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Lipopolysaccharide Architecture of Legionella pneumophila Grown in Broth and Host Cells, Page 1 of 2
< Previous page Next page > /docserver/preview/fulltext/10.1128/9781555815660/9781555813901_Chap64-1.gif /docserver/preview/fulltext/10.1128/9781555815660/9781555813901_Chap64-2.gifAbstract:
This chapter demonstrates for the first time to what extent the lipopolysaccharide (LPS) architecture is involved in extracellular structures of Legionella pneumophila bacteria. Furthermore, the intraphogosomal/ intracellular shedding of LPS components is investigated. The authors' investigation of the surface architecture of strain Lp02 and its dotA and letA mutants substantiate that the LPS equipment depends at least on both genes. Therefore, the valuation of the influence of dotA and letA on pathogenicity also has to consider the phenotypic changes of the LPS surface structures, because they initiate the first step of interaction between bacteria and host cells. The amounts of LPS were quantified by enzyme-linked immunosorbent assay. LPS was immobilized in microtiter wells and detected by monoclonal antibody (MAb) 3/1 followed by antimouse-IgG horseradish peroxidase. Moreover, until the postexponential growth phase in broth cultures only approximately 5% of bacteria of strains Corby and Lp02 can be labeled by MAb 59/1. After lysis of host cells it was observed that legionellae were released either as bacterial clusters positive for both MAbs or as single MAb 3/1-positive bacteria being MAb 59/1-positive or negative. The ability to modify and shed LPS allows L. pneumophila to build lamellar structures and vesicles and to release soluble LPS that may modulate host cells, enhance survival in aerosols, or stabilize biofilms. In this chapter, the authors have demonstrated that the whole LPS architecture is influenced by at least two systems, namely the type IV secretion apparatus and letA/letS regulatory elements.