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[PMID]: 26863118
[Au] Autor:Krezalek MA; DeFazio J; Zaborina O; Zaborin A; Alverdy JC
[Ad] Address:Department of Surgery, Center for Surgical Infection Research and Therapeutics Pritzker School of Medicine, University of Chicago, Chicago, Illinois.
[Ti] Title:The Shift of an Intestinal "Microbiome" to a "Pathobiome" Governs the Course and Outcome of Sepsis Following Surgical Injury.
[So] Source:Shock;45(5):475-82, 2016 May.
[Is] ISSN:1540-0514
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Sepsis following surgical injury remains a growing and worrisome problem following both emergent and elective surgery. Although early resuscitation efforts and prompt antibiotic therapy have improved outcomes in the first 24 to 48 h, late onset sepsis is now the most common cause of death in modern intensive care units. This time shift may be, in part, a result of prolonged exposure of the host to the stressors of critical illness which, over time, erode the health promoting intestinal microbiota and allow for virulent pathogens to predominate. Colonizing pathogens can then subvert the immune system and contribute to the deterioration of the host response. Here, we posit that novel approaches integrating the molecular, ecological, and evolutionary dynamics of the evolving gut microbiome/pathobiome during critical illness are needed to understand and prevent the late onset sepsis that develops following prolonged critical illness.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1604
[Cu] Class update date: 160416
[Lr] Last revision date:160416
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1097/SHK.0000000000000534

  2 / 96734 MEDLINE  
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[PMID]: 26717105
[Au] Autor:Young JS; Heffernan DS; Chung CS; Kettenmann ML; Young WA; Guillen VS; Cioffi WG; Ayala A
[Ad] Address:Division of Surgical Research, Department of Surgery, Warren Alpert Medical School of Brown University, Rhode Island Hospital, Providence, Rhode Island.
[Ti] Title:Effect of PD-1: PD-L1 in Invariant Natural Killer T-Cell Emigration and Chemotaxis Following Sepsis.
[So] Source:Shock;45(5):534-9, 2016 May.
[Is] ISSN:1540-0514
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Invariant natural killer T-cells (iNKT) are a subset of T-cells that play a regulatory role in sepsis. Following cecal ligation and puncture (CLP), iNKT cells emigrate from the liver and into the circulation and peritoneum in a manner dependent upon coinhibitory molecule Programmed Cell Death Receptor 1 (PD-1). We hypothesized that the effect of PD-1 on iNKT-cell emigration was dependent upon the direct PD-1:PD-L1 interaction, and that PD-1 and PD-L1 would play a role in chemotaxis and chemokine receptor expression. Adoptive transfer of Vybrant-labeled wild-type (WT) cells showed the donor iNKT cells migrated from the liver to the peritoneum following CLP, but PD-L1 deficient donor iNKT cells did not. In a chemotaxis assay, WT-iNKT cells chemotaxed to CXCL12, but PD-1 and PD-L1 deficient iNKT cells did not. Using flow cytometry to evaluate chemokine receptor expression, peritoneal iNKT expression of CXCR4 increased following CLP in the WT, PD-1, and PD-L1 deficient animals, and CXCR6 increased in the WT and PD-1 deficient animals. In conclusion here we document that the hepatic emigration of iNKT cells following CLP to the peritoneum appears dependent upon the direct PD-1:PD-L1 interaction; however, although PD-1 and PD-L1 appear to play a role in chemotaxis, this is unlikely a reflection of iNKT-cell chemokine receptor expression changes.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1604
[Cu] Class update date: 160416
[Lr] Last revision date:160416
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1097/SHK.0000000000000553

  3 / 96734 MEDLINE  
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[PMID]: 26682947
[Au] Autor:Di Caro V; Walko TD; Bola RA; Hong JD; Pang D; Hsue V; Au AK; Halstead ES; Carcillo JA; Clark RS; Aneja RK
[Ad] Address:*Department of Critical Care Medicine, University of Pittsburgh School of Medicine and Children's Hospital of Pittsburgh, Pittsburgh, Pennsylvania †University at Buffalo, State University of New York at Buffalo, Buffalo, New York ‡Department of Chemistry, Carnegie Mellon University §Departments of Critical Care Medicine and Pediatrics, University of Pittsburgh School of Medicine and Children's Hospital of Pittsburgh, Pittsburgh ||Department of Pediatrics, Division of Pediatric Critical Care Medicine, Penn State Hershey Children's Hospital, Pennsylvania State University College of Medicine, Hershey, Pennsylvania.
