A stealth adhesion factor contributes to Vibrio vulnificus pathogenicity: Flp pili play roles in host invasion, survival in the blood stream and resistance to complement activation
Fig 2
Significantly decreased adhesion to host cells by the Δtad123 mutant (A) and time-dependent recovery (B).
HeLa cells were treated with log-phase V. vulnificus cells at an MOI of 250 bacteria in the presence of 2 μg/ml tetracycline, and the bacterial cells that adhered to HeLa cells were counted at appropriate time points. The morphology of the infected HeLa cells was observed after Giemsa staining at ×1,000 magnification. Data shown represent the mean ± SEM of five independent experiments performed with six (A) or seventeen to forty-four replicates (B). WT (pLAFR3), wild type harboring pLAFR3; Δtad123 (pLAFR3), Δtad123 mutant harboring pLAFR3; Δtad123 (pLAFR3::tad1), Δtad123 mutant in trans complemented with pLAFR3::tad1 locus; Δtad123 (pLAFR3::tad2), Δtad123 mutant in trans complemented with pLAFR3::tad2 locus); Δtad123 (pLAFR3::tad3), Δtad123 mutant in trans complemented with pLAFR3::tad3 locus. Statistical analysis was carried out using Student’s t test (**, P < 0.01).