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3 "Endotoxemia"
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Original Articles
The Effects of CD11c/CD18 and CD14 Blocking on Lipopolysaccharide-induced Endotoxemia.
O Jun Kwon, Jong Kuk Kim, Jyung Sik Kwak
Korean J Pathol. 2000;34(1):11-19.
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We studied the morphologic changes and the expression of cytokines of major organs by blocking CD14 and CD11c/CD18, which are known to be receptors of lipopolysaccharide (LPS), in the LPS induced endotoxemic mice. In 2 and 8 hours after initial intraperitoneal injection of 10 mg/kg of LPS into the mice, 500 microgram/kg of anti-CD14 antibody (Ab) and/or the same dosage of the anti-CD11c/CD18 Ab were administered intravenously, respectively or concomitantly. Under the light microscope, the LPS only and the LPS with the anti-CD14 Ab injected groups (group 1 and 2) showed marked acute inflammation in the organs, especially in the lung and liver, but the LPS with the anti-CD11c/CD18 Ab only or with both anti-CD14 and anti-CD11c Abs injected groups (group 3 and 4) revealed only mild acute inflammation. Under the electron microscope, there was marked inflammation in the group 1 and 2 such as marked infiltration of neutrophils, monocytes/ macrophages, lymphocytes, aggregation of platelets, and marked edematous change of endothelial cells with separation from the basement membrane. However in the group 3 and 4, there was only mild inflammation such as mild infiltration of neutrophils in the tissue or aggregation of neutrophils in the capillaries and sinusoids with mild endothelial swelling. The expressions of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1alpha (IL-1alpha), detected by RT-PCR method, was remarkable in the group 2, but minimal in the group 3 and 4. We conclude that blocking the CD11c/CD18 with anti-CD11C/CD18 Ab is effective for the prohibition of biologic reactions and diminution of the inflammation induced by the LPS, even in the LPS induced endotoxemia.
The Effects of Proteolytic Agent on the Lung Injured by Endotoxemia.
Chang Ho Cho, Yoon Kyung Sohn, Jyung Sik Kwak, Tae Joong Sohn
Korean J Pathol. 1991;25(3):215-222.
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The authors studied the lung injury induced by endotoxemia and the effects of proteolytic agent on the lung changed by endotoxemia. Sprague-Dawley rats were intraperitoneally administrated with a single dose of endotoxin (4 mg/kg, E. coli 025 : B6 lipopolysaccharide) or with endotoxin and gabexate mesilate (200 mg/kg), a proteolytic agent, concomitantly. Rats of each group were scarificed at 9, 18, and 27 hours after injection. Light and electron microscopic examination were done. The results obtained were summarized as follows: Light microscopic exmination revealed congested capillaries and neutrophilic infiltration in both groups. Electron microscopic findings were interstitial and alveolar neutrophilic infiltration, endothelial swelling with increased pinocytotic vesicles and cytoplasmic process formation, and interstitial edema. Decrease of osmiophilic bodies in the type II pneumocytes had appeared at 9 hours after endotoxin injection. These changes were increased in severity at 18 hours and 27 hours after endotoxin injection. In the group of concomitant treatment of gabexate mesilated and endotoxin, there was no edema at 9 hours after injection. After 18 hours welling of endothelial cell and interstitial edema had appeared. However, the severity of the edema was markedly decreased. Type II pneumocytes showed well preserved osmiophilic bodies. According to these results, it is considered that administration of gabexate mesilate can significantly redeced the lung injury induced by endotoxemia.
Case Report
Neonatal Giant Cell Hepatitis: An autopsy case.
Sung Churl Lim, Moo Young Song, Un Jun Hyung, Je G Chi
Korean J Pathol. 1991;25(2):147-152.
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We report an autopsy case of neonatal giant cell hepatitis that was presumed to be related to bacterial sepsis, endotoxemia and to the subsequent parenteral alimentation and antibiotics treatment. The patient died of candidal endocarditis and multiple brain infarcts. This female baby was born by a normal full term spontaneous delivery. Six days after delivery she developed fever and lethargy as she suffered from Cheyne-Stokes respiration with severe grunting. Blood culture grew Enterobacter and Acinetobacter. After management of the sepsis her general condition improved. On the 23rd day of admission she was found to have deep jaundice and hepatosplenomegaly. The liver became larger progressively and the edge was palpable at the umbilical level. Grade II systolic murmur was heard along the left lower sternal border. She died on the 31st day of hospitalization. Postmortem examination showed severe jaundice, hepatosplenomegaly, a large vegetation on the mitral valve and multiple petechial hemorrhages of the viscera. Microscopically the liver showed features of massive giant cell transformation, mild fibrosis and inflammatory cells, suggestive of giant cell hepatitis. Numerous yeasts and candidal pseudohyphae were seen in the cardiac vegetation, focally extending into the myocardium. There was a focus of candidal vasculitis in the bowel wall. In addition there were multiple bilateral organizing infarcts in the cerebral hemisphere as well as diffuse white matter damage associated with septicemia.

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