SCYNAPSIS
#microbiology
#microbiology
#microbiology
Image credit by Jo Panuwat D via Shutterstock
Image credit by Jo Panuwat D via Shutterstock
Image credit by Jo Panuwat D via Shutterstock
Pablo Avalos Prado
Pablo Avalos Prado
Pablo Avalos Prado
Neuroscientist & Medical Writer
Neuroscientist & Medical Writer
Neuroscientist & Medical Writer
June 23, 2023
June 23, 2023
June 23, 2023
Fusobacterium infection facilitates the development of endometriosis
Fusobacterium infection facilitates the development of endometriosis
Fusobacterium infection facilitates the development of endometriosis
Bacterial infection triggers an immune response that might underlie endometriosis generation, according to a new article published in Science Translational Medicine.
Endometriosis is a painful and chronic disease affecting up to 10% of women of reproductive age that is characterized by the growth of endometrial-like tissue outside the uterus, resulting in inflammation, pelvic pain and infertility. Although retrograde menstruation (when menstrual blood flows back through the fallopian tubes) is a widely accepted cause, not all the women having this condition develop endometriosis.
A new study published in Science Translational Medicine shows that endometriosis is also associated with the presence of certain bacteria. Indeed, the uterine cavity is almost sterile compared to the vagina, which hosts millions of microbial communities. However, some of the residing bacteria, Fusobacterium nucleatum (F. nucleatum), can trigger an immune response resulting in the formation of endometrial-like tissue outside the uterus underlying endometriosis, according to this study.
Transgelin promotes the formation of endometriotic tissue
The authors initially identified the molecules leading to the proliferation of fibroblasts, a cellular type constituting many human tissues, including the endometrial-like tissue typical from endometriosis. After comparing different databases of genes from endometriotic tissues of patients, they observed the strong presence of transgelin (TALGN), a protein that confers contractile function on cells. Transgelin, which resulted to be particularly activated in fibroblasts of endometriotic tissue, was also essential for proliferation and migration in cultured fibroblasts.
Additional experiments with cells from endometriosis tissues revealed that fibroblast migration is mediated through interleukin-6 (IL-6), which promotes both inflammation and activation of transgelin. Finally, the investigators also found that the cellular transforming growth factor TGF-β1 induces the expression of transgelin in fibroblasts and their subsequent proliferation, resulting in formation of the endometrial-like tissue.
Fusobacterium infection influences the progression of endometriosis
The abundance of TGF-β in the endometrial microenvironment led to the hypothesis of bacterial influence in endometriosis. The authors observed by quantitative PCR that the bacterial symbiont F. nucleatum was highly present in endometrial tissues of women participating in the study, and significantly more abundant in those tissues from patients with endometriosis. Interestingly, these bacteria co-localised and activated a group of macrophages known to produce TGF-β1 in ovarian endometriotic tissue, the molecule promoting fibroblast proliferation. These data suggest that F. nucleatum within the endometrium may influence TAGLN abundance in fibroblasts via up-regulated TGF-β1 signaling.
The authors confirmed the role of F. nucleatum in endometriosis by performing experiments on mice. In their model, they transfer endometrium from a donor mouse to a receptor mouse and observed that only tissues containing F. nucleatum could induce both endometriotic lesions in the receptor mouse, and the proliferation of TALGN-fibroblasts and macrophages producing TGF-β1. Since other bacteria like Lactobacillum iners, which are the major indigenous bacteria of the vaginal microbiota in reproductive-age women, did not produce this effect, the investigators concluded that this immune response is specifically associated to F. nucleatum infection.
Supporting this theory, one week after specific antibiotic treatment against F.nucleatum macrophage presence, TGF-β1 expression, and TAGLN expression were all decreased. Consistently, recipient mice, which received endometrium from F. nucleatum–infected donor mice treated with antibiotics, developed significantly fewer endometriotic lesions than in the control group without antibiotics. Therefore, F.nucleatum infection facilitates the development of endometriosis through conversion of endometrial fibroblasts.
Original article
Bacterial infection triggers an immune response that might underlie endometriosis generation, according to a new article published in Science Translational Medicine.
Endometriosis is a painful and chronic disease affecting up to 10% of women of reproductive age that is characterized by the growth of endometrial-like tissue outside the uterus, resulting in inflammation, pelvic pain and infertility. Although retrograde menstruation (when menstrual blood flows back through the fallopian tubes) is a widely accepted cause, not all the women having this condition develop endometriosis.
A new study published in Science Translational Medicine shows that endometriosis is also associated with the presence of certain bacteria. Indeed, the uterine cavity is almost sterile compared to the vagina, which hosts millions of microbial communities. However, some of the residing bacteria, Fusobacterium nucleatum (F. nucleatum), can trigger an immune response resulting in the formation of endometrial-like tissue outside the uterus underlying endometriosis, according to this study.
Transgelin promotes the formation of endometriotic tissue
The authors initially identified the molecules leading to the proliferation of fibroblasts, a cellular type constituting many human tissues, including the endometrial-like tissue typical from endometriosis. After comparing different databases of genes from endometriotic tissues of patients, they observed the strong presence of transgelin (TALGN), a protein that confers contractile function on cells. Transgelin, which resulted to be particularly activated in fibroblasts of endometriotic tissue, was also essential for proliferation and migration in cultured fibroblasts.
