Biological relevance of these microbial-host interactions in the pathogenesis of E. coli meningitis is shown by the demonstrations that (a) exogenous OmpA and gp96 and anti-gp96 antibodies block E. coli invasion of HBMEC, but do not exhibit any blocking effect on the OmpA mutant [23,24], (b) addition of exogenous FimH- or CD48- antibodies inhibits E. coli invasion of the HBMEC [25], and (c) expression levels of 37LRP dictates the ability of E. coli to invade HBMEC, but exhibited no effect on the CNF1 mutant [26,27]. The gene discussed is HSP90B1; the disease is escherichia coli infection.