[Ti] Title:Plasma Mitochondrial DNA-a Novel DAMP in Pediatric Sepsis.
[So] Source:Shock;45(5):506-11, 2016 May.
[Is] ISSN:1540-0514
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Mitochondrial DNA (mtDNA) is a novel danger-associated molecular pattern that on its release into the extracellular milieu acts via toll-like receptor-9, a pattern recognition receptor of the immune system. We hypothesized that plasma mtDNA concentrations will be elevated in septic children, and these elevations are associated with an increase in the severity of illness. In a separate set of in vitro experiments, we test the hypothesis that exposing peripheral blood mononuclear cells (PBMC) to mtDNA activates the immune response and induces tumor necrosis factor (TNF) release. Children with sepsis/systemic inflammatory response syndrome or control groups were enrolled within 24 h of admission to the pediatric intensive care unit. Mitochondrial gene cytochrome c oxidase 1 (COX1) concentrations were measured by real-time quantitative PCR in the DNA extracted from plasma. PBMCs were treated with mtDNA (10 µg/mL) and supernatant TNF levels were measured. The median plasma mtDNA concentrations were significantly elevated in the septic patients as compared with the critically ill non-septic and healthy control patients [1.75E+05 (IQR 6.64E+04-3.67E+05) versus 5.73E+03 (IQR 3.90E+03-1.28E+04) and 6.64E+03 (IQR 5.22E+03-1.63E+04) copies/µL respectively]. The median concentrations of plasma mtDNA were significantly greater in patients with MOF as compared with patients without MOF (3.2E+05 (IQR 1.41E+05-1.08E+06) vs. 2.9E+04 (IQR 2.47E+04-5.43E+04) copies/µL). PBMCs treated with mtDNA demonstrated higher supernatant TNF levels as compared with control cells (6.5 ±â€Š1.8 vs. 3.5 ±â€Š0.5 pg/mL, P > 0.05). Our data suggest that plasma mtDNA is a novel danger-associated molecular pattern in pediatric sepsis and appears to be associated with MOF.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1604
[Cu] Class update date: 160416
[Lr] Last revision date:160416
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1097/SHK.0000000000000539

  4 / 96734 MEDLINE  
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[PMID]: 26767500
[Au] Autor:Yan J; Mitra A; Hu J; Cutrera JJ; Xia X; Doetschman T; Gagea M; Mishra L; Li S
[Ad] Address:Department of Pediatrics Research, The University of Texas MD Anderson Cancer Center, Houston, TX, United States....
[Ti] Title:Interleukin-30 (IL27p28) alleviates experimental sepsis by modulating cytokine profile in NKT cells.
[So] Source:J Hepatol;64(5):1128-36, 2016 May.