Additional experiments with cells from endometriosis tissues revealed that fibroblast migration is mediated through interleukin-6 (IL-6), which promotes both inflammation and activation of transgelin. Finally, the investigators also found that the cellular transforming growth factor TGF-β1 induces the expression of transgelin in fibroblasts and their subsequent proliferation, resulting in formation of the endometrial-like tissue.
Fusobacterium infection influences the progression of endometriosis
The abundance of TGF-β in the endometrial microenvironment led to the hypothesis of bacterial influence in endometriosis. The authors observed by quantitative PCR that the bacterial symbiont F. nucleatum was highly present in endometrial tissues of women participating in the study, and significantly more abundant in those tissues from patients with endometriosis. Interestingly, these bacteria co-localised and activated a group of macrophages known to produce TGF-β1 in ovarian endometriotic tissue, the molecule promoting fibroblast proliferation. These data suggest that F. nucleatum within the endometrium may influence TAGLN abundance in fibroblasts via up-regulated TGF-β1 signaling.
The authors confirmed the role of F. nucleatum in endometriosis by performing experiments on mice. In their model, they transfer endometrium from a donor mouse to a receptor mouse and observed that only tissues containing F. nucleatum could induce both endometriotic lesions in the receptor mouse, and the proliferation of TALGN-fibroblasts and macrophages producing TGF-β1. Since other bacteria like Lactobacillum iners, which are the major indigenous bacteria of the vaginal microbiota in reproductive-age women, did not produce this effect, the investigators concluded that this immune response is specifically associated to F. nucleatum infection.
Supporting this theory, one week after specific antibiotic treatment against F.nucleatum macrophage presence, TGF-β1 expression, and TAGLN expression were all decreased. Consistently, recipient mice, which received endometrium from F. nucleatum–infected donor mice treated with antibiotics, developed significantly fewer endometriotic lesions than in the control group without antibiotics. Therefore, F.nucleatum infection facilitates the development of endometriosis through conversion of endometrial fibroblasts.
Original article
Bacterial infection triggers an immune response that might underlie endometriosis generation, according to a new article published in Science Translational Medicine.
Endometriosis is a painful and chronic disease affecting up to 10% of women of reproductive age that is characterized by the growth of endometrial-like tissue outside the uterus, resulting in inflammation, pelvic pain and infertility. Although retrograde menstruation (when menstrual blood flows back through the fallopian tubes) is a widely accepted cause, not all the women having this condition develop endometriosis.
A new study published in Science Translational Medicine shows that endometriosis is also associated with the presence of certain bacteria. Indeed, the uterine cavity is almost sterile compared to the vagina, which hosts millions of microbial communities. However, some of the residing bacteria, Fusobacterium nucleatum (F. nucleatum), can trigger an immune response resulting in the formation of endometrial-like tissue outside the uterus underlying endometriosis, according to this study.
Transgelin promotes the formation of endometriotic tissue
The authors initially identified the molecules leading to the proliferation of fibroblasts, a cellular type constituting many human tissues, including the endometrial-like tissue typical from endometriosis. After comparing different databases of genes from endometriotic tissues of patients, they observed the strong presence of transgelin (TALGN), a protein that confers contractile function on cells. Transgelin, which resulted to be particularly activated in fibroblasts of endometriotic tissue, was also essential for proliferation and migration in cultured fibroblasts.
Additional experiments with cells from endometriosis tissues revealed that fibroblast migration is mediated through interleukin-6 (IL-6), which promotes both inflammation and activation of transgelin. Finally, the investigators also found that the cellular transforming growth factor TGF-β1 induces the expression of transgelin in fibroblasts and their subsequent proliferation, resulting in formation of the endometrial-like tissue.
Fusobacterium infection influences the progression of endometriosis
The abundance of TGF-β in the endometrial microenvironment led to the hypothesis of bacterial influence in endometriosis. The authors observed by quantitative PCR that the bacterial symbiont F. nucleatum was highly present in endometrial tissues of women participating in the study, and significantly more abundant in those tissues from patients with endometriosis. Interestingly, these bacteria co-localised and activated a group of macrophages known to produce TGF-β1 in ovarian endometriotic tissue, the molecule promoting fibroblast proliferation. These data suggest that F. nucleatum within the endometrium may influence TAGLN abundance in fibroblasts via up-regulated TGF-β1 signaling.
The authors confirmed the role of F. nucleatum in endometriosis by performing experiments on mice. In their model, they transfer endometrium from a donor mouse to a receptor mouse and observed that only tissues containing F. nucleatum could induce both endometriotic lesions in the receptor mouse, and the proliferation of TALGN-fibroblasts and macrophages producing TGF-β1. Since other bacteria like Lactobacillum iners, which are the major indigenous bacteria of the vaginal microbiota in reproductive-age women, did not produce this effect, the investigators concluded that this immune response is specifically associated to F. nucleatum infection.
Supporting this theory, one week after specific antibiotic treatment against F.nucleatum macrophage presence, TGF-β1 expression, and TAGLN expression were all decreased. Consistently, recipient mice, which received endometrium from F. nucleatum–infected donor mice treated with antibiotics, developed significantly fewer endometriotic lesions than in the control group without antibiotics. Therefore, F.nucleatum infection facilitates the development of endometriosis through conversion of endometrial fibroblasts.
Original article