Clinical Characteristics and Risk Factors of Surgical Site Infection in Patients with Open Abdomen with Fistula Undergoing the Abdominal Wall Reconstruction Utilizing Biological Mesh: A Single-Center Retrospective Study.

This study aimed to evaluate the clinical characteristics and identify risk factors for surgical site infection (SSI) following abdominal wall reconstruction using biological mesh. A retrospective analysis was conducted on patients with open abdomen (OA) with fistula who underwent abdominal wall reconstruction with biological mesh at Jinling Hospital between January 2010 and August 2023. Patients were divided into SSI and non-SSI groups, and their perioperative data were compared to identify potential risk factors.

Itaconate inhibits SYK through alkylation and suppresses inflammation against hvKP induced intestinal dysbiosis.

Hypervirulent Klebsiella pneumoniae (hvKP) is a highly lethal opportunistic pathogen that elicits more severe inflammatory responses compared to classical Klebsiella pneumoniae (cKP). In this study, we investigated the interaction between hvKP infection and the anti-inflammatory immune response gene 1 (IRG1)-itaconate axis. Firstly, we demonstrated the activation of the IRG1-itaconate axis induced by hvKP, with a dependency on SYK signaling rather than STING.

Precise Orchestration of Gasdermins' Pore-Forming Function by Posttranslational Modifications in Health and Disease.

Gasdermins (GSDMs) serve as pivotal executors of pyroptosis and play crucial roles in host defence, cytokine secretion, innate immunity, and cancer. However, excessive or inappropriate GSDMs activation is invariably accompanied by exaggerated inflammation and results in tissue damage. In contrast, deficient or impaired activation of GSDMs often fails to promptly eliminate pathogens, leading to the increasing severity of infections.

RIPK3-MLKL necroptotic signalling amplifies STING pathway and exacerbates lethal sepsis.

Backgrounds: The stimulator of interferon genes (STING) is an important driver in various inflammatory diseases.

Methods And Results: Here, we have demonstrated that inhibition of RIPK3 and MLKL dampens STING signaling, indicating that necroptosis may be involved in sustaining STING signaling. Furthermore, RIPK3 knockout in HT-29 cells significantly suppressed STING signaling.

Circulating mitochondrial DNA-triggered autophagy dysfunction via STING underlies sepsis-related acute lung injury.

The STING pathway and its induction of autophagy initiate a potent immune defense response upon the recognition of pathogenic DNA. However, this protective response is minimal, as STING activation worsens organ damage, and abnormal autophagy is observed during progressive sepsis. Whether and how the STING pathway affects autophagic flux during sepsis-induced acute lung injury (sALI) are currently unknown.

mtDNA-STING pathway promotes necroptosis-dependent enterocyte injury in intestinal ischemia reperfusion.

Intestinal ischemia reperfusion (I/R) injury is the important pathogenesis for acute intestinal barrier disruption. The STING signaling is associated with gut homeostasis and barrier integrity. However, the biological function and regulation of STING signaling in intestinal I/R injury are not yet fully understood.