Variable adherence of fimbriated Haemophilus influenzae type b to human cells.

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The attachment of isogenic fimbriated and nonfimbriated Haemophilus influenzae type b variants to human cells was studied by using a radioactive assay and an indirect immunofluorescent assay. As described previously, fimbriated H. influenzae variants adhered to a greater extent than nonfimbriated variants to human buccal epithelial cells (2.1 and 0.29 bacteria per cell, respectively, as determined by the radioactive assay [P less than 0.05]; 7.6 and 1.6 bacteria per cell, respectively, as determined by the immunofluorescent assay [P less than 0.01]). As the concentration of fimbriated bacteria was increased, so were the numbers of adherent bacteria; in contrast, increasing the bacterial concentration had a much smaller effect on adherence of nonfimbriated H. influenzae type b. The distribution of bacteria on the buccal cells also differed. Whereas 37% of the buccal cells failed to bind nonfimbriated H. influenzae type b, failure to bind was observed for only 4% of the buccal cells exposed to fimbriated H. influenzae. In contrast, adherence to human foreskin fibroblasts was low regardless of the presence of fimbriae. On the other hand, fimbriated H. influenzae type b adhered less well than nonfimbriated variants to HEp-2 cells (1.6 and 3.8 bacteria per cell, respectively, as determined by the radioactive assay [P less than 0.05]; 1.3 and 4.8 bacteria per cell, respectively, as determined by the immunofluorescent assay [P less than 0.02]). Whereas adherence to HEp-2 cells increased considerably as the concentration of nonfimbriated bacteria was increased, there was only a small enhancement of adherence with an increase in the concentration of fimbriated H. influenzae type b. Furthermore, only 16% of the HEp-2 cells failed to bind nonfimbriated H. influenzae type b, whereas 50% failed to bind fimbriated H. influenzae type b. These data indicate that H. influenzae type b may contain two adhesins. One is associated with fimbriae and enables adherence to buccal cells, whereas the other is nonfimbrial and is associated with adherence to HEp-2 cells. It is not known whether either of these adhesins plays a role in pathogenesis.

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