[Is] ISSN:1600-0641
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:BACKGROUND & AIMS: Sepsis is an acute systemic inflammatory response to infection associated with high patient mortality (28-40%). We hypothesized that interleukin (IL)-30, a novel cytokine protecting mice against liver injury resulting from inflammation, would generate a protective effect against systemic inflammation and sepsis-induced death. METHODS: Sepsis was induced by lipopolysaccharide (LPS) or cecal ligation and puncture (CLP). The inhibitory effects of IL-30 on septic inflammation and associated therapeutic effects were determined in wild-type, IL30 (p28)(-/-), IL10(-/-), and CD1d(-/-) mice. RESULTS: Mice treated with pIL30 gene therapy or recombinant IL-30 protein (rIL30) were protected from LPS-induced septic shock or CLP-induced polymicrobial sepsis and showed markedly less liver damage and lymphocyte apoptosis than control septic mice. The resulting reduction in mortality was mediated through attenuation of the systemic pro-inflammatory response and augmentation of bacterial clearance. Mice lacking IL-30 were more sensitive to LPS-induced sepsis. Natural killer-like T cells (NKT) produced much higher levels of IL-10 and lower levels of interferon-gamma and tumor necrosis factor-alpha in IL-30-treated septic mice than in control septic mice. Likewise, deficiency in IL-10 or NKT cells abolished the protective role of IL-30 against sepsis. Furthermore, IL-30 induced IL-10 production in purified and LPS-stimulated NKT cells. Blocking IL-6R or gp130 inhibited IL-30 mediated IL-10 production. CONCLUSIONS: IL-30 is important in modulating production of NKT cytokines and subsequent NKT cell-mediated immune regulation of other cells. Therefore, IL-30 has a role in prevention and treatment of sepsis via modulation of cytokine production by NKT.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1604
[Cu] Class update date: 160416
[Lr] Last revision date:160416
[Js] Journal subset:IM
[St] Status:In-Data-Review

  5 / 96734 MEDLINE  
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[PMID]: 26757165
[Au] Autor:Li D; Zou L; Feng Y; Xu G; Gong Y; Zhao G; Ouyang W; Thurman JM; Chao W
[Ad] Address:1Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA. 2Department of Anesthesia, the Third Xiangya Hospital, Xiangya School of Medicine, Changsha, China. 3Department of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, MA. 4Department of Medicine, University of Colorado School of Medicine, Aurora, CO.
[Ti] Title:Complement Factor B Production in Renal Tubular Cells and Its Role in Sodium Transporter Expression During Polymicrobial Sepsis.
[So] Source:Crit Care Med;44(5):e289-99, 2016 May.
[Is] ISSN:1530-0293
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:OBJECTIVES: Toll-like receptors and complement are two components of the innate immunity. Complement factor B is essential for the alternative pathway of complement activation. We have recently reported that complement factor B is significantly up-regulated in the kidney and may contribute to acute tubular injury in an animal model of sepsis. This study investigates the mechanisms responsible for the complement factor B up-regulation and its role in sodium transporter expression in tubular cells during sepsis. DESIGN: Animal study. SETTING: Laboratory investigation. SUBJECTS: C57BL/6 J wild-type, complement factor B, and Nfkb1 p50 mice. INTERVENTIONS: Human proximal tubular cells and mouse tubular epithelial cells were stimulated with Toll-like receptor agonists. Bay 11-7082 was used to block nuclear factor-κB pathway. Alternative pathway activation was detected by C3 zymosan deposition. Polymicrobial sepsis was created by cecal ligation and puncture. Sodium transporter gene expression was determined by quantitative reverse transcriptase-polymerase chain reaction. MEASUREMENTS AND MAIN RESULTS: The agonists for Toll-like receptor 4 (lipopolysaccharide) or Toll-like receptor 3 (polyinosinic-polycytidylic acid) induced a marked increase in complement factor B expression in human proximal tubular cells and mouse tubular epithelial cells both at gene and protein levels. The Toll-like receptor 1/2 agonist, Pam3cys, induced complement factor B production only in human proximal tubular cells, not in mouse tubular epithelial cells. The Toll-like receptor 9 ligand, CpG oligodeoxynucleotides failed to induce complement factor B production either in human proximal tubular cells or in mouse tubular epithelial cells. Lipopolysaccharide/polyinosinic-polycytidylic acid-induced complement factor B up-regulation was blocked by Bay 11-7082, a potent inhibitor of nuclear factor-κB signaling, and in mouse tubular epithelial cells deficient in p50 subunit of nuclear factor-κB. Media from the lipopolysaccharide-treated mouse tubular epithelial cell cultures contained de novo synthesized complement factor B and led to functional alternative pathway activation. In a cecal ligation and puncture model, wild-type septic mice had down-regulated expression of sodium transporters in the kidney compared with the sham. In comparison, complement factor B mice or mice treated with anti-complement factor B displayed preserved levels of Na/K ATPase-α1 following sepsis. CONCLUSIONS: 1) Toll-like receptor 3/4 activation is sufficient to induce complement factor B production via nuclear factor-κB pathway and to enhance alternative pathway activation in the kidney tubular epithelial cells. 2) Complement factor B may contribute to the down-regulation of certain sodium transporter expression during sepsis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1604
[Cu] Class update date: 160416
[Lr] Last revision date:160416
[Js] Journal subset:AIM; IM
[St] Status:In-Data-Review
[do] DOI:10.1097/CCM.0000000000001566

  6 / 96734 MEDLINE  
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[PMID]: 27076723
[Au] Autor:Ohsugi K; Kotani T; Fukuda S; Sato Y; Toyama S; Ozaki M
[Ad] Address:Department of Anesthesiology and Intensive Care Medicine, Tokyo Women's Medical University, Tokyo, Japan....
