Bacteria, toxins, and the peritoneum

T, Hau

doi:10.1007/bf01664869

Cited by 50 publications

(34 citation statements)

References 85 publications

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“…Of the numerous aerobic bacteria iso- lated from peritoneal infections, E. coli emerges as the predominate pathogen in over 60% of cases (18,24). E. coli seems particularly adept at making the transition from the environment of the gastrointestinal tract to that of the peritoneum.…”

Section: Discussionmentioning

confidence: 99%

“…Most intraperitoneal infections result from a breach in the integrity of the gastrointestinal system, allowing the introduction of both aerobic and anaerobic bacteria into the peritoneum. Escherichia coli emerges as the predominate pathogen in 60% of intraperitoneal infections (18,24). The characteristics that allow E. coli to adapt to the peritoneal environment and establish infection are not clearly understood.…”

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confidence: 99%

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Contribution of Escherichia coli Alpha-Hemolysin to Bacterial Virulence and to Intraperitoneal Alterations in Peritonitis

et al. 2000

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Alpha-hemolysin (Hly) is a common exotoxin produced by Escherichia coli that enhances virulence in a number of clinical infections. The addition of hemolysin production to laboratory bacterial strains is known to increase the lethality of E. coli peritonitis. However, the mechanisms involved have not been determined and the contribution of hemolysin to the alterations in the host intraperitoneal environment and the leukocyte response is not known. Utilizing a rat peritonitis model, we show that wild-type hemolytic E. coli strains have a significant competitive advantage over nonhemolytic strains within the peritoneum. To examine the specific contribution of Hly to E. coli-induced virulence and alterations within the peritoneum, a mixed peritonitis model of E. coli, Bacteroides fragilis, and sterile fecal adjuvant was used. Three transformed E. coli strains were utilized: one strongly secretes active hemolysin (WAF 270), a second secretes active hemolysin but a reduced amount (WAF 260), and the third does not produce hemolysin (WAF 108). After an equal inoculum of each of the three strains, WAF 270 produced a markedly increased lethality and an increased recovery of both E. coli and B. fragilis from the host relative to the other strains. Changes in the intraperitoneal pH, degree of erythrocyte lysis, and recruitment and viability of leukocytes within the peritoneum following the induction of peritonitis differed significantly between the strongly hemolytic and nonhemolytic strains. Induction of peritonitis with WAF 270 caused a pronounced decrease in intraperitoneal pH, lysis of most of the intraperitoneal erythrocytes, and a marked decrease in recoverable viable leukocytes compared to WAF 108. Thus, hemolysin production by E. coli within the peritoneum may alter not only the host's ability to control the hemolytic strain itself but also other organisms.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Contribution of Escherichia coli Alpha-Hemolysin to Bacterial Virulence and to Intraperitoneal Alterations in Peritonitis

et al. 2000

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“…Although the overall mortality of sepsis is ϳ35% (4), abdominal sepsis is associated with mortality rates up to 80% (5). Although different bacteria have been identified as causative organisms in peritonitis, Escherichia coli remains one of the most common pathogens (up to 60%) in intraperitoneal infections (6,7). Surgical and supportive treatment of peritonitis often do not suffice, and an increase in resistance to many antibiotic compounds has developed (8,9), especially among the Enterobacteriaceae, where some isolates have acquired extended spectrum ␤-lactamases (10,11).…”

Section: Il-10-deficient Mice Demonstrate Multiple Organ Failure and mentioning

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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“…Bacteria via the lymphatic system can easily pass into the systemic circulation and cause bacteriemia and septicemia [19] . Another possible pathway of septicemia is bacterial translocation defined as the passage of viable bacteria from the gastrointestinal tract through the epithelial mucosa into the lamina propria and then to the mesenteric lymph node and possibly other organs [20] , which may be important in immunosuppressive hosts.…”

Section: Discussionmentioning

confidence: 99%

Effects of granulocyte-colony stimulating factor on peritoneal defense mechanisms and bacterial translocation after administration of systemic chemotherapy in rats

Çerçi¹

2007

WJG

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activity of peritoneal fluid and phagocytic activity of polymorphonuclear leucocytes in the peritoneal fluid. G-CSF increased both bactericidal activity of the peritoneal fluid and phagocytic activity of polymorphonuclear leucocytes in the peritoneal fluid, and prevented the bacterial translocation. We conclude that intraperitoneal GCSF administration protects the effects of systemic 5-FU on peritoneal defense mechanisms. INTRODUCTIONChemotherapy is one of the most important methods in the therapy of malignant diseases. It has been widely used and it is well known that systemic chemotherapy has immunosuppressive effects [1] . 5-Fluorouracil (5-FU) has side effects, including leucopoenia, stomatitis, appetite loss, diarrhea, and mild fever like other chemotherapy agents [2,3] . It has been reported that a high dose of 5-FU often induces cytotoxicity in intestinal tissue that results in ulceration, diarrhea, and bacterial translocation [4][5][6][7][8] .Bacterial translocation is one of the most important causes of sepsis and multiple organ failure. Intestinal mucosa has a barrier function that prevents the colonization of the bacteria and the passage of bacteria and their toxins from the intestinal system into the systemic circulation. It has been shown that bacterial translocation is also augmented by shock, mesenteric ischemia, thermal injury, malnutrition, obstructive jaundice, and intestinal obstruction [9][10][11][12][13][14] . Granulocyte-colony stimulating factor (G-CSF) is a cytokine that is used to reverse the neutropenia associated with cytotoxic chemotherapy bone marrow and haemopoietic stem cell transplantation [15] . Abstract AIM: To investigate the effects of granulocyte-colony stimulating factor (G-CSF) on peritoneal defense mechanisms and bacterial translocation after systemic 5-Fluorouracil (5-FU) administration.

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Bacteria, toxins, and the peritoneum

Cited by 50 publications

References 85 publications

Contribution of Escherichia coli Alpha-Hemolysin to Bacterial Virulence and to Intraperitoneal Alterations in Peritonitis

Contribution of Escherichia coli Alpha-Hemolysin to Bacterial Virulence and to Intraperitoneal Alterations in Peritonitis

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

Effects of granulocyte-colony stimulating factor on peritoneal defense mechanisms and bacterial translocation after administration of systemic chemotherapy in rats

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