Chlamydia trachomatis (C. trachomatis) is an obligate intracellular bacterium that causes the most common sexually transmitted bacterial infection in humans worldwide. If undetected, such infections can cause severe genital diseases in women, which in the worst cases can lead to infertility. For ethical reasons, there are limitations in human studies, which is why mouse models can be used to study chlamydial infections. C. trachomatis and C. muridarum are genetically very similar, show about 90 % orthology of gene contents and belong to the same genus. Since human C. trachomatis and murine C. muridarum infections are clinically comparable and can lead to infertility in the end, a progesterone dependent C. muridarum mouse model is a suitable and well-established model system for human C. trachomatis infections. In mice as in humans, chlamydiae ascend after vaginal infection via the cervix, uterus and fallopian tubes to the ovaries. They can cause adhesions in human fallopian tubes and hydrosalpinges, which consist of serous inclusions, in mice. At worst, both pathology variants can cause infertility in the respective individuals. Considering that the environmental conditions are decisive for the development and progression of inflammations, the hypoxic environment present in the genital tract plays an important role in genital chlamydial infections. Hypoxic reactions in tissue and cells are mediated by transcription factors such as the Hypoxia Inducible Factor (HIF) 1?. After activation, HIF 1? interferes with the host's immune response via metabolic changes and cellular adaptations. In the present work, an established progesterone dependent C57BL/6 mouse model was extended by a HIF 1? knockout mouse model. The deletion of HIF 1? was related to myeloid cells and mice had a C57BL/6 background. Using this mouse model, the impact of HIF 1? on the vaginal chlamydial load, on the pathology formation at the ovaries and on the immune response of vaginal C. muridarum infections was investigated. After vaginal C. muridarum infection, a lower vaginal chlamydial load was detectable in the HIF 1? / mice compared to the wildtype (WT) animals at the beginning of the acute infection. This was determined using recovery assays of vaginally swabbed infective progeny of C. muridarum. The amount of local immune cells in the uterus of the mouse lines was determined by flow cytometry. Differences between the genotypes without statistical significance in the number of macrophages, granulocytes, CD4+- and CD8+-T cells could be shown. The absence of HIF 1? significantly accelerated the formation of macroscopically and microscopically visible hydrosalpinges at day 21 p. i. in the HIF 1? / mice compared to the WT controls. On day 43 p. i. this difference between the genotypes leveled out. After evaluating the C. muridarum specific Serum IgG levels in the blood serum of mice via ELISA, a significant difference between the mouse lines on day 21 and 43 p. i. was visible. It consisted in a reduction of the IgG levels in the HIF 1? / mice compared to the WT animals. The correlations between vaginal chlamydial colonization, the cellular changes of the local immune system, the development of ovarian pathologies and the systemic IgG antibody formation with HIF 1? are discussed and interpreted in the present work. Concluding, HIF 1? has a significant impact on the development of ovarian pathologies after chlamydial infections and on the formation of C. muridarum specific IgG in the blood serum. This could be due to a compensation of a reduced efficiency of HIF 1? deficient immune cells by an increase in the number of macrophages and granulocytes in the uterus. Furthermore, this cell increase could have led to increased tissue cell proliferation, which had a significantly increasing effect on the development of ovarian pathologies in the HIF 1? / mice. The significant reduction in the C. muridarum specific IgG response compared to the WT control animals was probably dose dependent, since the lack of HIF 1? resulted in lower chlamydial colonization in the knockout animals. Therefore, these mice developed lower IgG responses than the WT control animals. From a clinical point of view, it is of particular interest that the severity of the chlamydia infection and the length of time the chlamydia remain in the genital tract of the mice could have an impact on the development of pathologies. The development of the pathology could possibly have been caused by the expression of the innate and adaptive immune responses of the mice.