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Structural Relationship of the Lipid A Acyl Groups to Activation of Murine Toll-Like Receptor 4 by Lipopolysaccharides from Pathogenic Strains of Burkholderia mallei, Acinetobacter baumannii, and Pseudomonas aeruginosaстатья
Статья опубликована в высокорейтинговом журнале
Информация о цитировании статьи получена из
Web of Science,
Scopus
Статья опубликована в журнале из списка Web of Science и/или Scopus
Дата последнего поиска статьи во внешних источниках: 10 февраля 2016 г.
- Авторы: Korneev KV, Arbatsky NP, Molinaro A., Palmigiano A., Shaikhutdinova RZ, Shneider MM, Pier GB, Kondakova AN, Sviriaeva EN, Sturiale L., Garozzo D., Kruglov AA, Nedospasov SA, Drutskaya MS, Knirel YA, Kuprash DV
- Журнал: Frontiers in immunology
- Том: 6
- Номер: 595
- Год издания: 2015
- Издательство: Frontiers Research Foundation]
- Местоположение издательства: [Lausanne, Switzerland
- Первая страница: 1
- Последняя страница: 9
- DOI: 10.3389/fimmu.2015.00595
- Аннотация: Toll-like receptor 4 (TLR4) is required for activation of innate immunity upon recognition of lipopolysaccharide (LPS) of Gram-negative bacteria. The ability of TLR4 to respond to a particular LPS species is important since insufficient activation may not prevent bacterial growth while excessive immune reaction may lead to immunopathology associated with sepsis. Here, we investigated the biological activity of LPS from Burkholderia mallei that causes glanders, and from the two well-known opportunistic pathogens Acinetobacter baumannii and Pseudomonas aeruginosa (causative agents of nosocomial infections). For each bacterial strain, R-form LPS preparations were purified by hydrophobic chromatography and the chemical structure of lipid A, an LPS structural component, was elucidated by HR-MALDI-TOF mass spectrometry. The biological activity of LPS samples was evaluated by their ability to induce production of proinflammatory cytokines, such as IL-6 and TNF, by bone marrow-derived macrophages. Our results demonstrate direct correlation between the biological activity of LPS from these pathogenic bacteria and the extent of their lipid A acylation.
- Добавил в систему: Свиряева Екатерина Николаевна