Intraabdominal Infection: A Review

McClean, Karen L.; Sheehan, G; Harding, G. K. M.

doi:10.1093/clinids/19.1.100

Cited by 116 publications

(88 citation statements)

References 164 publications

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“…It is therefore necessary to aggressively manage the immediate postoperative resuscitation in the ICU with fluids combined with inotropic and vasopressor support. Progressive multiple organ dysfunction with death may follow if this cycle is not controlled [29][30][31][32][33].…”

Section: Tertiary Peritonitismentioning

confidence: 99%

Management of Peritonitis in the Critically Ill Patient

Ordóñez

Puyana

2006

Surgical Clinics of North America

111

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Section: Tertiary Peritonitismentioning

confidence: 99%

Management of Peritonitis in the Critically Ill Patient

Ordóñez

Puyana

2006

Surgical Clinics of North America

111

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“…Abdominal sepsis can be associated with multiple organ failure (37). To determine the role of endogenous IL-10 herein, we measured biochemical parameters of liver damage (ASAT, ALAT), pancreas damage (amylase), and renal failure (creatinine) at 24 h after i.p.…”

Section: Il-10 ϫ/ϫ Mice Have More Severe Multiple Organ Damagementioning

confidence: 99%

IL-10-Deficient Mice Demonstrate Multiple Organ Failure and Increased Mortality DuringEscherichia coliPeritonitis Despite an Accelerated Bacterial Clearance

Sewnath¹,

Olszyna

Birjmohun³

et al. 2001

The Journal of Immunology

151

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To determine the role of endogenous IL-10 in local antibacterial host defense and in the development of a systemic inflammatory response syndrome during abdominal sepsis, IL-10 gene-deficient (IL-10−/−) and wild-type (IL-10+/+) mice received an i.p. injection with Escherichia coli. Peritonitis was associated with a bacterial dose-dependent increase in IL-10 concentrations in peritoneal fluid and plasma. The recovery of E. coli from the peritoneal fluid, blood, and lungs was diminished in IL-10−/− mice, indicating that endogenous IL-10 impaired bacterial clearance. Despite a lower bacterial load, IL-10−/− mice had higher concentrations of TNF, macrophage inflammatory protein-2 and keratinocyte in peritoneal fluid and plasma, and demonstrated more severe multiple organ damage as indicated by clinical chemistry and histopathology. Furthermore, IL-10−/− mice showed an increased neutrophil recruitment to the peritoneal cavity. To examine the role of elevated TNF levels in the altered host response in IL-10−/− mice, the effect of a neutralizing anti-TNF mAb was determined. Anti-TNF did not influence the clearance of E. coli in either IL-10+/+ or IL-10−/− mice. Furthermore, anti-TNF did not affect leukocyte influx in the peritoneal fluid, multiple organ damage, or survival in IL-10+/+ mice. In IL-10−/− mice, anti-TNF partially attenuated neutrophil recruitment and multiple organ damage, and prevented the increased lethality. These data suggest that although endogenous IL-10 facilitates the outgrowth and dissemination of bacteria during E. coli peritonitis, it protects mice from lethality by attenuating the development of a systemic inflammatory response syndrome by a mechanism that involves inhibition of TNF release.

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“…Peritonitis is the second most common cause of sepsis (2), with Escherichia coli as one of the major pathogens involved (3). Because E. coli peritonitis is a life-threatening disease, an immediate and adequate host defense is necessary to contain and kill the pathogen.…”

mentioning

confidence: 99%

Matrix Metalloproteinase-9 Deficiency Impairs Host Defense against Abdominal Sepsis

Renckens¹,

Roelofs²,

Florquin³

et al. 2006

The Journal of Immunology

109

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Matrix metalloproteinase (MMP)-9 is involved in extracellular matrix degradation and leukocyte migration. To determine the role of MMP-9 in the innate immune response to peritonitis, MMP-9 gene-deficient (MMP-9−/−) and normal wild-type mice were i.p. infected with Escherichia coli. MMP-9 mRNA and pro-MMP-9 protein levels increased rapidly upon induction of peritonitis. Although MMP-9−/− neutrophils showed a normal phagocytosis of E. coli in vitro, MMP-9−/− mice displayed a reduced resistance against E. coli peritonitis, as indicated by an enhanced bacterial outgrowth in the peritoneal cavity and increased dissemination of the infection. Furthermore, the cytokine response to LPS was not influenced by MMP-9 deficiency. However, during E. coli peritonitis, MMP-9−/− mice showed much higher peritoneal chemokine and cytokine levels compared with wild-type mice. Despite the increased local chemokine concentrations, MMP-9−/− mice displayed a diminished recruitment of leukocytes to the site of infection, indicating that cellular migration was impaired. Moreover, MMP-9−/− mice developed more severe distant organ damage during infection. These data suggest that MMP-9 is an essential component of an effective host response to E. coli peritonitis.

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Intraabdominal Infection: A Review

Cited by 116 publications

References 164 publications

Management of Peritonitis in the Critically Ill Patient

Management of Peritonitis in the Critically Ill Patient

IL-10-Deficient Mice Demonstrate Multiple Organ Failure and Increased Mortality DuringEscherichia coliPeritonitis Despite an Accelerated Bacterial Clearance

Matrix Metalloproteinase-9 Deficiency Impairs Host Defense against Abdominal Sepsis

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