scholarly journals Neurogenic Inflammation in the Context of Endometriosis—What Do We Know?

2021 ◽  
Vol 22 (23) ◽  
pp. 13102
Author(s):  
Renata Voltolini Velho ◽  
Eliane Taube ◽  
Jalid Sehouli ◽  
Sylvia Mechsner
Keyword(s):  
Immune Cells ◽  
Neurotrophic Factors ◽  
Peripheral Nerves ◽  
Neurogenic Inflammation ◽  
Treatment Options ◽  
Uterine Cavity ◽  
Sensory Nerves ◽  
Tailored Treatment ◽  
Growth Phenotype

Endometriosis (EM) is an estrogen-dependent disease characterized by the presence of epithelial, stromal, and smooth muscle cells outside the uterine cavity. It is a chronic and debilitating condition affecting ~10% of women. EM is characterized by infertility and pain, such as dysmenorrhea, chronic pelvic pain, dyspareunia, dysuria, and dyschezia. Although EM was first described in 1860, its aetiology and pathogenesis remain uncertain. Recent evidence demonstrates that the peripheral nervous system plays an important role in the pathophysiology of this disease. Sensory nerves, which surround and innervate endometriotic lesions, not only drive the chronic and debilitating pain associated with EM but also contribute to a growth phenotype by secreting neurotrophic factors and interacting with surrounding immune cells. Here we review the role that peripheral nerves play in driving and maintaining endometriotic lesions. A better understanding of the role of this system, as well as its interactions with immune cells, will unearth novel disease-relevant pathways and targets, providing new therapeutics and better-tailored treatment options.

scholarly journals A Novel Model of Cancer-Induced Peripheral Neuropathy and the Role of TRPA1 in Pain Transduction

2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Ahmad Maqboul ◽  
Bakheet Elsadek
Keyword(s):  
Immune Cells ◽  
Peripheral Nerves ◽  
Morphological Changes ◽  
Nerve Fibres ◽  
Cold Allodynia ◽  
Sciatic Nerves ◽  
Pain Transduction ◽  
Thermal Stimuli ◽  
Novel Model

Background. Models of cancer-induced neuropathy are designed by injecting cancer cells near the peripheral nerves. The interference of tissue-resident immune cells does not allow a direct contact with nerve fibres which affects the tumor microenvironment and the invasion process. Methods. Anaplastic tumor-1 (AT-1) cells were inoculated within the sciatic nerves (SNs) of male Copenhagen rats. Lumbar dorsal root ganglia (DRGs) and the SNs were collected on days 3, 7, 14, and 21. SN tissues were examined for morphological changes and DRG tissues for immunofluorescence, electrophoretic tendency, and mRNA quantification. Hypersensitivities to cold, mechanical, and thermal stimuli were determined. HC-030031, a selective TRPA1 antagonist, was used to treat cold allodynia. Results. Nociception thresholds were identified on day 6. Immunofluorescent micrographs showed overexpression of TRPA1 on days 7 and 14 and of CGRP on day 14 until day 21. Both TRPA1 and CGRP were coexpressed on the same cells. Immunoblots exhibited an increase in TRPA1 expression on day 14. TRPA1 mRNA underwent an increase on day 7 (normalized to 18S). Injection of HC-030031 transiently reversed the cold allodynia. Conclusion. A novel and a promising model of cancer-induced neuropathy was established, and the role of TRPA1 and CGRP in pain transduction was examined.

scholarly journals Role of Mast Cells in the Pathogenesis of Pruritus in Mastocytosis

2021 ◽  
Author(s):  
Dominika Kwiatkowska ◽  
Adam Reich
Keyword(s):  
Mast Cells ◽  
Neurogenic Inflammation ◽  
Treatment Options ◽  
Sensory Nerve ◽  
Neurokinin A ◽  
Calcitonin Gene ◽  
Abnormal Accumulation ◽  
Mutual Communication

