| Depletion of phagocytes in the reticuloendothelial system causes increased inflammation and mortality in rabbits with Pseudomonas aeruginosa pneumonia. | |
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MedLine Citation:
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PMID: 19028978 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Phagocytes of the reticuloendothelial system are important in clearing systemic infection; however, the role of the reticuloendothelial system in the response to localized infection is not well-documented. The major goals of this study were to investigate the roles of phagocytes in the reticuloendothelial system in terms of bacterial clearance and inflammatory modulation in sepsis caused by Pseudomonas pneumonia. Macrophages in liver and spleen were depleted by administering liposome encapsulated dichloromethylene diphosphonate (clodronate) intravenously 36 h before the instillation of Pseudomonas aeruginosa into the lungs of anesthetized rabbits. Blood samples were analyzed for bacteria and cytokine concentrations. Lung injury was assessed by the bidirectional flux of albumin and by wet-to-dry weight ratios. Blood pressure and cardiac outputs decreased more rapidly and bacteremia occurred earlier in the clodronate-treated rabbits compared with the nondepleted rabbits. Plasma TNF-alpha (1.08 +/- 0.54 vs. 0.08 +/- 0.02 ng/ml) and IL-8 (6.8 +/- 1.5 vs. 0.0 +/- 0.0 ng/ml) were higher in the depleted rabbits. The concentration of IL-10 in liver of the macrophage-depleted rabbits was significantly lower than in normal rabbits at 5 h. Treatment of macrophage-depleted rabbits with intravenous IL-10 reduced plasma proinflammatory cytokine concentrations and reduced the decline in blood pressure and cardiac output. These results show that macrophages in the reticuloendothelial system have critical roles in controlling systemic bacteremia and reducing systemic inflammation, thereby limiting the systemic effects of a severe pulmonary bacterial infection. |
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Authors:
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Kiyoyasu Kurahashi; Teiji Sawa; Maria Ota; Osamu Kajikawa; Keelung Hong; Thomas R Martin; Jeanine P Wiener-Kronish |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2008-11-21 |
Journal Detail:
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Title: American journal of physiology. Lung cellular and molecular physiology Volume: 296 ISSN: 1040-0605 ISO Abbreviation: Am. J. Physiol. Lung Cell Mol. Physiol. Publication Date: 2009 Feb |
Date Detail:
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Created Date: 2009-01-27 Completed Date: 2009-03-10 Revised Date: 2010-09-22 |
Medline Journal Info:
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Nlm Unique ID: 100901229 Medline TA: Am J Physiol Lung Cell Mol Physiol Country: United States |
Other Details:
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Languages: eng Pagination: L198-209 Citation Subset: IM |
Affiliation:
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Dept. of Anesthesiology and Critical Care Medicine, Yokohama City Univ. Graduate School of Medicine, Kanazawa-ku, Yokohama, 236-0004, Japan. kiyok@med.yokohama-cu.ac.jp |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Bacteremia / etiology, mortality Blood Pressure Clodronic Acid / administration & dosage Cytokines / metabolism Enzyme-Linked Immunosorbent Assay Liposomes Liver / cytology, immunology, microbiology Lung Injury / etiology, pathology Macrophages / physiology Male Mononuclear Phagocyte System / metabolism* Phagocytes / physiology* Pneumonia, Bacterial / etiology*, mortality* Pseudomonas Infections / etiology*, mortality* Pseudomonas aeruginosa / pathogenicity Rabbits Spleen / cytology, immunology, microbiology Survival Rate |
| Grant Support | |
ID/Acronym/Agency:
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AI-29103/AI/NIAID NIH HHS; GM-37696/GM/NIGMS NIH HHS; HL-073996/HL/NHLBI NIH HHS; HL-30542/HL/NHLBI NIH HHS; HL-49810/HL/NHLBI NIH HHS; HL-55980/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Cytokines; 0/Liposomes; 10596-23-3/Clodronic Acid |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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