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  • 1
    Online Resource
    Online Resource
    Alterations of B Cells in Immunosuppressive Phase of Septic Shock Patients*
    Ovid Technologies (Wolters Kluwer Health) ; 2020
    In:  Critical Care Medicine Vol. 48, No. 6 ( 2020-06), p. 815-821
    Details
    In: Critical Care Medicine, Ovid Technologies (Wolters Kluwer Health), Vol. 48, No. 6 ( 2020-06), p. 815-821
    Abstract: Septic shock is a subset of sepsis related to acute circulatory failure characterized by severe immunosuppression and high mortality. Current knowledge about B-cell status in the immunosuppressive phase of septic shock is sparse. The aim of this study was to investigate the alterations of B Cells in the immunosuppressive phase of septic shock. Design: Prospective cohort study. Setting: Adult ICUs at a university hospital. Patients: Adult septic shock patients without any documented immune comorbidity. Interventions: None. Measurements and Main Results: The absolute counts of lymphocytes and B cells of 81 patients and 13 healthy controls, and serum immunoglobulin levels of 64 patients and 10 healthy controls were determined by clinical laboratory. The percentages and counts of B-cell subsets of 33 patients and 10 healthy controls and the immunoglobulin M expression on B-cell subsets of 20 patients and five healthy controls were quantified by flow cytometry. Immunoglobulin levels produced by B cells after stimulation in vitro of 20 patients and five healthy controls were tested by enzyme-linked immunosorbent assay. Redistribution and selective depletion of B-cell subsets in septic shock patients were discovered, and a decrease in immunoglobulin M levels was associated with a reduction in resting memory B-cell counts. These alterations were more pronounced in nonsurvivors compared with survivors. Additionally, receiver operating characteristic curve analysis showed that the data of B-cell subsets had the best predictive value for mortality risk. Conclusions: Severe B-cell abnormalities are present in the immunosuppressive phase of septic shock and are associated with prognosis.
    Type of Medium: Online Resource
    ISSN: 0090-3493
    URL: Article
    DOI: 10.1097/CCM.0000000000004309
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2020
    detail.hit.zdb_id: 2034247-0
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  • 2
    Online Resource
    Online Resource
    The Absence of Gasdermin D Reduces Nuclear Autophagy in a Cecal Ligation and Puncture-Induced Sepsis-Associated Encephalopathy Mouse Model
    MDPI AG ; 2023
    In:  Brain Sciences Vol. 13, No. 3 ( 2023-03-11), p. 478-
    Details
    In: Brain Sciences, MDPI AG, Vol. 13, No. 3 ( 2023-03-11), p. 478-
    Abstract: Sepsis-associated encephalopathy (SAE) is a common complication of sepsis, which is a life-threatening condition resulting from a dysregulated host response to infection. Pyroptosis, a pro-inflammatory mode of lytic cell death mediated by GSDMD (Gasdermin D), is involved in the pathogenesis of SAE. While autophagy has been extensively studied in SAE, the role of nuclear autophagy is not yet well understood. In this study, we aimed to investigate the involvement of pyroptosis and neural nuclear autophagy in the pathogenesis of SAE. We analyzed a CLP (cecal ligation and puncture)-induced SAE model in wild-type and GSDMD−/− mice to gain insights into the underlying mechanisms. Here, we show that in sepsis, neural nuclear autophagy is extremely activated, and nuclear LaminB decreases and is accompanied by an increase in the ratio of LC3BII/I. These effects can be reversed in GSDMD−/− mice. The behavioral outcomes of septic wild-type mice are impaired by the evidence from the novel object recognition test (NORT) and open field test (OFT), but are improved in septic GSDMD−/− mice. In conclusion, our study demonstrates the activation of neural nuclear autophagy in SAE. The absence of GSDMD inhibits nuclear autophagy and improves the behavioral outcomes of SAE.
