| Deficiency of mannose-binding lectin greatly increases susceptibility to postburn infection with Pseudomonas aeruginosa. | |
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MedLine Citation:
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PMID: 16424207 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Burn injury disrupts the mechanical and biological barrier that the skin presents against infection by symbionts like the Pseudomonas aeruginosa, a Gram-negative bacteria. A combination of local factors, antimicrobial peptides, and resident effector cells form the initial response to mechanical injury of the skin. This activity is followed by an inflammatory response that includes influx of phagocytes and serum factors, such as complement and mannose-binding lectin (MBL), which is a broad-spectrum pattern recognition molecule that plays a key role in innate immunity. A growing consensus from studies in humans and mice suggests that lack of MBL together with other comorbid factors predisposes the host to infection. In this study we examined whether MBL deficiency increases the risk of P. aeruginosa infection in a burned host. We found that both wild-type and MBL null mice were resistant to a 5% total body surface area burn alone or s.c. infection with P. aeruginosa alone. However, when mice were burned then inoculated s.c. with P. aeruginosa at the burn site, all MBL null mice died by 42 h from septicemia, whereas only one-third of wild-type mice succumbed (p = 0.0005). This result indicates that MBL plays a key role in containing and preventing a systemic spread of P. aeruginosa infection following burn injury and suggests that MBL deficiency in humans maybe a premorbid variable in the predisposition to infection in burn victims. |
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Authors:
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Mette Møller-Kristensen; W K Eddie Ip; Lei Shi; Lakshmi D Gowda; Michael R Hamblin; Steffen Thiel; Jens Chr Jensenius; R Alan B Ezekowitz; Kazue Takahashi |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural |
Journal Detail:
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Title: Journal of immunology (Baltimore, Md. : 1950) Volume: 176 ISSN: 0022-1767 ISO Abbreviation: J. Immunol. Publication Date: 2006 Feb |
Date Detail:
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Created Date: 2006-01-20 Completed Date: 2006-03-24 Revised Date: 2011-07-28 |
Medline Journal Info:
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Nlm Unique ID: 2985117R Medline TA: J Immunol Country: United States |
Other Details:
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Languages: eng Pagination: 1769-75 Citation Subset: AIM; IM |
Affiliation:
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Laboratory of Developmental Immunology, Department of Pediatrics, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Burns / blood, genetics, microbiology* Disease Models, Animal Inflammation / metabolism Interleukin-6 / blood Mannose-Binding Lectin / deficiency* Mice Mice, Knockout Organ Specificity / genetics, immunology Pseudomonas Infections* / blood Pseudomonas aeruginosa Risk Factors Sepsis / microbiology Tumor Necrosis Factor-alpha / metabolism |
| Grant Support | |
ID/Acronym/Agency:
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R01 AI050875-04/AI/NIAID NIH HHS; R01AI42788/AI/NIAID NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Interleukin-6; 0/Mannose-Binding Lectin; 0/Tumor Necrosis Factor-alpha |
| Comments/Corrections | |
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