Liver bacterial clearance following hepatic artery ligation and portacaval shunt

Katz, Schmuel; Jimenez, M. A.; Lehmkuhler, William E.; Grosfeld, Jay L.

doi:10.1016/0022-4804(91)90105-u

Cited by 37 publications

(15 citation statements)

References 13 publications

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“…Histological data revealed inflammatory hepatic and pulmonary damage in AP mice, which is consistent with the persistence of bacteria, as the liver is the major site of bacterial clearance (22,47) and pulmonary dysfunction is the complication most frequently observed after intra-abdominal sepsis (24,37). Although pulmonary infections in patients are usually a consequence of infections caused by nosocomial pathogens, in some cases this type of complication may arise secondary to hematologic dissemination from remote foci of infection.…”

Section: Discussionsupporting

confidence: 53%

Model of Polymicrobial Peritonitis That Induces the Proinflammatory and Immunosuppressive Phases of Sepsis

et al. 2011

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Severe sepsis is associated with early release of inflammatory mediators that contribute to the morbidity and mortality observed during the first stages of this syndrome. Although sepsis is a deadly, acute disease, high mortality rates have been observed in patients displaying evidence of sepsis-induced immune deactivation. Although the contribution of experimental models to the knowledge of pathophysiological and therapeutic aspects of human sepsis is undeniable, most of the current studies using animal models have focused on the acute, proinflammatory phase. We developed a murine model that reproduces the early acute phases but also the long-term consequences of human sepsis. We induced polymicrobial acute peritonitis (AP) by establishing a surgical connection between the cecum and the peritoneum, allowing the exit of intestinal bacteria. Using this model, we observed an acute phase with high mortality, leukopenia, increased interleukin-6 levels, bacteremia, and neutrophil activation. A peak of leukocytosis on day 9 or 10 revealed the persistence of the infection within the lung and liver, with inflammatory hepatic damage being shown by histological examination. Long-term (20 days) derangements in both innate and adaptive immune responses were found, as demonstrated by impaired systemic tumor necrosis factor alpha production in response to an inflammatory stimulus; a decreased primary humoral immune response and T cell proliferation, associated with an increased number of myeloid suppressor cells (Gr-1 ؉ CD11b ؉ ) in the spleen; and a low clearance capacity. This model provides a good approach to attempt novel therapeutic interventions directed to augmenting host immunity during late sepsis.Local inflammatory mechanisms triggered by an infection are usually enough to eradicate the pathogen. However, if the infection is not contained, the pathogen, its toxins, and diverse mediators of the host are released to the circulation, producing a systemic inflammatory response syndrome that can cause severe sepsis or septic shock (8). Sepsis is usually treated in intensive care units (ICUs), and about 30% of the patients with severe sepsis die; this percentage rises to 50 to 70% if septic shock, the main cause of mortality in the ICU, develops (46).As death by septic shock has been associated with an early excessive inflammatory response, most of the treatment strategies have been designed to block the inflammatory mediators involved in this phenomenon. This theory is based on animal models where the administration of large amounts of bacteria or lipopolysaccharide (LPS), a major component of the outer membrane of Gram-negative bacteria, generates a cytokine storm and where the blockade of these molecules increases the survival of animals (11). Nevertheless, clinical trials designed to neutralize inflammatory mediators have failed (45). The sepsis syndrome is not restricted to the activation of the inflammatory response, as compensatory anti-inflammatory mechanisms are also triggered, usually leading to immunosuppressio...

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Section: Discussionsupporting

confidence: 53%

Model of Polymicrobial Peritonitis That Induces the Proinflammatory and Immunosuppressive Phases of Sepsis

et al. 2011

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“…In experimental models impairment of Kupffer cells function resulted in the lower ability in clearing bacteria from the bloodstream and preventing uncontrolled bacteremia, especially when it originates from gut translocation. 19,20 In another animal model, a structural damage due to septal and sinusoidal fibrosis compromised the immune filter activity of the liver and promoted the occurrence of infections, mainly BSI and SBP. 15 Moreover, the liver is responsible for the production of complement proteins which act in the regulation and effector phase of adaptive immune response.…”

Section: Pathophysiology Of Bsis In Patients With Liver Cirrhosis: Inmentioning

confidence: 99%

Bloodstream infections in patients with liver cirrhosis

et al. 2016

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Bloodstream infections are a serious complication in patients with liver cirrhosis. Dysregulated intestinal bacterial translocation is the predominant pathophysiological mechanism of infections in this setting. For this reason enteric Gram-negative bacteria are commonly encountered as the first etiological cause of infection. However, through the years, the improvement in the management of cirrhosis, the recourse to invasive procedures and the global spread of multidrug resistant pathogens have importantly changed the current epidemiology. Bloodstream infections in cirrhotic patients are characterized by high mortality rate and complications including metastatic infections, infective endocarditis, and endotipsitis (or transjugular intrahepatic portosystemic shunt-related infection). For this reason early identification of patients at risk for mortality and appropriated therapeutic management is mandatory. Liver cirrhosis can significantly change the pharmacokinetic behavior of antimicrobials. In fact hypoproteinaemia, ascitis and third space expansion and impairment of renal function can be translated in an unpredictable drug exposure.

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“…In contrast, KCs are key cells involved in scavenging bacteria and endotoxin. The liver harbors approximately 80% of all macrophages in the human body as resident KCs [25]. Indeed, endotoxin clearance was impaired in the case of underlying liver disease, which could explain a higher susceptibility of the host to infection [26].…”

Section: Pathophysiological Aspectsmentioning

confidence: 99%

Clinical review: The liver in sepsis

et al. 2012

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During sepsis, the liver plays a key role. It is implicated in the host response, participating in the clearance of the infectious agents/products. Sepsis also induces liver damage through hemodynamic alterations or through direct or indirect assault on the hepatocytes or through both. Accordingly, liver dysfunction induced by sepsis is recognized as one of the components that contribute to the severity of the disease. Nevertheless, the incidence of liver dysfunction remains imprecise, probably because current diagnostic tools are lacking, notably those that can detect the early liver insult. In this review, we discuss the epidemiology, diagnostic tools, and impact on outcome as well as the pathophysiological aspects, including the cellular events and clinical picture leading to liver dysfunction. Finally, therapeutic considerations with regard to the weakness of the pertinent specific approach are examined.

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Liver bacterial clearance following hepatic artery ligation and portacaval shunt

Cited by 37 publications

References 13 publications

Model of Polymicrobial Peritonitis That Induces the Proinflammatory and Immunosuppressive Phases of Sepsis

Model of Polymicrobial Peritonitis That Induces the Proinflammatory and Immunosuppressive Phases of Sepsis

Bloodstream infections in patients with liver cirrhosis

Clinical review: The liver in sepsis

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