    Type of Medium: Online Resource
    ISSN: 2076-3425
    URL: Article
    DOI: 10.3390/brainsci13030478
    Language: English
    Publisher: MDPI AG
    Publication Date: 2023
    detail.hit.zdb_id: 2651993-8
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  • 3
    Online Resource
    Online Resource
    Inhibition of Ferroptosis Attenuates Glutamate Excitotoxicity and Nuclear Autophagy in a CLP Septic Mouse Model
    Ovid Technologies (Wolters Kluwer Health) ; 2022
    In:  Shock Vol. 57, No. 5 ( 2022-05), p. 694-702
    Details
    In: Shock, Ovid Technologies (Wolters Kluwer Health), Vol. 57, No. 5 ( 2022-05), p. 694-702
    Abstract: Sepsis-associated encephalopathy (SAE) often manifests in severe diffuse cerebral dysfunction due to an aberrant systemic immune response to infection. The underlying pathophysiology of SAE is not entirely understood but is likely a multifactorial process that involves disruption in cell death mechanism. Ferroptosis is a novel form of programmed cell death characterized by iron accumulation and lipid peroxidation, leading to inflammatory cascade and glutamate release. We hypothesized that ferroptosis is involved in the glutamate-mediated excitotoxic neuron injury during the uncontrolled neural inflammatory process of SAE. Inhibiting ferroptosis with ferrostatin-1 (Fer-1) could alleviate glutamate excitotoxicity and reduce neuron death of SAE, potentially improving prognosis. We found that in the cecal ligation and puncture (CLP) sepsis model, ferroptosis occurred increasingly in the cerebrum, characterized by glutathione-dependent antioxidant enzyme glutathione peroxidase 4 (GPX4) inactivation, transferrin upregulation, mitochondria shrink and malondialdehyde (MDA) increased. Fer-1 treatment downregulated cerebral ferroptosis and alleviated glutamate excitotoxicity via dampening system xc-(SXC) and glutamate receptor N-methyl-D-asperate receptor subunit 2. Combined with an observed reduction in calcium transporter PLCG and PLCB activation, these processes ultimately protected the integrities of synapses and neurons during SAE. Fer-1 treatment also rescued sepsis-induced nuclear autophagy and improved the behaviors of tail suspension test and novel object recognition test in septic mice. Conclusively, our results suggested that inhibition of ferroptosis could attenuate glutamate excitotoxicity and SAE outcomes.
    Type of Medium: Online Resource
    ISSN: 1073-2322 , 1540-0514
    URL: Article
    DOI: 10.1097/SHK.0000000000001893
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2022
    detail.hit.zdb_id: 2011863-6
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  • 4
    Online Resource
    Online Resource
    Early plasma monocyte chemoattractant protein 1 predicts the development of sepsis in trauma patients : A prospective observational study
    Ovid Technologies (Wolters Kluwer Health) ; 2018
    In:  Medicine Vol. 97, No. 14 ( 2018-04), p. e0356-
    Details
    In: Medicine, Ovid Technologies (Wolters Kluwer Health), Vol. 97, No. 14 ( 2018-04), p. e0356-
    Type of Medium: Online Resource
    ISSN: 0025-7974
    URL: Article
    DOI: 10.1097/MD.0000000000010356
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2018
    detail.hit.zdb_id: 2049818-4
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  • 5
    Online Resource
    Online Resource
    Table_1.docx
    Frontiers Media SA ; 2021
    In:  Frontiers in Immunology Vol. 11 ( 2021-1-8)
    Details
    In: Frontiers in Immunology, Frontiers Media SA, Vol. 11 ( 2021-1-8)
    Abstract: Severe trauma is believed to disrupt the homeostasis of the immune system, and lead to dramatic changes in the circulating immune-cell count (ICC). The latter fluctuates widely over time. Knowledge about the relationship between these dramatic changes and dynamic fluctuations and the late prognosis of trauma patients is sparse. We investigated the relationship between the trajectory of alterations in the circulating ICC within 7 days in severe-trauma patients and subsequent sepsis and mortality. Methods A retrospective analysis of 917 patients with an Injury Severity Score ≥16 was undertaken. The absolute neutrophil, lymphocyte, and monocyte counts (ANC, ALC, and AMC, respectively) on days 1, 3, and 7 (D1, D3, and D7, respectively) after trauma, and whether sepsis or death occurred within 60 days, were recorded. As the disordered circulating ICCs fluctuated widely, their time-varying slopes (D3/D1 and D7/D3) were calculated. Patients were divided into “sepsis” and “non-sepsis” groups, as well as “alive” and “death” groups. Comparative studies were conducted between every two groups. Univariate and multivariate logistic regression analyses were used to identify variables related to the risk of sepsis and mortality. Receiver operating characteristic curves were plotted to assess the predictive value of various risk factors. Results More severe trauma caused more pronounced increases in the ANC and slower recovery of the ALC within 7 days. The ALC (D3), ANC (D7), ALC (D3/D1), and ANC (D7/D3) were independent risk factors for sepsis. The ALC (D3), ALC (D7), AMC (D7), and ALC (D3/D1) were independent risk factors for mortality. A combination of the ALC (D3) and ALC (D3/D1) exerted a good predictive value for sepsis and death. Conclusions The trajectory of alterations in the circulating ICC in the early stage after trauma is related to subsequent sepsis and mortality.
