelium system in health, disease, and infection. The evolution from 2D to 3D cell biology and to more advanced technological integrated models for studying respiratory host–pathogen interactions are reviewed and provide a reference point for understanding the in vitro modeling requirements. Finally, the current limitations and future perspectives for advancing this field are presented.
Highlights
Respiratory diseases and lower respiratory tract infections are among the gens can be highly contagious and those leading cause of death worldwide and, especially given the recent severe acute respiratory syndrome coronavirus-2 pandemic, are of high and prevalent socio-economic importance
We describe the pulmonary immune system, contributes a substantial burden on society, especially providing a primer on its response to common respiratory lower respiratory tract infections which account for 4 million pathogen, and remodeling of the respiratory epithelium in disease
In vivo examples include bioresorbable patches[196,197] and implantable electrocorticography devices for monitoring neuronal epileptiform discharge.[198,199]. In each of these applications, organic electrochemical transistors (OECTs) devices have shown superior performance when compared to conventional electrode recordings, including lower operational voltages, increased signal-to-noise ratio (SNR), and increased biocompatibility
Summary
The human respiratory system is responsible for essential breathing processes and gas exchange. Surfactant directly binds/traps pathogen and cell debris; activates immune cells; initiates opsonization for pathogen clearance; Initiates microbial phagocytosis.[44,45]. Quiescent macrophages suppress the overstimulation of immune system; activated macrophages secrete cytokines, stimulate dendritic cells and phagocytose cell debris and pathogens; can present antigens in some cases.[20,29]. Regulatory T-cells suppress the overstimulation of immune system; Helper T-cell, for example, CD4+T regulate the adaptive immune response, especially B-cells and macrophages; cytotoxic T-cell, for example, CD8+ bind and lyse infected cells; memory T-cells remain and circulate after infection to ensure rapid response to reinfection.[35,37,48]. Plasma cells secrete specific antibodies which neutralize pathogens or bind and lyse infected cells; memory B-cells remain and circulate after infection to ensure rapid response to reinfection.[38,49]
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