Sepsis-induced acute liver injury (SALI), a manifestation of sepsis multi-organ dysfunction syndrome, is associated with poor prognosis and high mortality. The diversity and plasticity of liver macrophage subpopulations explain their different functional responses in different liver diseases. Kupffer macrophages, liver capsular macrophages, and monocyte-derived macrophages are involved in pathogen recognition and clearance and in the regulation of inflammatory responses, exacerbating the progression of SALI through different pathways of pyroptosis, ferroptosis, and autophagy. Concurrently, they play an important role in maintaining hepatic homeostasis and in the injury and repair processes of SALI. Other macrophages are recruited to diseased tissues under pathological conditions and are polarized into various phenotypes (mainly M1 and M2 types) under the influence of signaling molecules, transcription factors, and metabolic reprogramming, thereby exerting different roles and functions. This review provides an overview of the immune role of macrophages in SALI and discusses the multiple roles of macrophages in liver injury and repair to provide a reference for future studies.

Sepsis is a syndrome that causes dysfunction of multiple organs due to the host's uncontrolled response to infection and is a significant contributor to morbidity and mortality in intensive care units worldwide. Surviving patients are often left with acute brain injury and long-term cognitive impairment, known as sepsis-associated encephalopathy (SAE). In recent years, researchers have directed their focus towards the pathogenesis of SAE. However, due to the complexity of its development, there remains a lack of effective treatment measures that arise as a serious issue affecting the prognosis of sepsis patients. Further research on the possible causes of SAE aims to provide clinicians with potential therapeutic targets and help develop targeted prevention strategies. This paper aims to review recent research on the pathogenesis of SAE, in order to enhance our understanding of this syndrome.

Background: Songling virus (SGLV) within the genus Orthonairovirus, family Nairoviridae, is an emerging tick-borne virus associated with human febrile illness. However, no rapid detection method for SGLV has been established. Methods: In this study, four primer sets targeting the nucleocapsid protein gene of SGLV were designed for use in the LAMP assay and evaluated to identify the optimal primer set. Recombinant plasmids were constructed and utilized for assessing the sensitivity of the assay. Tacheng tick virus 1 (TcTV-1)-, Beiji nairovirus (BJNV)-, Yezo virus (YEZV)-, severe fever with thrombocytopenia syndrome virus (SFTSV)-, and tick-borne encephalitis virus (TBEV)-positive tick samples were utilized to assess the specificity. Field-collected ticks were also evaluated as biological specimens to validate the assay. Results: A SGLV-specific LAMP assay was established with a detection limit of 1 × 10^–2 copies/μl and could be visually confirmed by a color change from purple to blue in SGLV-positive samples. No cross-reactivity was observed in the detection of TcTV-1, BJNV, YEZV, SFTSV, and TBEV using the LAMP assay. In addition to the detection of the same seven high-copy numbers of SGLV as the SYBR Green quantitative RT-PCR assay within a reduced timeframe, the developed LAMP method also effectively identified an additional sample with a low copy number in the field-collected tick samples. Conclusions: We successfully developed a sensitive, specific, and cost-effective visual method for the rapid detection of SGLV using the LAMP assay, which can be applied in pathogenesis and epidemiological surveillance studies of SGLV. Graphical

Sepsis is a critical condition characterized by a dysregulated immune response to infection, leading to widespread inflammation, tissue damage, organ failure, and often death. It is a leading cause of morbidity and mortality, particularly in intensive care units, due to its complex pathophysiology involving immune dysregulation, coagulation abnormalities, and metabolic disturbances. Pyogenic liver abscess (PLA) is a significant cause, especially in developing countries where its incidence is rising. PLA, an infectious liver disease, can lead to sepsis, termed sepsis secondary to PLA (SLA). This study aimed to identify key genes and non-coding RNAs involved in the pathogenesis and treatment of SLA. We performed RNA sequencing on peripheral blood samples from healthy individuals, SLA patients, and SLA patients after seven days of therapy. Integrated bioinformatics analysis identified 4549 differentially expressed (DE) mRNAs, 9808 DE lncRNAs, 467 DE circRNAs, and 292 DE miRNAs between SLA patients and healthy controls. Additionally, 3199 mRNAs, 6018 lncRNAs, 161 circRNAs, and 132 miRNAs were differentially expressed between SLA patients before and after seven days of therapy. DE mRNAs in both comparisons were associated with immune responses; DE lncRNAs were linked to the B cell receptor signaling pathway and osteoclast differentiation; DE circRNAs were connected to Chagas disease and the B cell receptor signaling pathway; and DE miRNAs were implicated in the MAPK and estrogen signaling pathways. We constructed lncRNA/circRNA-miRNA-mRNA networks to explore regulatory relationships, validating 16 ceRNAs through RT-PCR. These findings provide new insights into SLA pathogenesis and treatment, potentially guiding the development of novel therapies.