GlgA plays an important role in the induction of hydrosalpinx by chlamydia muridarum.

While glycogen synthase A deficiency can reduce the growth and proliferation of Chlamydia muridarum, the effect of glycogen synthase A on the pathogenic process of Chlamydia muridarum remains unclear. To characterize the effect of glycogen synthase A deficiency on the pathogenicity of Chlamydia muridarum in the genital tract, BALB/c mice were intravaginally inoculated with wild-type, plasmid-free, and glycogen synthase A-deficient Chlamydia muridarum, and the genital tract tissue was isolated to assess the severity of hydrosalpinx and the levels of oviduct dilatation at day 60 after infection. The glycogen storage capacity and in vitro infection ability of different Chlamydia muridarum strains were analyzed by periodic acid-Schiff staining and quantification of progeny EB formation. The tissue homogenate was used to determine the recovery of different Chlamydia muridarum strains. The results show that glycogen synthase A-deficient Chlamydia muridarum induced reduction of hydrosalpinx and attenuated the extent of oviduct dilatation in mice, and exhibited reduced growth and proliferation in the mouse lower genital tract. In addition, glycogen synthase A point mutations at different sites reduced the glycogen storage capacity and in vitro infectivity of Chlamydia muridarum to different degrees. Glycogen synthase A deficiency also reduced the host inflammatory reaction and ascending infection of Chlamydia muridarum.