Biomedical subjects

G Wollenberg

Publications and source records attributed to G Wollenberg.

3 recordsLinked to original sources

PubMed2000

Peliosis hepatis in a dog infected with Bartonella henselae.

A 6-year-old spayed female Golden Retriever was examined because of generalized weakness and abdominal distention. Abdominal ultrasonography revealed a large quantity of peritoneal fluid. In addition, the liver appeared larger than normal and contained multiple, small, nodular masses and cyst-like structures. Abdominal exploratory surgery was performed, and 5 L of serosanguineous peritoneal fluid was removed. Gross lesions were not found in the stomach, kidneys, intestines, adrenal glands, or urinary bladder. There were diffuse cystic nodules in all liver lobes. The dog did not recover from anesthesia. A diagnosis of peliosis hepatis was made on the basis of gross and histologic appearance of the liver. A polymerase chain reaction assay revealed Bartonella henselae DNA in liver specimens. To our knowledge, this is the first report of molecular evidence of B henselae infection in a dog with peliosis hepatis.

Animals↗

PubMed1998

Exogenous interleukin-10 fails to decrease the mortality or morbidity of sepsis.

OBJECTIVE: To determine if exogenous interleukin (IL)-10 will decrease the morbidity or mortality of sepsis induced by cecal ligation and puncture. DESIGN: Prospective, randomized, controlled study. SETTING: University research laboratory. SUBJECTS: Adult, female, Balb¿c mice. INTERVENTIONS: Balb¿c mice were subjected to cecal ligation and puncture with an 18- or 23-gauge needle and treated with triple antibiotics. Mice were injected subcutaneously with recombinant human IL-10 (diluted in normal saline with 0.1% mouse serum albumin) and followed until death. In a separate experiment, IL-10 was also injected subcutaneously and lipopolysaccharide (LPS) injected intraperitoneally and plasma tumor necrosis factor concentrations measured 90 mins later. MEASUREMENTS AND MAIN RESULTS: In the LPS experiments, IL-10 decreased tumor necrosis factor (TNF) production by nearly 90%. For the cecal ligation and puncture experiments, temperature and movement were recorded continuously via implanted transmitters. Studies on mortality indicated that exogenous IL-10 given at 0, +6 and +12 hrs after surgery failed to increase survival when using an 18-gauge needle (alive:total cecal ligation and puncture alone 4:21; IL-10 10 microg/mouse 2:12; 1 microg/mouse 8:25; 0.1 microg/mouse 1:12) or a 23-gauge needle (cecal ligation and puncture alone 13:29; IL-10 1 microg 18:30). There was no difference in the number of hours to death between the groups. IL-10 did not prevent the hypothermia after cecal ligation and puncture or increase the animals' activity. To examine parameters of inflammation, mice were killed 8 hrs after 18-gauge cecal ligation and puncture. IL-10 (1 microg/mL) failed to reduce pulmonary neutrophil sequestration (lung myeloperoxidase, cecal ligation and puncture 107 +/- 10 [SEM], IL-10 107 +/- 5) or recruitment of neutrophils to the peritoneum (neutrophils x 10(6), cecal ligation and puncture 3.72 +/- 0.62; IL-10 3.49 +/- 0.37). IL-10 also failed to reduce the appearance of TNF or IL-6 in the plasma or peritoneal fluid. The chemokine KC was reduced in the peritoneal fluid but not the plasma and endogenous IL-10 production was not reduced in the peritoneum. CONCLUSION: Our data indicate that exogenous IL-10 fails to improve morbidity or mortality in the clinically relevant cecal ligation and puncture model of sepsis.

Animals↗

PubMed1995

Blockade of tumor necrosis factor reduces lipopolysaccharide lethality, but not the lethality of cecal ligation and puncture.

Inhibition of tumor necrosis factor (TNF) bioactivity has afforded protection in several animal models of sepsis. We examined whether inhibition of TNF could improve survival after lethal lipopolysaccharide (LPS) or cecal ligation and puncture (CLP) in CD-1 or BALB/c mice. Neutralizing rabbit anti-TNF antisera were evaluated in CD-1 mice by injecting the antisera 3 h before intravenous (i.v.) LPS (600 micrograms). Implantable radiotransmitters were used for continuous monitoring of temperature. No decrease in mortality was observed, and the anti-TNF failed to prevent the drop in temperature. In BALB/c mice injected with antisera before LPS (200 micrograms) mortality was reduced (dead/total: control sera, 14/14; anti-TNF, 4/12; p = .007 control sera vs. anti-TNF). CD-1 mice were pretreated with anti-TNF or control sera; CLP was performed followed by administration of antibiotics. Anti-TNF did not decrease pulmonary neutrophil sequestration, improve survival, or prevent the decrease in temperature observed as sepsis developed. CLP was performed in the BALB/c mice using antibiotics plus anti-TNF antisera, but no protection was observed. Our results demonstrate that anti-TNF treatment prevents LPS mortality only when using certain strains of mice and inhibition of TNF fails to reduce mortality in a more clinically relevant model of sepsis.

Animals↗