Lack of the receptor for advanced glycation end-products attenuates E. coli pneumonia in mice
| Autor: | Lasse Ramsgaard, Ruben Zamora, Lauren T. Crum, Michelle L. Manni, Jacob M. Tobolewski, Judson M. Englert, Tim D. Oury, Yoram Vodovotz, Gina M. Coudriet, Jon D. Piganelli, Jan J. Enghild, Julia V. Gefter, Pavle S. Milutinovic |
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| Jazyk: | angličtina |
| Rok vydání: | 2011 |
| Předmět: |
Male
Critical Care and Emergency Medicine Lipopolysaccharide Pulmonology endocrine system diseases medicine.medical_treatment Receptor for Advanced Glycation End Products Interleukin-1beta lcsh:Medicine RAGE (receptor) chemistry.chemical_compound Mice 0302 clinical medicine Medicine Receptors Immunologic lcsh:Science Lung Cells Cultured Chemokine CCL2 Chemokine CCL3 Mice Knockout 0303 health sciences Multidisciplinary biology Interleukin-12 Cytokine Infectious Diseases 030220 oncology & carcinogenesis cardiovascular system Cytokines Tumor necrosis factor alpha medicine.symptom Bronchoalveolar Lavage Fluid Research Article medicine.medical_specialty Histology Immunology Blotting Western Inflammation Lung injury In Vitro Techniques HMGB1 03 medical and health sciences Internal medicine Sepsis Escherichia coli Animals cardiovascular diseases Biology 030304 developmental biology Peroxidase business.industry Interleukin-6 Tumor Necrosis Factor-alpha lcsh:R Wild type nutritional and metabolic diseases Pneumonia Mice Inbred C57BL Endocrinology chemistry Immune System Respiratory Infections biology.protein lcsh:Q business Infectious Disease Modeling human activities |
| Zdroj: | Ramsgaard, L, Englert, J M, Manni, M L, Milutinovic, P S, Gefter, J, Tobolewski, J, Crum, L, Coudriet, G M, Piganelli, J, Zamora, R, Vodovotz, Y, Enghild, J J & Oury, T D 2011, ' Lack of the receptor for advanced glycation end-products attenuates E. coli pneumonia in mice ', P L o S One, vol. 6, no. 5, pp. e20132 . https://doi.org/10.1371/journal.pone.0020132 PLoS ONE PLoS ONE, Vol 6, Iss 5, p e20132 (2011) |
| Popis: | Background: The receptor for advanced glycation end-products (RAGE) has been suggested to modulate lung injury in models of acute pulmonary inflammation. To study this further, model systems utilizing wild type and RAGE knockout (KO) mice were used to determine the role of RAGE signaling in lipopolysaccharide (LPS) and E. coli induced acute pulmonary inflammation. The effect of intraperitoneal (i.p.) and intratracheal (i.t.) administration of mouse soluble RAGE on E. coli injury was also investigated. Methodology/Principal Findings: C57BL/6 wild type and RAGE KO mice received an i.t. instillation of LPS, E. coli, or vehicle control. Some groups also received i.p. or i.t. administration of mouse soluble RAGE. After 24 hours, the role of RAGE expression on inflammation was assessed by comparing responses in wild type and RAGE KO. RAGE protein levels decreased in wild type lung homogenates after treatment with either LPS or bacteria. In addition, soluble RAGE and HMGB1 increased in the BALF after E. coli instillation. RAGE KO mice challenged with LPS had the same degree of inflammation as wild type mice. However, when challenged with E. coli, RAGE KO mice had significantly less inflammation when compared to wild type mice. Most cytokine levels were lower in the BALF of RAGE KO mice compared to wild type mice after E. coli injury, while only monocyte chemotactic protein-1, MCP-1, was lower after LPS challenge. Neither i.p. nor i.t. administration of mouse soluble RAGE attenuated the severity of E. coli injury in wild type mice. Conclusions/Significance: Lack of RAGE in the lung does not protect against LPS induced acute pulmonary inflammation, but attenuates injury following live E. coli challenge. These findings suggest that RAGE mediates responses to E. coli-associated pathogen-associated molecular pattern molecules other than LPS or other bacterial specific signaling responses. Soluble RAGE treatment had no effect on inflammation. © 2011 Ramsgaard et al. |
| Databáze: | OpenAIRE |
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