Abstract

Mice are valuable models extensively used to test vaccine candidates against Chlamydia abortus and to clarify immunopathological mechanisms of the bacteria. As this pathogen has the ability to reactivate during pregnancy, it is important to deepen the knowledge and understanding of some of the effects of female hormones on immunity and vaccination. This study is aimed at describing the role of sex hormones in the pathology of OEA during chlamydial clearance using ovariectomised mice and also gaining an understanding of how 17-oestradiol or progesterone may impact the effectiveness of vaccination. Animals were treated with sex hormones and infected with C. abortus, and the kinetics of infection and immune response were analysed by means of bacterial isolation, histopathology, and immunohistochemistry. In a second phase of the study, protection conferred by an experimental vaccine after hormone treatment was assessed. Oestradiol showed a stimulatory effect on the immune response during infection, with a more efficient recruitment of macrophages and T-cells at the infection site. Furthermore, after vaccination, oestradiol-treated animals showed a stronger protection against infection, indicating that this hormone has a positive effect, stimulating a specific memory response to the pathogen.

Highlights

  • Chlamydia abortus is the cause of ovine enzootic abortion (OEA)

  • In the case of C. abortus, we have previously showed that was the infection rate increased in both endometrial and trophoblast cell lines after treatment with progesterone or oestrogen, but C. abortus aberrant forms were induced by hormonal treatment in ovine endometrial cell line [13]

  • Bacterial Isolation C. abortus was isolated from the liver of infected mice, and the results were expressed as Log Inclusion Forming Units per gram (Log inclusion-forming units (IFUs)/g)

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Summary

Introduction

Chlamydia abortus is the cause of ovine enzootic abortion (OEA) This pathogen with zoonotic potential is recognised as the main cause of reproductive failure in small ruminants and other domestic animals. The bacteria can infect non-pregnant ewes and produce latency, and once the ewe becomes pregnant, the infection reactivates and multiplies in the placental tissue, producing lesions and leading to late abortions or weak lambs ([3], reviewed in [4]). These foetal membranes and vaginal discharges can be a source of infection for both animals and humans [5,6]

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