Characterizing the endometrial fluid cytokine profile in women with endometriosis

Llarena, Natalia C.; Richards, Elliott G.; Priyadarshini, Anju; Fletcher, David; Bonfield, Tracey L.; Flyckt, Rebecca

doi:10.1007/s10815-020-01989-y

Cited by 15 publications

(10 citation statements)

References 36 publications

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“…In contrast, cytokines, including IL-1a, IL-1b, and IL-6, were found elevated in women with advanced stage endometriosis but were unchanged in women with mild endometriosis, compared with women without endometriosis. 42 A plausible explanation for such a variation may be the result of macrophage activity and secretions during inflammation, which can vary between proinflammatory and prorepair throughout the various stages of disease. 36,39 In mice, a recent study found increased levels of neutrophils and inflammatory cytokines G-CSF, TNFa, IL-6, and VEGF, in the peritoneal fluid during in the early stages (days 1-3) of endometriosis development.…”

Section: Discussionmentioning

confidence: 99%

A syngeneic inoculation mouse model of endometriosis that develops multiple comorbid visceral and cutaneous pain like behaviours

Maddern

Grundy

Harrington

et al. 2021

Pain

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Section: Discussionmentioning

confidence: 99%

A syngeneic inoculation mouse model of endometriosis that develops multiple comorbid visceral and cutaneous pain like behaviours

Maddern

Grundy

Harrington

et al. 2021

Pain

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“…Lessey et al found that PF has a detrimental effect on the endometrium (LIF and integrin αvβ3) in women with EMS [ 38 ], suggesting that the inflammatory cytokines in the PF of EMS patients exert a direct influence on the endometrium. In addition, Llarena et al examined the endometrial fluid of women with EMS to assess the endometrial microenvironment and found that the levels of proinflammatory cytokines (IL-1α, IL-1β, and IL-6) in the endometrial secretions of EMS patients were significantly higher [ 39 ]. Thus, EMS can impair fertility by increasing the concentration of proinflammatory cytokines ( Figure 2 ).…”

Section: Inflammationmentioning

confidence: 99%

“…[ 48 ]. IL-6 expression is significantly higher in the peripheral blood [ 49 ], PF [ 50 ], and endometrial fluid [ 39 ].…”

Section: Inflammationmentioning

confidence: 99%

Towards a Better Understanding of Endometriosis-Related Infertility: A Review on How Endometriosis Affects Endometrial Receptivity

Shan

Wang

2023

Biomolecules

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Endometriosis is the most common cause of infertility. Endometrial receptivity has been suggested to contribute to infertility and poor reproductive outcomes in affected women. Even though experimental and clinical data suggest that the endometrium differs in women with endometriosis, the pathogenesis of impaired endometrial receptivity remains incomplete. Therefore, this review summarizes the potential mechanisms that affect endometrial function and contribute to implantation failure. Contemporary data regarding hormone imbalance, inflammation, and immunoregulatory dysfunction will be reviewed here. In addition, genetic, epigenetic, glycosylation, metabolism and microRNA in endometriosis-related infertility/subfertility will be summarized. We provide a brief discussion and perspectives on their future clinical implications in the diagnosis and therapy to improve endometrial function in affected women.

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“…The inflammatory environment of endometriosis has been widely recognized over these years 6 . It was reported that the inflammatory cytokines were significantly increased in peritoneal fluid, 7,8 eutopic endometria, 9 and endometriotic lesions 10 . Furthermore, studies found that the immune cells, including macrophages, T cells and NK cells, and so on, were dramatically changed in both aspects of amount and function, which greatly aggravated the inflammatory response 11,12 .…”

Section: Introductionmentioning

confidence: 99%

Lipoxin A4 depresses inflammation and promotes autophagy via AhR/mTOR/AKT pathway to suppress endometriosis

Huang

Ding

et al. 2022

American J Rep Immunol

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Background: Endometriosis is a benign gynecological disease with the feature of estrogen dependence and inflammation. The function of autophagy and the correlation with inflammation were not yet revealed.Methods: Autophagosomes were detected by transmission electron microscopy.Gene Expression Omnibus (GEO) database was referred to analyze the expression of autophagy-related genes. Quantification of mRNA and protein expression was examined by qRT-PCR and Western Blot. Immunohistochemistry was performed to explore the expression of proteins in tissues. The mouse model of endometriosis was performed to analyze the autophagic activity and effect of LXA4. Results:The expression of autophagy-related genes in endometriotic lesions were unusually changed. The number of autophagosomes and LC3B-II expression was diminished, and p62 was increased in ectopic lesions from both patients and mice.Interleukin 1β (IL1β) attenuated the expression of LC3B and promoted the level p62.The autophagy activator MG-132 upregulated the expression of LC3B and reduced IL1β, IL6, and p62. LXA4 reversed the inhibitory effect of IL1β on the expression of LC3B and p62, and blocking the receptor of LXA4 AhR (aryl hydrocarbon receptor) resulted in the incapacitation of LXA4 to influence the effect of IL1β. LXA4 depressed the phosphorylation of AKT and mTOR to against IL1β, and blocking AhR negatively regulated the effect of LXA4 on AKT/mTOR pathway. LXA4 reduced the ectopic lesions and the expression of IL1β and p62, but enhanced LC3B-II in endometriotic mouse models. Conclusion:In endometriosis, increased inflammation of ectopic lesions prominently depresses autophagy. LXA4 could regulate autophagy by suppressing inflammatory response through AhR/AKT/mTOR pathway.

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Characterizing the endometrial fluid cytokine profile in women with endometriosis

Cited by 15 publications

References 36 publications

A syngeneic inoculation mouse model of endometriosis that develops multiple comorbid visceral and cutaneous pain like behaviours

A syngeneic inoculation mouse model of endometriosis that develops multiple comorbid visceral and cutaneous pain like behaviours

Towards a Better Understanding of Endometriosis-Related Infertility: A Review on How Endometriosis Affects Endometrial Receptivity

Lipoxin A4 depresses inflammation and promotes autophagy via AhR/mTOR/AKT pathway to suppress endometriosis

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