Chlamydia Infection Causes Loss of Pacemaker Cells and Inhibits Oocyte Transport in the Mouse Oviduct1

We have investigated the role of oviduct contractions in egg transport and found that underlying electrical pacemaker activity is responsible for oviduct motility and egg transport

Rose Ellen Dixon; Sung Jin Hwang; Grant W. Hennig; Kyle H. Ramsey; Justin H. Schripsema; Kenton M. Sanders; Sean M. Ward


Scholarcy highlights

  • Chlamydia trachomatis is the most common bacterial sexually transmitted disease, presenting an enormous public health challenge worldwide
  • Loss of Interstitial cells of Cajal was associated with an absence of pacemaker activity and propulsive contractions in oviducts, but membrane potentials of smooth muscle cells were unchanged from untreated oviducts
  • We investigated whether the loss of ICC in the oviduct was associated with upregulation of PTGS2 and NOS2 in response to C. muridarum infection
  • The results using in vitro Spatiotemporal maps in the present study contradict this concept, because we found that small, 15 to 25 lm particles, possibly cellular debris, were moved in the oviduct by ciliary beating, but eggs are approximately 70–90 lm and are not effectively propelled by ciliary beating
  • Results we obtained with video imaging experiments demonstrate that spontaneous contractile activity of the myosalpinx is essential for oocyte movement
  • 4) pacemaker activity was absent in the oviducts of mice infected with C. muridarum, and KIT immunohistochemistry revealed that the likely cause of the loss of pacemaker activity was a depletion of ICC-OVI
  • Interstitial cells of Cajal-OVI pace the smooth muscle cells of the oviduct to produce propulsive phasic contractions

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