    Type of Medium: Online Resource
    ISSN: 1664-3224
    URL: Article
    URL: Article
    DOI: 10.3389/fimmu.2020.603353
    DOI: 10.3389/fimmu.2020.603353.s001
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2021
    detail.hit.zdb_id: 2606827-8
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  • 6
    Online Resource
    Online Resource
    Extension domain of amyloid processor protein inhibits amyloidogenic cleavage and balances neural activity in a traumatic brain injury mouse model
    Wiley ; 2023
    In:  CNS Neuroscience & Therapeutics
    Details
    In: CNS Neuroscience & Therapeutics, Wiley
    Abstract: Mechanisms underlying cognitive dysfunction following traumatic brain injury (TBI) partially due to abnormal amyloid processor protein (APP) cleavage and neural hyperactivity. Binding of the extension domain of APP (ExD17) to the GABAbR1 receptor results in reduced neural activity, which might play a role in the mechanisms of cognitive dysfunction caused by TBI. Methods Stretch‐induced injury was utilized to establish a cell injury model in HT22 cells. The TBI model was created by striking the exposed brain tissue with a free‐falling weight. Topical or intraperitoneal administration of ExD17 was performed. Cell viability was assessed through a cell counting kit‐8 assay, while intracellular Ca 2+ was measured using Fluo‐4. Western blotting was used to investigate the expression of APP amyloidogenic cleavage proteins, GABAbR1, phospholipase C (PLC), PLCB3, and synaptic proteins. ELISA was performed to analyze the levels of Aβ42. Seizures were assessed using electroencephalography (EEG). Behaviors were evaluated through the novel object recognition test, open field test, elevated plus maze test, and nest‐building test. Results ExD17 improved cell viability and reduced intracellular calcium in the cell injury model. The treatment also suppressed the increased expression of APP amyloidogenic cleavage proteins and Aβ42 in both cell injury and TBI models. ExD17 treatment reversed the abnormal expression of GABAbR1, GRIA2, p‐PLCG1/PLCG1 ratio, and p‐PLCB3/PLCB3 ratio. In addition, ExD17 treatment reduced neural activity, seizure events, and their duration in TBI. Intraperitoneal injection of ExD17 improved behavioral outcomes in the TBI mouse model. Conclusions ExD17 treatment results in a reduction of amyloidogenic APP cleavage and neuroexcitotoxicity, ultimately leading to an improvement in the behavioral deficits observed in TBI mice.