Pruritus can be defined as an unpleasant sensation that evokes a desire to scratch and significantly impairs patients’ quality of life. Pruritus is widely observed in many dermatoses, including mastocytosis, a rare disease characterized by abnormal accumulation of mast cells, which can involve skin, bone marrow, and other organs. Increasing evidence highlights the role of mast cells in neurogenic inflammation and itching. Mast cells release various pruritogenic mediators, initiating subsequent mutual communication with specific nociceptors on sensory nerve fibres. Among important mediators released by mast cells that induce pruritus, one can distinguish histamine, serotonin, proteases, as well as various cytokines. During neuronal-induced inflammation, mast cells may respond to numerous mediators, including neuropeptides, such as substance P, neurokinin A, calcitonin gene-related peptide, endothelin 1, and nerve growth factor. Currently, treatment of pruritus in mastocytosis is focused on alleviating the effects of mediators secreted by mast cells. However, a deeper understanding of the intricacies of the neurobiology of this disease could help to provide better treatment options for patients.

scholarly journals The interaction between the immune system and the peripheral sensory nerves in pruritus

2021 ◽  
Author(s):  
Hiroyuki Irie ◽  
Kenji Kabashima
Keyword(s):  
Mental Health ◽  
Atopic Dermatitis ◽  
Immune Cells ◽  
Peripheral Nerves ◽  
Skin Diseases ◽  
Daily Life ◽  
Sensory Nerves ◽  
Inflammatory Skin Diseases ◽  
Heavy Burden ◽  
Peripheral Sensory

Abstract Pruritus is a skin-specific sensation that is observed in various skin diseases, especially in inflammatory skin diseases such as atopic dermatitis, and is deeply involved in their pathogenesis. Pruritus also adversely affects patients’ sleep and mental health, placing a heavy burden on daily life. As such, pruritus control is important to the maintenance of health. The mechanism of pruritus has recently been clarified and the discovery of various pruritus mediators, the identification of specific nerves that transmit pruritus and the accumulation of knowledge on pruritus perception have led to a better understanding of all aspects of pruritus generation, transmission and recognition. In the case of pruritus caused by dermatitis, immune cells infiltrating the skin secrete inflammatory cytokines, which also act on peripheral nerves as pruritus mediators and induce an inflammatory response. Interestingly, there has been accumulating evidence that peripheral nerves are also involved in the inflammation via neuropeptides. In this article, we summarize the findings on pruritus mediators secreted by immune cells and the roles of peripheral nerves in pruritus in terms of their interactions with immunity.

Involvement of neurogenic inflammation in antigen-induced bronchoconstriction in guinea pigs

1993 ◽  
Vol 265 (5) ◽  
pp. L507-L511 ◽  
Author(s):  
C. Bertrand ◽  
P. Geppetti ◽  
P. D. Graf ◽  
A. Foresi ◽  
J. A. Nadel
Keyword(s):  
Guinea Pigs ◽  
Neurogenic Inflammation ◽  
Neutral Endopeptidase ◽  
Receptor Activation ◽  
Sensory Nerves ◽  
Pulmonary Resistance ◽  
Receptor Antagonists ◽  
Tachykinin Receptor ◽  
Nk2 Receptor

The role of tachykinins released from sensory nerves in bronchoconstriction induced by antigen was studied in sensitized guinea pigs anesthetized with pentobarbital sodium and pretreated with atropine. The combination of NK2 (SR-48968) and NK1 (CP-96,345) tachykinin-receptor antagonists abolished the increase in total pulmonary resistance (RL) evoked by intravenous capsaicin but did not affect the response evoked by intravenous histamine. A small dose of aerosolized ovalbumin (OVA, 0.1%) produced a small increase in RL that was further increased and markedly prolonged by the neutral endopeptidase (NEP) inhibitor phosphoramidon; this bronchoconstrictor effect of OVA was markedly reduced by the NK2-receptor antagonist and was abolished by the combination of the NK1 and NK2-receptor antagonists together. When a larger dose of OVA (0.5%) was used, a maximal bronchoconstrictor response was obtained. Phosphoramidon did not potentiate this response significantly. The combination of NK1- and NK2-receptor antagonists blunted the response at 5 min only slightly but markedly attenuated the later (10–20 min) response. These results show that tachykinins released from sensory nerves play a significant role in antigen-induced bronchoconstriction in guinea pigs. This effect is exaggerated when the normal modulation of neuropeptides by NEP is inhibited and is mediated predominantly by NK2-receptor activation, with a smaller contribution by NK1 receptors.

