scholarly journals Postoperative Rise of Circulating Mitochondrial DNA Is Associated with Inflammatory Response in Patients following Pancreaticoduodenectomy

2021 ◽  
pp. 1-7
Author(s):  
Niv Pencovich ◽  
Nadav Nevo ◽  
Roi Weiser ◽  
Ekaterina Bonder ◽  
Yoel Bogoch ◽  
...  
Keyword(s):  
Mitochondrial Dna ◽  
Inflammatory Response ◽  
Delayed Gastric Emptying ◽  
Clinical Course ◽  
Severe Trauma ◽  
Postoperative Fever ◽  
Postoperative Course ◽  
Cell Counts ◽  
White Blood Cell Counts ◽  
The Relationship

<b><i>Introduction:</i></b> Accumulation of plasma mitochondrial DNA (mtDNA) following severe trauma has been shown to correlate with the development of systemic inflammatory response syndrome (SIRS) and may predict mortality. Our objective was to investigate the relationship between levels of circulatory mtDNA following pancreaticoduodenectomy (PD) and the postoperative course. <b><i>Methods:</i></b> Levels of plasma mtDNA were assessed by real-time PCR of the mitochondrial genes <i>ND1</i> and <i>COX3</i> in 23 consecutive patients who underwent PD 1 day prior to surgery, within 8 h after surgery, and on postoperative day (POD)1 and POD5. The abundance of mtDNA was assessed relative to preoperative levels and in relation to parameters reflecting the postoperative clinical course. <b><i>Results:</i></b> When pooled for all patients, the circulating mtDNA levels were significantly increased after surgery. However, while a significant (at least &#x3e;2-fold and up to &#x3e;20-fold) rise was noted in 11 patients, no change in mtDNA levels was noted in the other 12 following surgery. Postoperative rise in circulating mtDNA was associated with an increased rate of postoperative fever until day 5, decreased hemoglobin and albumin levels, and increased white blood cell counts. These patients also suffered from increased rates of delayed gastric emptying. No significant differences were demonstrated in other postoperative parameters. <b><i>Conclusion:</i></b> Circulating mtDNA surge is associated with an inflammatory response following PD and may potentially be used as an early marker for postoperative course. Studies of larger patient cohorts are warranted.

scholarly journals Cell-free nuclear, but not mitochondrial, DNA concentrations correlate with the early host inflammatory response after severe trauma

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Julie A. Stortz ◽  
Russell B. Hawkins ◽  
David C. Holden ◽  
Steven L. Raymond ◽  
Zhongkai Wang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Mitochondrial Dna ◽  
Inflammatory Response ◽  
Nuclear Dna ◽  
Severe Trauma ◽  
Organ Injury ◽  
Trauma Patients ◽  
Chronic Critical Illness ◽  
Molecular Patterns ◽  
The Relationship

Abstract Severe blunt trauma is associated with an early ‘genomic storm’ which causes simultaneous up- and down-regulation of host protective immunity. Excessive inflammation can lead to organ injury. In the absence of infection, the inflammatory response is presumably driven by release of endogenous alarmins called danger-associated molecular patterns (DAMPs), which initiate immune responses through pattern-recognition receptors (PRR). Here we examined the relationship between concentrations of cell-free (cf) nuclear DNA (ncDNA) and mitochondrial DNA (mtDNA) within 24 hours post trauma with circulating leukocyte transcriptomics and plasma IL-6 concentrations, as well as the patients’ clinical trajectories. In 104 patients enrolled from two level-1 trauma centers, ncDNA and mtDNA concentrations were increased within 24 hours of severe trauma, but only ncDNA concentrations correlated with leukocyte gene expression and outcomes. Surprisingly, ncDNA, not mtDNA concentrations, were significantly elevated in trauma patients who developed chronic critical illness versus rapid clinical recovery. Plasma IL-6 and leukocyte transcriptomics were better predictors of outcomes than cfDNA levels. Although mtDNA and ncDNA are significantly increased in the immediate post-trauma period, the dramatic inflammatory and gene expression changes seen after severe trauma are only weakly correlated with ncDNA concentrations, and more importantly, mtDNA concentrations are not associated with adverse clinical trajectories.