    Type of Medium: Online Resource
    ISSN: 1755-5930 , 1755-5949
    URL: Article
    DOI: 10.1111/cns.14402
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 2423467-9
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  • 7
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    Online Resource
    Alpinetin Attenuates Persistent Inflammation, Immune Suppression, and Catabolism Syndrome in a Septic Mouse Model
    Hindawi Limited ; 2021
    In:  Journal of Immunology Research Vol. 2021 ( 2021-7-5), p. 1-9
    Details
    In: Journal of Immunology Research, Hindawi Limited, Vol. 2021 ( 2021-7-5), p. 1-9
    Abstract: Patients who survive the acute phase of sepsis can progress to persistent inflammation, immunosuppression, and catabolism syndrome (PICS), which usually results in extended recovery periods and multiple complications. Alpinetin is a flavonoid isolated from Alpinia katsumadai Hayata that has been demonstrated to have anti-inflammatory, antibacterial, and antioxidant activities. The aim of this study was to investigate whether the administration of alpinetin could attenuate PICS in a septic mouse model. Mice were randomly divided into four groups: the (1) sham-operated group, (2) sham+alpinetin (1 mg/kg intravenously infused for once per day after sham operation), (3) cecal ligation and puncture (CLP), and (4) CLP+alpinetin (50 mg/kg intravenously infused for once per day after CLP). Eight days after sham operation or CLP surgery, mice were euthanized for subsequent examination. Alpinetin significantly improved the survival of septic mice. Also, it attenuated the CLP-induced persistent inflammation, immunosuppression, and catabolism syndrome. The level of plasma proinflammatory cytokines and apoptosis of T lymphocytes were obviously decreased by alpinetin as well. Moreover, oxidative stress in the organs was compelling lower in the alpinetin-treated CLP mice. In this clinically relevant model of sepsis, alpinetin ameliorates CLP-induced organ dysfunction and improves the likelihood of survival, possibly through suppressing the inflammatory response, oxidative stress, and apoptosis. These findings suggested that alpinetin could be a potential novel therapeutic approach to prevent sepsis-induced PICS.
    Type of Medium: Online Resource
    ISSN: 2314-7156 , 2314-8861
    URL: Article
    DOI: 10.1155/2021/9998517
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2021
    detail.hit.zdb_id: 2817541-4
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  • 8
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    Online Resource
    Caspase-1-Dependent Pyroptosis of Peripheral Blood Mononuclear Cells Is Associated with the Severity and Mortality of Septic Patients
    Hindawi Limited ; 2020
    In:  BioMed Research International Vol. 2020 ( 2020-02-29), p. 1-8
    Details
    In: BioMed Research International, Hindawi Limited, Vol. 2020 ( 2020-02-29), p. 1-8
    Abstract: Purpose . Pyroptosis has been known to play a vital role in the inflammation process which was induced by infection, injury, or inflammatory disease. The present study was aimed at evaluating the percentage of peripheral blood mononuclear cell (PBMC) pyroptosis in septic patients and assessing the correlation of PBMC pyroptosis with the severity and the mortality of septic patients. Methods . 128 trauma-induced patients with sepsis were enrolled in this prospective cohort study. Blood samples were collected, and PBMC pyroptosis was measured by flow cytometry within 24 hours after sepsis was diagnosed. Results . Percentage of PBMC pyroptosis was positively correlated with the acute physiology and chronic health evaluation (APACHE) II score and sequential organ failure assessment (SOFA) score (all P 〈 0.01 ). The area under the curve (AUC) for the percentage of PBMC pyroptosis on a receiver operating characteristic curve was 0.79 (95% confidence interval (CI), 0.68–0.90). A Cox proportional hazard model identified an association between an increased percentage of PBMC pyroptosis ( 〉 14.17%) and increased risk of the 28-day mortality (hazard ratio = 1.234 , 95% CI, 1.014–1.502). Conclusion . The percentage of PBMC pyroptosis increases in septic patients, and the increased percentage of PBMC pyroptosis is associated with the severity of sepsis and the 28-day mortality of patients with sepsis.
