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Infectious agents of the female genital tract must interact with innate defenses of genital mucosal epithelial cells, along with the immune cells recruited to the site of infection. Chlamydia muridarum, along with other chlamydial species, has evolved host-specific mechanisms to evade some of these innate defenses out of necessity, as its obligate-intracellular nature requires parts of the host’s enzymatic and nutritional machinery to survive. However, to its detriment, C. muridarum ultimately incites a robust immune response that recruits both bacterial-clearing and tissue-damaging immune cells to the genital tract. One such host-defense mechanism is the inflammasome. Microbial- or stress-associated stimuli induce a signaling cascade that results in the rapid activation of canonical inflammasome caspase-1, which cleaves and activates inflammatory cytokines interleukin-1b (IL-1b) and IL-18 before driving the cell to an inflammatory death. The noncanonical inflammasome, caspase-11, is able to directly sense cytosolic lipopolysaccharide (LPS), and results in the release of IL-1a and IL-1b. The release of IL-1a and IL-1b, the two pro-inflammatory cytokines that can signal through the type I interleukin receptor (IL-1R1), results in NF-kB activation and the production of several pro-inflammatory cytokines that recruit immune cells like neutrophils, macrophages, and T cells to sites of infection and inflammation. However, though the downstream consequences of either IL-1a or IL-1b binding to IL-1R1 are identical, these two cytokines are produced in differential and non-redundant ways, and as such often play different roles in infection-induced pathologies. Similarly, caspase-1 and caspase-11 are induced by different stimuli, and can have differential effects in response to infection. In this dissertation, we examine and compare the roles of inflammasome activation and IL-1a/b during Chlamydia muridarum infection, and how each affects the long-term pathology that ultimately destroys the female reproductive tract. We begin Chapter 1 by summarizing Chlamydia’s life cycle and the significant immune pathways identified here, and review inflammasome and IL-1R1 signaling. In Chapter 2, we compare and contrast the roles for caspase-1 and caspase-11 during infection, and how each impacts long-term pathology in the oviduct. Similarly, Chapter 3 will first compare the effects of IL-1a and IL-1b on pathology, and then will explore the immunologic and long-term consequences of IL-1a activation in the genital tract. We will conclude in Chapter 4 with a discussion about how these pathways influence each other, along with implications for women with pelvic inflammatory disease.