scholarly journals Leukogram Profile and Clinical Status invivaxandfalciparumMalaria Patients from Colombia

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Alberto Tobón-Castaño ◽  
Esteban Mesa-Echeverry ◽  
Andrés Felipe Miranda-Arboleda
Keyword(s):  
Hematological Parameters ◽  
Clinical Status ◽  
Clinical Complications ◽  
Cell Counts ◽  
Leukocyte Counts ◽  
White Blood Cell Counts ◽  
Hematologic Profile ◽  
Monitoring Treatment ◽  
The Relationship ◽  
Hematological Alterations

Introduction. Hematological alterations are frequent in malaria patients; the relationship between alterations in white blood cell counts and clinical status in malaria is not well understood. In Colombia, with low endemicity and unstable transmission for malaria, with malariavivaxpredominance, the hematologic profile in malaria patients is not well characterized. The aim of this study was to characterize the leukogram in malaria patients and to analyze its alterations in relation to the clinical status.Methods. 888 leukogram profiles of malaria patients from different Colombian regions were studied: 556 withP. falciparuminfection (62.6%), 313 withP. vivaxinfection (35.2%), and 19 with mixed infection by these species (2.1%).Results. Leukocyte counts at diagnosis were within normal range in 79% of patients and 18% had leucopenia; the most frequent alteration was lymphopenia (54%) followed by monocytosis (11%); the differential granulocyte count in 298 patients revealed eosinophilia (15%) and high basophil counts (8%). Leukocytosis, eosinopenia, and neutrophilia were associated with clinical complications. The utility of changes in leukocyte counts as markers of severity should be explored in depth. A better understanding of these hematological parameters will allow their use in prompt diagnosis of malaria complications and monitoring treatment response.

scholarly journals Ionizing radiation induces iNOS-mediated epithelial dysfunction in the absence of an inflammatory response

2000 ◽  
Vol 278 (2) ◽  
pp. G243-G250 ◽  
Author(s):  
Samara L. Freeman ◽  
Wallace K. MacNaughton
Keyword(s):  
Ionizing Radiation ◽  
Inflammatory Response ◽  
Electrical Field Stimulation ◽  
Chloride Secretion ◽  
Inos Mrna ◽  
Myeloperoxidase Activity ◽  
Mrna Levels ◽  
Cell Counts ◽  
White Blood Cell Counts ◽  
Deficient Mice

Ionizing radiation induces intestinal epithelial hyporesponsiveness to secretagogues through an unknown mechanism. We investigated the role of the inducible isoform of nitric oxide (NO) synthase (iNOS)-derived NO in radiation-induced hyporesponsiveness. C57BL/6 mice were sham treated or exposed to 10-Gy γ-radiation and were studied 3 days later. Tissues were mounted in Ussing-type diffusion chambers to assess chloride secretion in response to electrical field stimulation (EFS) and forskolin (10 μM). Transport studies were also repeated in iNOS-deficient mice. White blood cell counts were significantly lower in irradiated mice, and there was no inflammatory response as shown by myeloperoxidase activity and histological assessment. iNOS mRNA levels and nitrate/nitrite concentrations were significantly elevated in irradiated colons. iNOS immunoreactivity localized to the epithelium. Colons from irradiated wild-type, but not iNOS-deficient, mice exhibited a significant reduction in the responsiveness of the tissue to EFS and forskolin. The hyporesponsiveness was reversed byl- N6-(1-iminoethyl)lysine, 1400W, and dexamethasone treatments. iNOS-derived NO mediates colonic hyporesponsiveness 3 days after irradiation in the mouse in the absence of an inflammatory response.

scholarly journals The Trajectory of Alterations in Immune-Cell Counts in Severe-Trauma Patients Is Related to the Later Occurrence of Sepsis and Mortality: Retrospective Study of 917 Cases

2021 ◽  
Vol 11 ◽  
Author(s):  
Xijie Dong ◽  
Chuntao Wang ◽  
Xinghua Liu ◽  
Xiangjun Bai ◽  
Zhanfei Li
Keyword(s):  
Risk Factors ◽  
Predictive Value ◽  
Injury Severity ◽  
Immune Cell ◽  
Early Stage ◽  
Severe Trauma ◽  
Trauma Patients ◽  
Cell Counts ◽  
Independent Risk Factors ◽  
The Relationship

BackgroundSevere 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.MethodsA 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.ResultsMore 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.ConclusionsThe trajectory of alterations in the circulating ICC in the early stage after trauma is related to subsequent sepsis and mortality.

