Intestinal barrier damage, systemic inflammatory response syndrome, and acute lung injury: A troublesome trio for acute pancreatitis

• Published in: Biomedicine & pharmacotherapy 2020-12, Vol.132, p.110770-110770, Article 110770
• Main Authors: Ge, Peng, Luo, Yalan, Okoye, Chukwuemeka Samuel, Chen, Haiyang, Liu, Jiayue, Zhang, Guixin, Xu, Caiming, Chen, Hailong
• Format: Article
• Language: English
• Subjects: Acute Lung Injury - etiology; Acute Lung Injury - physiopathology; Acute Lung Injury - prevention & control; Animals; Damage-associated molecular patterns; Endotoxins - metabolism; Humans; Intestinal barrier; Intestines - pathology; Lung injury; Multiple Organ Failure - etiology; Multiple Organ Failure - physiopathology; Pancreatitis - complications; Pancreatitis - physiopathology; Pancreatitis, Acute Necrotizing - etiology; Pancreatitis, Acute Necrotizing - pathology; Pathogen-associated molecular patterns; Severe acute pancreatitis; Systemic inflammatory response syndrome; Systemic Inflammatory Response Syndrome - etiology; Systemic Inflammatory Response Syndrome - physiopathology
• ISSN: 0753-3322; 1950-6007
• DOI: 10.1016/j.biopha.2020.110770

[Display omitted] •Severe acute pancreatitis involves a troublesome trio: intestinal barrier damage, inflammation, and acute lung injury.•Damage-associated molecular patterns, activated trypsin, and hemodynamic changes promote intestinal barrier damage.•Pathogen-associated molecular patterns and microRNAs amplify inflammatory response and aggravate the lung injury. Severe acute pancreatitis (SAP), a serious inflammatory disease of the pancreas, can easily lead to systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndromes (MODS). Acute lung injury (ALI) is one of the most serious complications of SAP. However, the specific pathogenesis of SAP-associated ALI is not fully understood. Crosstalk and multi-mechanisms involving pancreatic necrosis, bacteremia, intestinal barrier failure, activation of inflammatory cascades and diffuse alveolar damage is the main reason for the unclear pathological mechanism of SAP-associated ALI. According to previous research on SAP-associated ALI in our laboratory and theories put forward by other scholars, we propose that the complex pattern of SAP-associated ALI is based on the “pancreas-intestine-inflammation/endotoxin-lung (P-I-I/E–L) pathway”. In this review, we mainly concentrated on the specific details of the “P-I-I/E–L pathway” and the potential treatments or preventive measures for SAP-associated ALI.