EVALUATION OF BACTERIAL TRANSLOCATION IN THE PATHOGENESIS OF MODS IN SEPSIS
EVALUATION OF BACTERIAL TRANSLOCATION IN THE PATHOGENESIS OF MODS IN SEPSIS
批准号:
7604894
负责人:
ALIX ASHARE
金额:
$0.13万
依托单位:
依托单位国家:
美国
项目类别:
财政年份:
2007
资助国家:
美国
项目状态:
已结题
起止时间:
2007-03-01 至 2007-09-16
关键词:
Acute Liver FailureBacteremiaBacteriaBacterial TranslocationBlood CirculationCirrhosisComplicationComputer Retrieval of Information on Scientific Projects DatabaseDefense MechanismsDepressed moodEndotoxinsEvaluationFunctional disorderFundingGastrointestinal tract structureGrantHepaticImmunityIncidenceInjuryInstitutionLeadLeukocyte ChemotaxisLiverLiver diseasesOrganPathogenesisPatientsPopulationResearchResearch PersonnelResourcesReticuloendothelial SystemRiskSepsisSourceT-LymphocyteUnited States National Institutes of Healthmortalitytheories
中文摘要
这个子项目是许多研究子项目中的一个
由NIH/NCRR资助的中心赠款提供的资源。子项目和
研究者(PI)可能从另一个NIH来源获得了主要资金,
因此可在其他CRISP条目中表示。所列机构为
研究中心,而研究中心不一定是研究者所在的机构。
健康的肝脏是细菌和内毒素从胃肠道进入体循环的有效屏障。 然而,在严重的肝脏疾病如肝硬化中,受损的防御机制导致菌血症的发生率增加。 菌血症是肝硬化的常见并发症,估计发生率为4.5- 8.8%。 菌血症患者的死亡率很高。 急性肝衰竭患者也有菌血症的风险增加。 该患者人群中菌血症的病理生理学尚不完全清楚。 已经假设了几种机制,包括受损的T细胞免疫和异常的白细胞趋化性。 然而,最令人信服的理论是,肝网状内皮系统功能低下易使这些患者发生菌血症。 这些研究者推测肝损伤与清除细菌能力下降有关。 此外,在脓毒症诱导的肝损伤的情况下,他们假设细菌移位将导致继发性菌血症并增加器官损伤。
英文摘要
This subproject is one of many research subprojects utilizing the
resources provided by a Center grant funded by NIH/NCRR. The subproject and
investigator (PI) may have received primary funding from another NIH source,
and thus could be represented in other CRISP entries. The institution listed is
for the Center, which is not necessarily the institution for the investigator.
The healthy liver serves as an effective barrier to the passage of bacteria and endotoxin from the GI tract into the systemic circulation. However, in severe liver disease such as cirrhosis, impaired defense mechanisms lead to an increased incidence of bacteremia. Bacteremia is a common complication of cirrhosis, with an estimated incidence of 4.5-8.8%. Bacteremia in cirrhotic subjects is associated with a high mortality. Patients with acute liver failure also have an increased risk of bacteremia. The pathophysiology of bacteremia in this patient population is not entirely clear. Several mechanisms have been postulated including impaired T-cell immunity and abnormal leukocyte chemotaxis. However, the most compelling theory is that depressed hepatic reticuloendothelial system function predisposes these patients to bacteremia. These investigators hypothosize that liver injury is associated with decreased ability to clear bacteria. Further, in the setting of sepsis-induced liver injury, they hypothesize that bacterial translocation will result in secondary bacteremia and increase organ injury.
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海外基金