An Alternative Elastase-mediated Degradation of Fibrinogen and Fibrin Observed in a Patient with Herpes Simplex Encephalitis and Pneumonia

1996 ◽  
Vol 76 (02) ◽  
pp. 184-186 ◽  
Author(s):  
Kenji lijima ◽  
Fumiyo Murakami ◽  
Yasushi Horie ◽  
Katsumi Nakamura ◽  
Shiro Ikawa ◽  
...  
Keyword(s):  
Herpes Simplex ◽  
Blood Cell ◽  
White Blood Cell ◽  
Herpes Simplex Encephalitis ◽  
Pmn Elastase ◽  
Cell Counts ◽  
Blood Cell Counts ◽  
Sds Page ◽  
White Blood Cell Counts ◽  
Pmn Élastase

SummaryA 74-year-old female developed pneumonia following herpes simplex encephalitis. Her white blood cell counts reached 28,400/μl, about 90% of which consisted of granulocytes. The polymorphonuclear (PMN) elastase/α1-arantitrypsin complex levels increased and reached the maximum of 5,019 ng/ml, indicating the release of a large amount of elastase derived from the granulocytes. The mechanism of PMN elastase release was most likely to be granulocyte destruction associated with phagocytosis. The cleavage of fibrinogen and fibrin by PMN elastase, independent of plasmin, was indicated by the presence of the fragments in immunoprecipitated plasma from the patient corresponding to elastase-induced FDP D and DD fragments and the absence of fragments corresponding to plasmin-induced FDP D and DD fragments on SDS-PAGE. These findings suggested that the large amount of PMN elastase released from the excessive numbers of granulocytes in this patient with herpes simplex encephalitis and pneumonia, induced the cleavage of fibrinogen and fibrin without the participation of plasmin.

COVID-19 in children: Pathogenesis and current status

2020 ◽  
Author(s):  
Lawrence Frenkel ◽  
Fernando Gomez ◽  
Joseph A Bellanti
Keyword(s):  
Respiratory Disease ◽  
Respiratory Symptoms ◽  
Distress Syndrome ◽  
Clinical Course ◽  
Current Status ◽  
Current Evidence ◽  
Initial Description ◽  
Relationship Of ◽  
Inflammatory Syndrome ◽  
The Relationship

Background: Since its initial description in December 2019 in Wuhan, China, coronavirus disease 2019 (COVID-19) has rapidly progressed into a worldwide pandemic, which has affected millions of lives. Unlike the disease in adults, the vast majority of children with COVID-19 have mild symptoms and are largely spared from severe respiratory disease. However, thereare children who have significant respiratory disease, and some may develop a hyperinflammatory response similar to thatseen in adults with COVID-19 and in children with Kawasaki disease (KD), which has been termed multisystem inflammatory syndrome in children (MIS-C).Objective: The purpose of this report was to examine the current evidence that supports the etiopathogenesis of COVID-19 in children and the relationship of COVID-19 with KD and MIS-C as a basis for a better understanding of the clinical course, diagnosis, and management of these clinically perplexing conditions.Results: The pathogenesis of COVID-19 is carried out in two distinct but overlapping phases of COVID-19: the first triggered by the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) itself and the second by the host immune response. Children with KD have fewer of the previously described COVID-19–associated KD features with less prominent acute respiratory distress syndrome and shock than children with MIS-C.Conclusion: COVID-19 in adults usually includes severe respiratory symptoms and pathology, with a high mortality. Ithas become apparent that children are infected as easily as adults but are more often asymptomatic and have milder diseasebecause of their immature immune systems. Although children are largely spared from severe respiratory disease, they canpresent with a SARS-CoV-2–associated MIS-C similar to KD.

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