The adherence mechanism of Aeromonas caviae Sch3N to HEp-2 cells was initia
lly investigated through four mini-Tn5 mutants that showed a ill-fold decre
ase in adherence. These mutants lost motility, flagella, and their lipopoly
saccharide (LPS) O antigen (O-Ag), Three genes, flmB-neuA-flmD, were found
to be interrupted by the transposon insertions; additionally, two other gen
es, one lying upstream flmA) and one downstream (neuB), were found to be cl
ustered in the same operon, While the flmA and flmB genes were present in a
ll mesophilic Aeromonas spp, (A. hydrophila, A. caviae, A. veronii by. vero
nii, and A. veronii by. sobria) tested, this was not the case for the neuA-
flmD-neuB genes. Construction and characterization of flmB insertion mutant
s in five other mesophilic Aeromonas strains revealed the loss of motility,
flagella, and adherence but did not alter the LPS composition of these str
ains. Taking the above findings into consideration, we conclude (i) that fl
agella and possibly the LPS O-Ag are involved in the adherence of the mesop
hilic Aeromonas to human epithelial cells; (ii) flmA and flmB are genes wid
ely distributed in the mesophilic Aeromonas and are involved in flagella as
sembly, and thus adherence; and (iii) in A, caviae Sch3N the flmA and flmB
genes are found in a putative operon together with neuA,flmD, and neuB and
are involved in LPS O-Ag biosynthesis and probably have a role in flagellum
assembly.