transmitting from the genital to gastrointestinal tract and inducing tubal disease: Double attack pattern.

( ) genital tract infection is insidious, and patients often have no conscious symptoms.Delayed treatment after infection can lead to serious complications. ( ) genital tract infection in female mice can simulate genital tract infection in women, which is an ideal model to investigate the pathogenesis of . plasmid protein pGP3, chromosomal protein TC0237/TC0668, -specific CD8 T cells, TNF-α, and IL-13 can induce genital tract inflammation, CD4 T cells are responsible for clearance. However, tubal inflammation persists after genital tract is removed. Genital tract can spread spontaneously in vivo and colonize the gastrointestinal (GI) tract, but the GI tract cannot reverse spread to the genital tract. The survival time and number of transmitted from genital tract to GI tract are positively correlated with the long-term lesion of oviduct, while the inoculated directly into the GI tract has no pathogenicity in both the genital and GI tract. The double attack pattern of -induced genital tract inflammatory lesions is as follows: infection of oviduct epithelial cells initiates the process of oviduct repair as the first attack. After genital spreads to the GI tract, activated chlamydia-specific CD8 T cells are recruited to the genital tract and secreted pro-fibrotic cytokines such as TNF-α and IL-13. This process is called the second attack which transform tubal repair initiated by the first attack into long-term tubal fibrosis/hydrosalpinx. Elucidating the pathogenic mechanism of infection can provide new ideas for the development of vaccine, which is expected to solve the problems of infertility caused by repeated infection in women.