[Ti] Title:Does vasopressin improve the mortality of septic shock patients treated with high-dose NA.
[So] Source:Indian J Crit Care Med;20(3):137-40, 2016 Mar.
[Is] ISSN:0972-5229
[Cp] Country of publication:India
[La] Language:eng
[Ab] Abstract:AIM OF STUDY: In Surviving Sepsis Campaign Guidelines 2012, noradrenalin (NA) is recommended as a first choice vasopressor. Although vasopressin (VP) is recommended for the treatment of NA-resistant septic shock, the optimal parameters for its administration remain unclear. MATERIALS AND METHODS: We conducted a retrospective study to evaluate the clinical outcomes of the administration of VP to adult septic shock patients who were undergoing high-dose NA (≥0.25 µg/kg/min) therapy in our Intensive Care Unit between January 2010 and December 2013. We defined high-dose NA as a dose of >0.25 µg/kg/min, based on the definition of low-dose NA as a dose of 5-14 µg/min because the average body weight of the patients in this study was 53.0 kg. RESULTS: Among 29 patients who required the administration of high-dose NA, 18 patients received VP. Although the patient background physiological conditions and NA dose did not differ between the two groups, the survival rate of the VP-treated patients was significantly lower (33%) than that of the patients who were managed with a high-dose of NA-alone (82%) (P = 0.014). The lactate clearance did not change after the administration of VP, whereas it improved when in NA treatment alone. CONCLUSION: The results suggest that the administration of VP did not improve the mortality among septic shock patients when administered in addition to high-dose NA.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1604
[Cu] Class update date: 160416
[Lr] Last revision date:160416
[Da] Date of entry for processing:160414
[St] Status:PubMed-not-MEDLINE
[do] DOI:10.4103/0972-5229.178175

  7 / 96734 MEDLINE  
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[PMID]: 27075205
[Au] Autor:Shankar-Hari M; Ambler M; Mahalingasivam V; Jones A; Rowan K; Rubenfeld GD
[Ad] Address:Guy's and St Thomas' NHS Foundation Trust, ICU support Offices, 1st Floor, East Wing, St Thomas' Hospital, London, SE1 7EH, UK. Manu.Shankar-Hari@kcl.ac.uk....
[Ti] Title:Evidence for a causal link between sepsis and long-term mortality: a systematic review of epidemiologic studies.
[So] Source:Crit Care;20(1):101, 2016.
