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The incompletely eliminated <i>Treponema pallidum</i> (<i>T. pallidum</i>) during wound infection can result in the progression of secondary, tertiary, or latent syphilis in individuals, suggesting that <i>T. pallidum</i> has successfully evaded the immune response and spread to distant sites. The mechanism underlying the dissemination of<i> T. pallidum</i> is unclear. Here, rabbit model of syphilis was established to evaluate the effects of <i>T. pallidum</i> protein Tp0136 on bacterial transmission. An increase in Tp0136 concentration decreased <i>T. pallidum</i> load in the skin lesions and increased <i>T. pallidum</i> load in the testes. Tp0136 antibody inhibited dissemination of <i>T. pallidum</i>, leading to the concentrated load of <i>T. pallidum</i> in skin lesions, and the low load of <i>T. pallidum</i> in the testis. This effect is reversed when Tp0136 antibody was interrupted. Furthermore, Tp0136 promoted angiogenesis <i>in vivo</i> and <i>in vitro</i>, leading to an increase in vascular permeability. PI3K/AKT signaling pathway is involved in regulating angiogenesis and an increase in vascular permeability. These findings elucidate the strategy employed by <i>T. pallidum</i> in evading immune clearance during the infection.