    Type of Medium: Online Resource
    ISSN: 2314-6133 , 2314-6141
    URL: Article
    DOI: 10.1155/2020/9152140
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2020
    detail.hit.zdb_id: 2698540-8
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  • 9
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    Online Resource
    GPA Peptide Attenuates Sepsis-Induced Acute Lung Injury in Mice via Inhibiting Oxidative Stress and Pyroptosis of Alveolar Macrophage
    Hindawi Limited ; 2021
    In:  Oxidative Medicine and Cellular Longevity Vol. 2021 ( 2021-12-28), p. 1-12
    Details
    In: Oxidative Medicine and Cellular Longevity, Hindawi Limited, Vol. 2021 ( 2021-12-28), p. 1-12
    Abstract: Acute lung injury (ALI) has been known to be a devastating form of respiratory infection and an important contributor to mortality in intensive care, due to its lacking of effective treatment. Inflammation, oxidative stress, and pyroptosis are associated with multiple kinds of inflammatory diseases such as ALI. It is commonly accepted that Gly-Pro-Ala (GPA) peptide regulates oxidative stress and pyroptosis in different kinds of inflammatory diseases. Our study is aimed at exploring the regulatory function and protective effects of GPA peptides on ALI. In the current study, the cecal ligation and puncture (CLP) technique was used to evoke sepsis in mice, and GPA peptide was administered intraperitoneally with different concentrations (50, 100, and 150 mg/kg) after CLP. Histopathological changes and the ratio of wet-to-dry in lung were recorded and analyzed. We also investigated the level of oxidative stress, inflammation, and pyroptosis. Results showed that GPA peptide significantly ameliorated CLP-stimulated lung tissue injury, impeded proinflammatory cytokine release, and reduced inflammatory cell infiltration. Additionally, GPA peptide suppressed oxidative stress and caspase-1-dependent pyroptosis in alveolar macrophages. Furthermore, our study showed that the GPA peptide prevents alveolar macrophage from undergoing pyroptosis by attenuating ROS. In conclusion, results demonstrated that GPA peptide has protective effects in CLP-stimulated ALI by inhibiting oxidative stress as well as pyroptosis of alveolar macrophage.
    Type of Medium: Online Resource
    ISSN: 1942-0994 , 1942-0900
    URL: Article
    DOI: 10.1155/2021/5589472
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2021
    detail.hit.zdb_id: 2455981-7
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  • 10
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    Lessons Learned Comparing Immune System Alterations of Bacterial Sepsis and SARS-CoV-2 Sepsis
    Frontiers Media SA ; 2020
    In:  Frontiers in Immunology Vol. 11 ( 2020-11-30)
    Details
    In: Frontiers in Immunology, Frontiers Media SA, Vol. 11 ( 2020-11-30)
    Abstract: Bacterial sepsis has been used as a prototype to understand the pathogenesis of severe coronavirus disease 2019 (COVID-19). In addition, some management programs for critically ill COVID-19 patients are also based on experience with bacterial sepsis. However, some differences may exist between these two types of sepsis. Methods This retrospective study investigated whether there are differences in the immune system status of these two types of sepsis. A total of 64 bacterial sepsis patients and 43 patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) sepsis were included in this study. Demographic data were obtained from medical records. Laboratory results within 24 h after the diagnosis of sepsis were provided by the clinical laboratory. Results The results of blood routine (neutrophil, lymphocyte, and monocyte counts), infection biomarkers (C-reactive protein, ferritin, and procalcitonin levels), lymphocyte subset counts (total T lymphocyte, CD4+ T cell, CD8+ T cell, B cell, and NK cell counts), and lymphocyte subset functions (the proportions of PMA/ionomycin-stimulated IFN-γ positive cells in CD4+, CD8+ T cells, and NK cells) were similar in bacterial sepsis patients and SARS-CoV-2 sepsis patients. Cytokine storm was milder, and immunoglobulin and complement protein levels were higher in SARS-CoV-2 sepsis patients. Conclusions There are both similarities and differences in the immune system status of bacterial sepsis and SARS-CoV-2 sepsis. Our findings do not support blocking the cytokine storm or supplementing immunoglobulins in SARS-CoV-2 sepsis, at least in the early stages of the disease. Treatments for overactivation of the complement system and lymphocyte depletion may be worth exploring further.
    Type of Medium: Online Resource
    ISSN: 1664-3224
    URL: Article
    DOI: 10.3389/fimmu.2020.598404
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2020
    detail.hit.zdb_id: 2606827-8
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