[Is] ISSN:1466-609X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: In addition to acute hospital mortality, sepsis is associated with higher risk of death following hospital discharge. We assessed the strength of epidemiological evidence supporting a causal link between sepsis and mortality after hospital discharge by systematically evaluating the available literature for strength of association, bias, and techniques to address confounding. METHODS: We searched Medline and Embase using the following 'mp' terms, MESH headings and combinations thereof - sepsis, septic shock, septicemia, outcome. Studies published since 1992 where one-year post-acute mortality in adult survivors of acute sepsis could be calculated were included. Two authors independently selected studies and extracted data using predefined criteria and data extraction forms to assess risk of bias, confounding, and causality. The difference in proportion between cumulative one-year mortality and acute mortality was defined as post-acute mortality. Meta-analysis was done by sepsis definition categories with post-acute mortality as the primary outcome. RESULTS: The literature search identified 11,156 records, of which 59 studies met our inclusion criteria and 43 studies reported post-acute mortality. In patients who survived an index sepsis admission, the post-acute mortality was 16.1 % (95 % CI 14.1, 18.1 %) with significant heterogeneity (p < 0.001), on random effects meta-analysis. In studies reporting non-sepsis control arm comparisons, sepsis was not consistently associated with a higher hazard ratio for post-acute mortality. The additional hazard associated with sepsis was greatest when compared to the general population. Older age, male sex, and presence of comorbidities were commonly reported independent predictors of post-acute mortality in sepsis survivors, challenging the causality relationship. Sensitivity analyses for post-acute mortality were consistent with primary analysis. CONCLUSIONS: Epidemiologic criteria for a causal relationship between sepsis and post-acute mortality were not consistently observed. Additional epidemiologic studies with recent patient level data that address the pre-illness trajectory, confounding, and varying control groups are needed to estimate sepsis-attributable additional risk and modifiable risk factors to design interventional trials.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1604
[Cu] Class update date: 160416
[Lr] Last revision date:160416
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1186/s13054-016-1276-7

  8 / 96734 MEDLINE  
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[PMID]: 26671885
[Au] Autor:Arshad M; Goller CC; Pilla D; Schoenen FJ; Seed PC
[Ad] Address:Department of Pediatrics....
[Ti] Title:Threading the Needle: Small-Molecule Targeting of a Xenobiotic Receptor to Ablate Escherichia coli Polysaccharide Capsule Expression Without Altering Antibiotic Resistance.
[So] Source:J Infect Dis;213(8):1330-9, 2016 Apr 15.
[Is] ISSN:1537-6613
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Uropathogenic Escherichia coli (UPEC), a leading cause of urinary tract and invasive infections worldwide, is rapidly acquiring multidrug resistance, hastening the need for selective new anti-infective agents. Here we demonstrate the molecular target of DU011, our previously discovered potent, nontoxic, small-molecule inhibitor of UPEC polysaccharide capsule biogenesis and virulence. METHODS: Real-time polymerase chain reaction analysis and a target-overexpression drug-suppressor screen were used to localize the putative inhibitor target. A thermal shift assay quantified interactions between the target protein and the inhibitor, and a novel DNase protection assay measured chemical inhibition of protein-DNA interactions. Virulence of a regulatory target mutant was assessed in a murine sepsis model. RESULTS: MprA, a MarR family transcriptional repressor, was identified as the putative target of the DU011 inhibitor. Thermal shift measurements indicated the formation of a stable DU011-MprA complex, and DU011 abrogated MprA binding to its DNA promoter site. Knockout of mprA had effects similar to that of DU011 treatment of wild-type bacteria: a loss of encapsulation and complete attenuation in a murine sepsis model, without any negative change in antibiotic resistance. CONCLUSIONS: MprA regulates UPEC polysaccharide encapsulation, is essential for UPEC virulence, and can be targeted without inducing antibiotic resistance.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1603
[Cu] Class update date: 160416
[Lr] Last revision date:160416
[Js] Journal subset:AIM; IM
[St] Status:In-Data-Review
[do] DOI:10.1093/infdis/jiv584

  9 / 96734 MEDLINE  
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[PMID]: 26111103
[Au] Autor:Kaplan D; Casper TC; Elliott CG; Men S; Pendleton RC; Kraiss LW; Weyrich AS; Grissom CK; Zimmerman GA; Rondina MT
[Ti] Title:VTE Incidence and Risk Factors in Patients With Severe Sepsis and Septic Shock.
[So] Source:Chest;148(5):1224-30, 2015 Nov.
