Nerve fibres in peritoneal endometriosis

Tokushige, Natsuko; Markham, Robert; Russell, Peter; Fraser, Ian S.

doi:10.1093/humrep/del260

Cited by 250 publications

(214 citation statements)

References 38 publications

(37 reference statements)

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“…We have demonstrated in this study that NGF protein is preferentially localized to the glands in endometriotic lesions, which is consistent with previous reports [19,20]. In rodent models of endometriosis, NGF exprestime RT-PCR analysis of NGF and GAPDH mRNA derived from 19 different ovarian endometriomas, eight peritoneal endometriotic lesions and 11 intrauterine endometrial samples without endometriosis.…”

Section: Discussionsupporting

confidence: 91%

“…Recently, Anaf et al have demonstrated that a prominence of NGF expression together with perineurial and endoneurial invasion are preferentially observed in deep adenomyotic nodules, the most symptomatic form of endometriosis [19]. Furthermore, Tokushige et al have reported that peritoneal endometriotic lesions are intensely positive for NGF and possess significantly more nerve fibers than normal peritoneum [20].…”

Section: Semi-quantitative Rt-pcr and Real-time Rt-pcrmentioning

confidence: 99%

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Possible involvement of nerve growth factor in dysmenorrhea and dyspareunia associated with endometriosis

et al. 2013

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Section: Discussionsupporting

confidence: 91%

Section: Semi-quantitative Rt-pcr and Real-time Rt-pcrmentioning

confidence: 99%

Possible involvement of nerve growth factor in dysmenorrhea and dyspareunia associated with endometriosis

et al. 2013

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“…Our studies in a mouse model of endometriosis have revealed that macrophages resident in peritoneal lesions can originate from both the peritoneum and the endometrium. 9 Sensory C, sensory Ad, cholinergic, and adrenergic nerve fibers have been identified within lesions, 10,11 with greater nerve fiber density in areas that exhibit high macrophage density. 6 Studies in zebrafish have shown that macrophages will migrate toward damaged peripheral nerves, 12 consistent with a role for neuron-derived factors in immune-nerve cross talk.…”

mentioning

confidence: 99%

Estradiol Is a Critical Mediator of Macrophage-Nerve Cross Talk in Peritoneal Endometriosis

Greaves

Temp

Esnal-Zufiurre

et al. 2015

The American Journal of Pathology

131

121

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Endometriosis occurs in approximately 10% of women and is associated with persistent pelvic pain. It is defined by the presence of endometrial tissue (lesions) outside the uterus, most commonly on the peritoneum. Peripheral neuroinflammation, a process characterized by the infiltration of nerve fibers and macrophages into lesions, plays a pivotal role in endometriosis-associated pain. Our objective was to determine the role of estradiol (E2) in regulating the interaction between macrophages and nerves in peritoneal endometriosis. By using human tissues and a mouse model of endometriosis, we demonstrate that macrophages in lesions recovered from women and mice are immunopositive for estrogen receptor b, with up to 20% being estrogen receptor a positive. In mice, treatment with E2 increased the number of macrophages in lesions as well as concentrations of mRNAs encoded by Csf1, Nt3, and the tyrosine kinase neurotrophin receptor, TrkB. By using in vitro models, we determined that the treatment of rat dorsal root ganglia neurons with E2 increased mRNA concentrations of the chemokine C-C motif ligand 2 that stimulated migration of colony-stimulating factor 1edifferentiated macrophages. Conversely, incubation of colony-stimulating factor 1 macrophages with E2 increased concentrations of brainderived neurotrophic factor and neurotrophin 3, which stimulated neurite outgrowth from ganglia explants. In summary, we demonstrate a key role for E2 in stimulating macrophage-nerve interactions, providing novel evidence that endometriosis is an estrogen-dependent neuroinflammatory disorder. Endometriosis affects 10% of reproductive age women and is associated with persistent pelvic pain. 1 It is defined by the presence of endometrial-like tissue (lesions) found outside the uterus, most commonly on the peritoneum. The mechanisms underlying endometriosis-associated pain are poorly understood, but it has been postulated that estrogen-dependent neuroinflammation may be involved. 2 Notably, the presence of endometrial tissue fragments on the peritoneum elicits an immune response, including recruitment of macrophages, 3 blood vessels, and nerve fibers into the resultant lesions. 4,5 Within the lesions, CD68 þ macrophages have been detected in close association with nerve fibers. 6 Studies investigating macrophage activation and recruitment have revealed that endometriosis-associated macrophages exhibit a phenotype consistent with the alternative end of the macrophage activation spectrum. 7,8 In a mouse model of endometriosis that included cell transfer of polarized macrophages, Bacci et al 7 reported that mice injected with proinflammatory macrophages [macrophage (interferon g)] developed microscopic lesions, but those injected with alternatively activated macrophages [macrophage (IL-4)] developed larger lesions with a well-developed vasculature. Our studies in a mouse model of endometriosis have revealed that macrophages resident in peritoneal lesions can originate from both the peritoneum and the endometrium. 9

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“…Имеется очень небольшое число работ, посвященных изучению нервных волокон в очагах перитонеального эндоме-триоза, эндометриоза яичников и в эндометрии и миометрии женщин, больных эндометриозом. По-казано, что в очагах перитонеального эндометриоза количество и плотность расположения нервных во-локон значительно выше по сравнению с нормаль-ной брюшиной женщин без эндометриоза (16,3 и 2,5/мм 2 соответственно) [12,13]. G. Wang и соавт.…”

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Pain syndrome in endometriosis: clinical, morphological and molecular mechanisms

Ovakimyan¹,

Adamyan²,

Kogan³

et al. 2015

Probl. reprod.

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Nerve fibres in peritoneal endometriosis

Abstract: Peritoneal endometriotic lesions were innervated by sensory Adelta, sensory C, cholinergic and adrenergic nerve fibres. These nerve fibres may play an important role in the mechanisms of pain generation in this condition.

Cited by 250 publications

References 38 publications

Possible involvement of nerve growth factor in dysmenorrhea and dyspareunia associated with endometriosis

Possible involvement of nerve growth factor in dysmenorrhea and dyspareunia associated with endometriosis

Estradiol Is a Critical Mediator of Macrophage-Nerve Cross Talk in Peritoneal Endometriosis

Pain syndrome in endometriosis: clinical, morphological and molecular mechanisms

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