Mechanistic Understanding of Lung Inflammation: Recent Advances and Emerging Techniques

Abstract

Acute respiratory distress syndrome (ARDS) is a life-threatening lung injury characterized by an acute inflammatory response in the lung parenchyma. Hence, it is considered as the most appropriate clinical syndrome to study pathogenic mechanisms of lung inflammation. ARDS is associated with increased morbidity and mortality in the intensive care unit (ICU), while no effective pharmacological treatment exists. It is very important therefore to fully characterize the underlying pathobiology and the related mechanisms, in order to develop novel therapeutic approaches. In vivo and in vitro models are important pre-clinical tools in biological and medical research in the mechanistic and pathological understanding of the majority of diseases. In this review, we will present data from selected experimental models of lung injury/acute lung inflammation, which have been based on clinical disorders that can lead to the development of ARDS and related inflammatory lung processes in humans, including ventilation-induced lung injury (VILI), sepsis, ischemia/reperfusion, smoke, acid aspiration, radiation, transfusion-related acute lung injury (TRALI), influenza, Streptococcus ( S .) pneumoniae and coronaviruses infection. Data from the corresponding clinical conditions will also be presented. The mechanisms related to lung inflammation that will be covered are oxidative stress, neutrophil extracellular traps, mitogen-activated protein kinase (MAPK) pathways, surfactant, and water and ion channels. Finally, we will present a brief overview of emerging techniques in the field of omics research that have been applied to ARDS research, encompassing genomics, transcriptomics, proteomics, and metabolomics, which may recognize factors to help stratify ICU patients at risk, predict their prognosis, and possibly, serve as more specific therapeutic targets.

Construction and validation of a pulmonary complication score for patients after liver transplantation

“…The relationship between the inflammatory factors and PCS‐LT were analyzed in our study. TNF‐α and IL‐1 were pro‐inflammatory mediators 20 and IL‐8 could also induce inflammation in lung injury 21 . At the same time, IL‐2Rwas an inflammatory factor that expresses a pro‐inflammatory response 22 and IL‐6 was involved in the inflammatory response to lung injury 23 .…”

Heparin-Binding Protein Promotes Acute Lung Injury in Sepsis Mice by Blocking the Aryl Hydrocarbon Receptor Signaling Pathway

“…Because severe inflammatory response induced by sepsis is an important cause of lung injury, 28 we further investigated whether HBP degradation regulated the pulmonary inflammatory response. The ELISA results showed that the levels of pulmonary cytokines (TNF-α, IL-1β, IL-6, and IFN-γ) in lung homogenate of mice in the LPS group were significantly higher compared with those in the Control group (P < 0.01).…”

Ferroptosis in Rat Lung Tissue during Severe Acute Pancreatitis-Associated Acute Lung Injury: Protection of Qingyi Decoction

“…Through a thorough investigation of metabolite alterations before and after illness onset, metabolomics directly reflects the disease phenotype at the functional level. Currently, metabolomic methods are frequently used in the research of ALI/ARDS and are crucial for identifying biomarkers and assessing medication effectiveness [ 7 ]. Moreover, the alterations of the lung microbiome before and after illness have been reported recently and have gained increasing attention.…”