Sepsis and mechanical ventilation alter the tight junction proteins in rat lungs in vivo

Helguera, G. Sánchez; Silva, Anthony; Murillo, Raquel; Ferruelo, Antonio; Lorente, José A.; Herrero, Raquel

doi:10.1183/13993003.congress-2019.pa4116

Cited by 1 publication

(1 citation statement)

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“…One of the key strengths of the ventilated model was its notable capability to facilitate the establishment and maintenance of tight junctions between lung epithelial cells, as evidenced by the presence of ZO-1, which was not detected in A549 cell cultures in previous publications (59)(60)(61) . Ventilation, with its cyclic inflow and outflow of air, played a pivotal role in enhancing the formation of these tight junctions and promoting their robustness over time (62,63). Ventilation-induced mechanical forces effectively simulated the dynamic nature of the breathing process in the human lung.…”

Section: Discussion and Outlookmentioning

confidence: 99%

A 3D Printed Ventilated Perfused Lung Model Platform to Dissect the Lung’s Response to Viral Infection in the Presence of Respiration

Derman,

Alioglu,

Banerjee

et al. 2023

Preprint

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In this study, we developed a three-dimensionally (3D) printed lung model that faithfully recapitulates the intricate lung environment. This 3D model incorporated alveolar and vascular components that allow for a comprehensive exploration of lung physiology and responses to infection in vitro. In particular, we investigated the intricate role of ventilation on formation of the alveolar epithelial layer and its response to viral infections. In this regard, we subjected our 3D printed, perfused lung model to a continuous respiratory cycle at the air-liquid interface (ALI) for up to 10 days followed by infection with two viruses: influenza virus (Pr8) and respiratory syncytial virus (RSV), at two different concentrations for 24 or 48 h. The results revealed that ventilation induced increased tight-junction formation with better epithelial barrier function over time, facilitated higher expression of alveolar epithelial specific genes, enabled higher level of infection with an increased progression of viral spread and replication over time, and modulated the production of pro-inflammatory cytokines and chemokines. Our findings represent a critical step forward in advancing our understanding of lung-specific viral responses and respiratory infections in response to ventilation, which sheds light on vital aspects of pulmonary physiology and pathobiology.

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