Both the cgtB and the wlaN genes encode β-1,3- galactosyltransferases thought to be involved in synthesis of the C. jejuni outer membrane lipo-oligosaccharide. All strains in this

study possessed cgtB, and all except D2600 possessed wlaN. Muller et al. [57, 58] studied the associations of these genes with the ability to invade Caco-2 cells in culture and to colonize chickens; their results suggest this website that possession of one or both genes is associated with the ability to invade eukaryotic cells and to colonize the chicken GI tract, but one strain that lacked both loci was fully invasive. Adaptation to the host by serial passage altered the outcome of infection for three of five C. jejuni strains Entinostat price Three of five C. jejuni strains (11168, D0835, and D2600) became more virulent during serial passage in mice as shown by increased colonization of the jejunum, decreased time to develop clinical disease, and increased levels of both gross pathology (particularly increased incidence of bloody diarrhea) and histopathology. Fecal population sizes of two of the three strains that became more virulent increased during serial passage. The change toward increased pathogenicity in the three evolving strains find more occurred after one passage in two strains and after three passages in one strain. This observation suggests that the strain that increased in pathogenicity only after three passages may

have had to undergo more extensive PLEK2 genetic change than the other two strains. An increase in pathogenicity is consistent both with a large body of theoretical work and with previous experimental studies of pathogenicity evolution; in this case, since the mice were individually housed, virulence trade-offs with transmission dynamics between hosts would not be expected to occur. Since all mice in all passages of the serial passage experiment experienced the same dietary conditions (transition

from the ~12% fat breeder diet to the ~6% fat NIH-31 formula maintenance diet), differences in the behavior of a C. jejuni strain in different passages cannot be attributed to differences in diet, particularly for strain D2600, which did not show increased colonization of the jejunum or marked increases in pathology until after the third passage. Two C. jejuni strains, D2586 and NW, did not increase in pathogenicity during four serial passages. Although we cannot rule out the possibility that continued passage might have produced an increase in pathogenicity in these strains, this result shows that the initial genetic complements of the two strains affected their ability to respond to the selection pressure imposed by the novel host environment of the mouse GI tract. Microarray comparison of the gene content of strain NW to that of strain 11168 revealed that strain NW did not possess a detectable homologue of C. jejuni gmhA, a gene involved in LOS/LPS synthesis encoding sedoheptulose-7-phosphate isomerase.