Abstract
Patients with liver diseases are at high risk for the development of acute respiratory distress syndrome (ARDS). The liver is an important organ that regulates a complex network of mediators and modulates organ interactions during inflammatory disorders. Liver function is increasingly recognized as a critical determinant of the pathogenesis and resolution of ARDS, significantly influencing the prognosis of these patients. The liver plays a central role in the synthesis of proteins, metabolism of toxins and drugs, and in the modulation of immunity and host defense. However, the tools for assessing liver function are limited in the clinical setting, and patients with liver diseases are frequently excluded from clinical studies of ARDS. Therefore, the mechanisms by which the liver participates in the pathogenesis of acute lung injury are not totally understood. Several functions of the liver, including endotoxin and bacterial clearance, release and clearance of pro-inflammatory cytokines and eicosanoids, and synthesis of acute-phase proteins can modulate lung injury in the setting of sepsis and other severe inflammatory diseases. In this review, we summarized clinical and experimental support for the notion that the liver critically regulates systemic and pulmonary responses following inflammatory insults. Although promoting inflammation can be detrimental in the context of acute lung injury, the liver response to an inflammatory insult is also pro-defense and pro-survival. A better understanding of the liver–lung axis will provide valuable insights into new diagnostic targets and therapeutic strategies for clinical intervention in patients with or at risk for ARDS.
Highlights
Acute respiratory distress syndrome (ARDS) is a severe respiratory failure, due to noncardiogenic pulmonary edema [1, 2], associated with a hospital mortality between 35% and 46% [1, 3, 4]
It has been observed that established ARDS during acute liver allograft rejection is resolved within hours of Despite the well-recognized liver–lung interaction in the pathogenesis of ARDS, its underlying mechanisms and its effects on the outcome of these patients have been barely studied due to several reasons
Liver dysfunction is common in critical care patients The frequency of liver damage in critical illness has considerably increased over the last decades [23, 33,34,35], reaching up to 20% of Intensive care unit (ICU) patients in some series and elevating their morbi-mortality [33, 34, 36]
Summary
Acute respiratory distress syndrome (ARDS) is a severe respiratory failure, due to noncardiogenic pulmonary edema [1, 2], associated with a hospital mortality between 35% and 46% [1, 3, 4]. Activation of these hepatic mononuclear cells enhances the production and release of inflammatory mediators, such as IL-1, IL-6, TNF-α, platelet-activating factor (PAF), and leukotrienes, into the systemic circulation [61], where they play an important role in the lung–liver interaction [18, 31, 51, 61,62,63,64] These liverderived inflammatory mediators alter lung structure function early in acute inflammatory diseases (such as sepsis) and contribute to some extent to lung damage upon activation of pulmonary alveolar macrophages The potential role of circulating EVs in mediating liver–lung communication in the context of ARDS is not currently understood, representing an interesting topic for further investigation
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