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Role of Flagella in Campylobacter Pathogenesis, Page 1 of 2
< Previous page Next page > /docserver/preview/fulltext/10.1128/9781555818340/9781555810825_Chap25-1.gif /docserver/preview/fulltext/10.1128/9781555818340/9781555810825_Chap25-2.gifAbstract:
The thermophilic Campylobacters Campylobacter jejuni and C. coli together constitute one of the major causes of bacterial diarrhea worldwide. Variations in growth temperature, pH, and inorganic ion contents led to increases in expression of flaB up to 2.6-fold over the basal level of expression in standard medium, suggesting that Campylobacters can modulate the compositions of their flagellar filaments and their motilities in direct response to environmental signals. Kanamycin-resistant, motile revertants were never obtained in the presence of DNase, indicating that these recombinational events were due to autolysis of cells and natural transformation mediated, intergenomic recombinational events. The lack of a suitable nonprimate disease model has precluded examination of nonflagellated isogenic mutants in a pathogenesis model, but several groups have examined the role of flagella in the invasion and adherence of eukaryotic cells in vitro. Flagellin genes were among the first Campylobacter genes to be cloned and mutated by site-specific mutagenesis protocols. The subsequent manipulation of these genes not only has led to greater understanding about the structure of an unusual flagellar filament but also has increased understanding of other aspects of the biology of these organisms. An understanding of the mechanisms by which Campylobacters regulate expression of flagellin genes and genes encoding alternate posttranslational modifications on the flagellins will contribute further to understanding of the molecular pathogenesis of these important pathogens.