scholarly journals The role of regulatory neuropeptides and neurotrophic factors in asthma pathophysiology

2019 ◽  
Vol 8 (4) ◽  
Author(s):  
Oxana Yu. Kytikova ◽  
Tatyana P. Novgorodtseva ◽  
Marina V. Antonyuk ◽  
Tatyana A. Gvozdenko
Keyword(s):  
Growth Factors ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Neurotrophic Factors ◽  
Neurogenic Inflammation ◽  
Allergic Inflammation ◽  
Research Area ◽  
Calcitonin Gene ◽  
The Relationship

In the last decade, the attention of scientists in the field of biomedicine is focused on studying the relationship between the immunological and neurogenic components of the inflammatory response and their contribution to the pathophysiology of allergic inflammation in asthma. The review is devoted to detailing the mechanism of neurogenic inflammation involving regulatory neuropeptides (substance P, vasoactive intestinal peptide, calcitonin gene-related peptide) in the pathogenesis of bronchial hyperreactivity in asthma. The role of neurotrophic growth factors (nerve growth factor, brain-derived neurotrophic factor) in the regulation of remodeling of bronchi in asthma has been analyzed. The study of neuroimmune mechanisms in the pathophysiology of asthma will it possible to find new therapeutic targets in this research area.

Treatment Options in COVID-19: The Role of Bioavailable Antiviral Ribonucleoside Analog on NHC in vitro

2020 ◽  
Author(s):  
Lara Bittmann
Keyword(s):  
World Health Organization ◽  
Clinical Picture ◽  
Treatment Options ◽  
World Health ◽  
Wuhan City ◽  
The World ◽  
Novel Coronavirus ◽  
Health Organization

On December 31, 2019, WHO was informed of cases of pneumonia of unknown cause in Wuhan City, China. A novel coronavirus was identified as the cause by Chinese authorities on January 7, 2020 and was provisionally named "2019-nCoV". This new Coronavirus causes a clinical picture which has received now the name COVID-19. The virus has spread subsequently worldwide and was explained on the 11th of March, 2020 by the World Health Organization to the pandemic.

Microbiota, Immune System and Autism Spectrum Disorders: An Integrative Model towards Novel Treatment Options

2020 ◽  
Vol 27 (31) ◽  
pp. 5119-5136 ◽  
Author(s):  
Barbara Carpita ◽  
Donatella Marazziti ◽  
Lionella Palego ◽  
Gino Giannaccini ◽  
Laura Betti ◽  
...  
Keyword(s):  
Immune System ◽  
Familial Aggregation ◽  
Treatment Options ◽  
Autism Spectrum ◽  
Integrative Model ◽  
Neural Basis ◽  
Integrative Framework ◽  
Intermediate Phenotypes ◽  
Close Relatives

Background: Autism Spectrum Disorder (ASD) is a condition strongly associated with genetic predisposition and familial aggregation. Among ASD patients, different levels of symptoms severity are detectable, while the presence of intermediate autism phenotypes in close relatives of ASD probands is also known in literature. Recently, increasing attention has been paid to environmental factors that might play a role in modulating the relationship between genomic risk and development and severity of ASD. Within this framework, an increasing body of evidence has stressed a possible role of both gut microbiota and inflammation in the pathophysiology of neurodevelopment. The aim of this paper is to review findings about the link between microbiota dysbiosis, inflammation and ASD. Methods: Articles ranging from 1990 to 2018 were identified on PUBMED and Google Scholar databases, with keyword combinations as: microbiota, immune system, inflammation, ASD, autism, broad autism phenotype, adult. Results: Recent evidence suggests that microbiota alterations, immune system and neurodevelopment may be deeply intertwined, shaping each other during early life. However, results from both animal models and human samples are still heterogeneous, while few studies focused on adult patients and ASD intermediate phenotypes. Conclusion: A better understanding of these pathways, within an integrative framework between central and peripheral systems, might not only shed more light on neural basis of ASD symptoms, clarifying brain pathophysiology, but it may also allow to develop new therapeutic strategies for these disorders, still poorly responsive to available treatments.

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