Campylobacter concisus is a heterogeneous species complex comprised of several phenotypically indistinguishable but genetically distinct taxa (“”genomospecies”"). Numerous methods can be used to genetically separate the genomospecies, including PCR analysis

of the 23S rRNA gene [11] and cluster analysis of amplified fragment length polymorphism (AFLP) or random amplified polymorphic DNA (RAPD) profiles [1, 2]. Based on these typing methods, at Quisinostat concentration least two main C. concisus genomospecies have been identified [1, 2, 4, 11]. Differences in pathogenicity amongst distinct genomospecies of some bacterial taxa [12, 13] support the notion that certain C. concisus genomospecies may be more likely than others to cause click here intestinal disease. While an early study by Van Etterijck et al. [10] concluded that C. concisus was not pathogenic given similar isolation rates from diarrheic and healthy children, genetic diversity of the isolates with respect to clinical presentation was not considered.

A more recent study showed that isolates from healthy individuals were genetically distinct from those of diarrheal origin; however, differences in epithelial cytotoxicity between the two groups were not evident [2]. Additionally, cluster analysis of diarrheic isolate AFLP profiles delineated two main C. concisus EPZ015666 concentration genomospecies (designated genomospecies 1 and 2), which where characterized by type strains of oral and diarrheal origin, respectively [1]. Genomospecies 2 isolates were more frequently isolated from the stool of patients presenting with diarrhea in which no other pathogens were found, and bloody diarrhea was associated only with genomospecies 2 isolates. While

these studies suggest that distinct C. concisus genomospecies may vary in their pathogenic ability, this has yet to be empirically examined. Our understanding of Campylobacter pathogenesis is based primarily on C. jejuni. Its small, spiral shape coupled with flagella-mediated motility, allow C. jejuni to penetrate intestinal mucus [14] where it can then adhere to and invade intestinal epithelial cells. This bacterium can also translocate across the intestinal epithelium via a paracellular mechanism involving disruption of epithelial Chloroambucil tight junctions [15, 16] or via a lipid raft-mediated transcellular mechanism [17]. C. jejuni also causes cellular cytotoxicity through the production of various toxins; cytolethal distending toxin (CDT) is a well-characterized toxin produced by most strains. The cytolethal distending toxin blocks cell proliferation in the G2/M phase resulting in cellular distension leading to the induction of apoptotic cell dealth [18]. This bacterium also induces intestinal epithelial secretion of interleukin-8 (IL-8), a pro-inflammatory chemoattractant that recruits neutrophils to the site of infection [19]. Cytolethal distending toxin-like activity has been reported for a majority of clinical C.