[Is] ISSN:1931-3543
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Prospective studies on the incidence of VTE during severe sepsis and septic shock remain absent, hindering efficacy assessments regarding VTE prevention strategies in sepsis. METHODS: We prospectively studied 113 consecutively enrolled patients in the ICU with severe sepsis and septic shock at three hospitals. All patients provided informed consent. VTE thromboprophylaxis was recorded for all patients. Patients underwent ultrasonography and were followed for VTE prior to ICU discharge. All-cause 28-day mortality was recorded. Variables from univariate analyses that were associated with VTE (including central venous catheter [CVC] insertion, age, length of stay, and mechanical ventilation) were included in a multivariable logistic regression analysis using backward stepwise elimination to determine VTE predictors. RESULTS: Mean APACHE (Acute Physiology and Chronic Health Evaluation) II score was 18.2 ± 7.0, and age was 50 ± 18 years. Despite all patients receiving guideline-recommended thromboprophylaxis, the incidence of VTE was 37.2% (95% CI, 28.3-46.8). Most VTE events were clinically significant (defined as pulmonary embolism, proximal DVT, and/or symptomatic distal DVT) and associated with an increased length of stay (18.2 ± 9.9 days vs 13.4 ± 11.5 days, P < .05). Mortality was higher in patients with acute VTE but did not reach statistical significance. Insertion of a CVC and longer mechanical ventilation duration were significant VTE risk factors. VTE incidence did not differ by thromboprophylaxis type. CONCLUSIONS: To our knowledge this is the first multicenter prospective study to identify a high incidence of VTE in patients with severe sepsis and septic shock, despite the use of universal, guideline-recommended thromboprophylaxis. Our findings suggest that the systemic inflammatory milieu of sepsis may uniquely predispose patients with sepsis to VTE. More effective VTE prevention strategies are necessary in patients with sepsis. TRIAL REGISTRY: ClinicalTrials.gov; No.: NCT02353910; URL: www.clinicaltrials.gov.
[Mh] MeSH terms primary: Risk Assessment/methods
Sepsis/complications
Shock, Septic/complications
Venous Thromboembolism/epidemiology
[Mh] MeSH terms secundary: Female
Humans
Incidence
Male
Middle Aged
Prospective Studies
Risk Factors
Survival Rate/trends
Utah/epidemiology
Venous Thromboembolism/etiology
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Em] Entry month:1602
[Cu] Class update date: 160416
[Lr] Last revision date:160416
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:151103
[St] Status:MEDLINE
[do] DOI:10.1378/chest.15-0287

  10 / 96734 MEDLINE  
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[PMID]: 25887317
[Au] Autor:Franks Z; Carlisle M; Rondina MT
[Ad] Address:Program in Molecular Medicine, Salt Lake City, 84112, , Utah, USA. zfranks@u2m2.utah.edu....
[Ti] Title:Current challenges in understanding immune cell functions during septic syndromes.
[So] Source:BMC Immunol;16:11, 2015.
[Is] ISSN:1471-2172
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Sepsis is a dynamic infectious disease syndrome characterized by dysregulated inflammatory responses. RESULTS: Despite decades of research, improvements in the treatment of sepsis have been modest. These limited advances are likely due, in part, to multiple factors, including substantial heterogeneity in septic syndromes, significant knowledge gaps in our understanding of how immune cells function in sepsis, and limitations in animal models that accurately recapitulate the human septic milieu. The goal of this brief review is to describe current challenges in understanding immune cell functions during sepsis. We also provide a framework to guide scientists and clinicians in research and patient care as they strive to better understand dysregulated cell responses during sepsis. CONCLUSIONS: Additional, well-designed translational studies in sepsis are critical for enhancing our understanding of the role of immune cells in sepsis.
[Mh] MeSH terms primary: Immunity, Cellular
Systemic Inflammatory Response Syndrome/immunology
[Mh] MeSH terms secundary: Animals
Disease Models, Animal
Humans
Inflammation
Patient Care
Translational Medical Research
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Em] Entry month:1601
[Cu] Class update date: 160416
[Lr] Last revision date:160416
[Js] Journal subset:IM
[Da] Date of entry for processing:150418
[St] Status:MEDLINE
[do] DOI:10.1186/s12865-015-0073-4


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