Infertility, IL-17, IL-33 and Microbiome Cross-Talk: The Extended ARIA-MeDALL Hypothesis
Samir Hamamah1,2, Fatima Barry1,2, Sarah Vannier3
1Biologie de la Reproduction, Hôpital Arnaud de Villeneuve, 34295 Montpellier, France.
International Journal of Molecular Sciences
|November 27, 2024
Summary
Infertility may be linked to gut dysbiosis, which increases estrogen levels and activates key cytokines. This suggests a gut-endometrial axis contributes to infertility and endometriosis.
Area of Science:
- Reproductive immunology
- Microbiome research
- Endocrinology
Background:
- Infertility prevalence is rising, mirroring increases in chronic inflammatory and autoimmune diseases.
- The ARIA-MeDALL hypothesis links these conditions to dysbiosis and cytokines like interleukin-17 (IL-17) and interleukin-33 (IL-33).
Purpose of the Study:
- To investigate the link between endometriosis, a major cause of infertility, and endometrial dysbiosis.
- To explore the role of IL-17 and IL-33 in the gut-endometrial axis and their interaction with intestinal dysbiosis.
Main Methods:
- The study proposes a connection between endometrial dysbiosis, IL-17, and IL-33.
- It hypothesizes that intestinal dysbiosis elevates estrogen levels, promoting endometriosis.
Main Results:
- Elevated estrogen levels, driven by intestinal dysbiosis, are identified as a key factor in endometriosis.
- Estrogens are shown to strongly activate IL-17 and IL-33, supporting the proposed axis.
Conclusions:
- Endometriosis and infertility are potentially linked through a gut-endometrial axis.
- Dysbiosis and specific cytokine interactions (IL-17, IL-33) play a significant role in this axis and contribute to infertility.
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