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- Expression of Surfactant-D Protein and TNF-alpha in the Interaction of Pneumocystis Carinii and Alveolar Macrophages in Pneumocystis Carinii Pneumonia.
- Kun Young Kwon, Kwan Kyu Park, Chang Kwon Park, Young June Jeon, Eun Sook Chang
- Korean J Pathol. 1999;33(9):684-694.
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Abstract
PDF - Alveolar macrophages participate in the host defense against P. carinii, but the mechanisms in degradation and clearance of the organism from lung has not been well established. We observed the transmission and scanning electron microscopic features and evaluated the expression of TNF-alpha and Surfactant-D in the interaction of P. carinii with alveolar macrophages. Expression of TNF-alpha and Surfactant-D in the experimentally induced P. carinii pneumonia in rat was examined by immunohistochemistry and immunoelectron microscopy. Electron microscopically, the alveolar macrophages phagocytized trophozoites and cysts of P. carinii micro-organisms. Immunohistochemically TNF-alpha was strongly expressed in the cytoplasms of alveolar macrophages. Postembedding immunogold labeling for Surfactant-D protein was expressed on the pellicles of trophozoites and cysts, P. carinii micro-organisms in the cytoplasms of macrophages, free floating surfactant materials and multilamellar bodies of type II epithelial cells. We conclude that alveolar macrophages interacted with P. carinii micro-organisms respond with increased expression of TNF-alpha. TNF-alpha may bind to P. carinii and exert a direct toxic effect upon the micro-organisms. Surfactant-D protein may augment binding of P. carinii to the alveolar macrophages and enhance the clearance of the micro-organisms.
- 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.
- 1,610 View
- 16 Download
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Abstract
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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.
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