Case Report: Multiple Organ Failure Caused by Hemorrhagic Fever with Renal Syndrome.

Hemorrhagic fever with renal syndrome (HFRS), a natural epidemic disease caused by hantavirus (HV), is one of the viral diseases that pose a major threat to our health. Considering the increasing number of atypical-onset cases reported in some countries, it is important to be familiar with the symptoms of HFRS and the signs of HV infection. This report describes the case of a 55-year-old man with complaints of fever, vomiting, and diarrhea. His symptoms showed no significant improvement after routine anti-infective, antipyretic, and other symptomatic supportive treatments administered at a local clinic. During these treatments, the patient had progressive oliguria; after 3 days, he also developed multiple organ failures, such as the liver and kidney, and was examined for positive serum IgM antibodies to hemorrhagic fever during treatment at our hospital. The patient was finally diagnosed with HFRS followed by multiple organ failure. After antiviral therapy, including ribavirin, piperacillin, and tazobactam, continuous renal replacement therapy, fluid metabolism adjustment, and related supportive therapy were administered, which improved his liver and kidney function. He was discharged on the 25th day after hospitalization. It is difficult to manage patients who develop multiple organ failure after HFRS. Moreover, this condition is rare in clinical settings, with fever being the initial indication. For diseases with unknown origin such as refractory fever and diarrhea, it is crucial to differentiate them from common pathogenic infection and HV infections to provide timely treatment that improves the prognosis of patients.

Taraxasterol Inhibits Hyperactivation of Macrophages to Alleviate the Sepsis-induced Inflammatory Response of ARDS Rats.

To explore the effect and mechanism of taraxasterol on sepsis-induced acute respiratory distress syndrome (ARDS). Twenty-four male SD rats were randomly divided into four groups: the control group, model (lipopolysaccharide, LPS) group, lipopolysaccharide+taraxasterol (LPS + TXL) group, and lipopolysaccharide+ulinastatin (LPS + UTI) group. The model of sepsis-induced ARDS was established by intraperitoneal injection of LPS. The lung water content of the rats in each group was determined by the dry/wet ratio. Pathology of rat lung tissue was observed through H&E staining. Wright staining was applied to count the number of neutrophils, macrophages, and total cells. ELISA was utilized to measure the levels of the inflammatory factors TNF-α, IL-1ß, and IL-6 in bronchoalveolar lavage fluid (BALF). Biochemical detection was adopted to check the levels of myeloperoxidase (MPO), superoxide dismutase (SOD) and catalase (CAT) in lung tissue. Western blotting was performed to check the protein expression of IL-12, iNOS, Arg-1, and Mrc1 in lung tissue. Compared with the LPS group, both taraxasterol and ulinastatin significantly decreased lung tissue water content, improved lung tissue injury, reduced the number of neutrophils, macrophages and total cells, and decreased the level of inflammatory factors. In addition, taraxasterol and ulinastatin also reduced the content of MPO and the expression of IL-12 and iNOS and increased the activity of SOD and CAT as well as the protein expression of Arg-1 and Mrc1. Taraxasterol can suppress macrophage M1 polarization to alleviate the inflammatory response and oxidative stress, thereby treating sepsis-induced ARDS.

Protectin D1 protects against lipopolysaccharide-induced acute lung injury through inhibition of neutrophil infiltration and the formation of neutrophil extracellular traps in lung tissue.

Protectin D1 (PD1), a DHA-derived lipid mediator, has recently been shown to possess anti-inflammatory and pro-resolving properties. To date, little is known about the effect of PD1 on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice. The aim of the present study was to investigate the therapeutic effects of PD1 on LPS-induced ALI and its potential mechanisms of action. ALI was induced via an intraperitoneal injection of LPS, where PD1 (2 ng/mouse) was administered intravenously 30 min after LPS challenge. Mice were sacrificed 24 h after modeling. Lung histopathological changes were assessed using hematoxylin and eosin staining and myeloperoxidase (MPO) activity was tested using immunohistochemistry. Tumor necrosis-α and interleukin-6 levels in the bronchoalveolar lavage fluid (BALF) and serum were measured using ELISA. To detect neutrophil extracellular traps produced by infiltrated neutrophils in the lung tissue, immunofluorescence staining was performed using anti-MPO and anti-histone H3 antibodies. The results indicated that PD1 significantly attenuated histological damage and neutrophil infiltration in lung tissue, reduced the lung wet/dry weight ratio, protein concentration and proinflammatory cytokine levels in BALF and decreased proinflammatory cytokine levels in serum. Moreover, neutrophil citrullinated histone H3 (CitH3) expression was also reduced after PD1 administration. In conclusion, PD1 attenuated LPS-induced ALI in mice via inhibition of neutrophil extracellular trap formation in lung tissue. Therefore, PD1 administration may serve to be a new strategy for treating ALI.

Curcumin protects the pancreas from acute pancreatitis via the mitogen­activated protein kinase signaling pathway.

Curcumin has been demonstrated to reduce markers of inflammation during acute pancreatitis (AP). However, the underlying mechanisms of the protective effects of curcumin are unknown. In the present study the effects of curcumin in an AP animal model and cell models was examined and the underlying mechanisms were investigated. An AP animal model was established by injection of 5% sodium taurocholate into the biliopancreatic duct of rats, and the cell model was established by treatment with 0.5 nM cerulein with an optimal concentration of lipopolysaccharide in AR42J rat pancreatic cancer cells. Amylase activity and arterial blood gas composition were assessed by automatic biochemical and blood gas analyzers. Pathological alteration of the pancreas was determined by hematoxylin and eosin staining. Interleukin (IL­6), tumor necrosis factor (TNF)­α and C­reactive protein (CRP) levels were measured by ELISA. Cell viability was determined by Cell Counting Kit­8 and protein expression levels were assessed by western blotting. Curcumin reduced the ascites volume after 12 and 24 h, the weight of pancreas after 12, 24 and 36 h of surgery, but also attenuated injury to the pancreas. Serum expression levels of TNF­α and CRP were reduced by curcumin. In addition, curcumin decreased the cell viability, amylase activity and the phosphorylation of p38 in AR42J cells, but did not affect the intracellular levels of IL­6 and TNF­α. Curcumin may lower the severity and inflammatory response via the mitogen­activated protein kinase­signaling pathway, to some extent. However, future studies are required to fully understand the protective effects of curcumin on AP.