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Blood, 1 September 2006, Vol. 108, No. 5, pp. 1751-1757. Prepublished online as a Blood First Edition Paper on May 30, 2006; DOI 10.1182/blood-2005-11-011932. This Article Full Text (PDF) All Versions of this Article: blood-2005-11-011932v1 108/5/1751    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Shah, C. Articles by Raynes, J. G. Search for Related Content PubMed PubMed Citation Articles by Shah, C. Articles by Raynes, J. G. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted November 21, 2005 Accepted April 17, 2006 Serum amyloid A is an innate immune opsonin for Gram-negative bacteria Chandrabala Shah, Ranjeeta Hari-Dass, and John Graham Raynes* Immunology Unit, London School of Hygiene and Tropical Medicine * Corresponding author; email: john.raynes{at}lshtm.ac.uk. Serum amyloid A (SAA) is the major acute phase protein in man and most mammals. Recently we demonstrated that SAA binds to many Gram-negative bacteria including Escherichia coli and Pseudomonas aeruginosa through outer membrane protein A (OmpA) family members. Therefore we investigated whether SAA altered the response of innate phagocytic cells to bacteria. Both the percentage of neutrophils containing E. coli and the number of bacteria per neutrophil were greatly increased by SAA-opsonisation, equivalent to that seen for serum. In contrast no change was seen for Streptoccocus pneumoniae, a bacteria that did not bind SAA. Neutrophil reactive oxygen intermediate production in response to bacteria was also increased by opsonisation with SAA. SAA-opsonisation also increased phagocytosis of E.coli by peripheral blood mononuclear cell derived macrophages. These macrophages showed strong enhancement of TNF-; and IL-10 production in response to SAA- opsonised E. coli and P. aeruginosa. SAA did not enhance responses in the presence of bacteria to which it did not bind. These effects of SAA occur at normal and acute phase concentrations consistent with SAA binding properties and a role in innate recognition. SAA therefore represents a novel innate recognition protein for Gram-negative bacteria. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: P. Gross, K. Brandl, C. Dierkes, J. Scholmerich, B. Salzberger, T. Gluck, and W. 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