&lt;p&gt;Frontal Fibrosing Alopecia. An Example of Disrupted Aryl Hydrocarbon Receptor-Mediated Immunological Homeostasis in the Skin?&lt;/p&gt;

Noakes, Rowland

doi:10.2147/ccid.s262803

Cited by 12 publications

(11 citation statements)

References 41 publications

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“…Given that IDO is the first rate-limiting and inflammatory-inducing enzyme in the KP [ 39 ], we explored the molecular mechanisms underlying stress-induced depression. Accordingly, we measured two IDO isoforms, IDO1and IDO2, KP and its metabolites in the serum and brain tissue of mice harvested at the end of behavioral experiments by q-PCR, ELISA and HPLC.…”

Section: Resultsmentioning

confidence: 99%

Involvement of kynurenine pathway between inflammation and glutamate in the underlying etiopathology of CUMS-induced depression mouse model

Chen

et al. 2022

BMC Neurosci

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Inflammation and glutamate (GLU) are widely thought to participate in the pathogenesis of depression, and current evidence suggests that the development of depression is associated with the activation of the kynurenine pathway (KP). However, the exact mechanism of KP among the inflammation, GLU and depression remain poorly understood. In this study, we examined the involvement of KP, inflammation and GLU in depressive phenotype induced by chronic unpredictable mild stress (CUMS) in C57B/6 J mice. Our results showed that CUMS caused depressive like-behavior in the sucrose preference test, tail suspension test and forced swimming test. From a molecular perspective, CUMS upregulated the peripheral and central inflammatory response and activated indoleamine 2,3-dioxygenase (IDO), the rate-limiting enzyme of KP, which converts tryptophan (TRP) into kynurenine (KYN). KYN is a precursor for QA in microglia, which could activate the N-methyl-D-aspartate receptor (NMDAR), increasing the GLU release, mirrored by increased IDO activity, quinolinic acid and GLU levels in the hippocampus, prefrontal cortex and serum. However, intervention with IDO inhibitor 1-methyl-DL-tryptophan (50 mg/kg/s.c.) and 1-methyl-L-tryptophan (15 mg/kg/i.p.) reversed the depressive-like behaviors and adjusted central and peripheral KP’s metabolisms levels as well as GLU content, but the inflammation levels were not completely affected. These results provide certain evidence that KP may be a vital pathway mediated by IDO linking inflammation and glutamate, contributing to depression.

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Section: Resultsmentioning

confidence: 99%

Involvement of kynurenine pathway between inflammation and glutamate in the underlying etiopathology of CUMS-induced depression mouse model

Chen

et al. 2022

BMC Neurosci

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“…A new hypothesis proposes that FFA may arise as a result of excessive facial photo-protection, with a resultant disturbance in immunological homeostasis mediated via the aryl hydrocarbon receptor-kynurenine pathway axis (AhR/KP), leading to the collapse of immune privilege at the hair bulge [ 43 ]. Overexpression of the aryl hydrocarbon receptor (AhR) in the epidermis of FFA and LPP has been newly described in both unaffected and affected scalp [ 44 ].…”

Section: Aetiopathogenesismentioning

confidence: 99%

Frontal Fibrosing Alopecia: A Review

Porriño‐Bustamante

Fernández‐Pugnaire

Arias‐Santiago

2021

JCM

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Frontal fibrosing alopecia is a scarring alopecia, the prevalence of which is increasing worldwide since its first description in 1994. The reason for this emerging epidemic may be a higher exposure to an unknown trigger, although its aethiology and pathogenesis still remain enigmatic. Clinical, trichoscopic, sonographic, and histopathologic findings are allowing clinicians to understand more aspects about this type of cicatricial alopecia. Several treatments have been used in frontal fibrosing alopecia, although the 5-alpha reductase inhibitors seem to be the most promising. The aim of this report is to provide a compilation about the published data regarding frontal fibrosing alopecia in a narrative review.

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“…How to reverse the immune response in the early stage of EMT, or develop a corresponding targeting carrier for PPARγ, so that the PPARγ inhibitors can accumulate around the hair follicle, will become the future treatment direction or strategy to help us integrate the recent FFA pathobiological insights and translate them into specific therapeutic benefits. Commonly, it is reported that FFA is related to thyroid disease and some other autoimmune diseases, such as scalp discoid lupus erythematosus, vitiligo, lichen planus, lichen planus pigmentosa, and Sjögren’s syndrome ( 51 ).…”

Section: Discussionmentioning

confidence: 99%

“…One hypothesis is that the light protection provided by many facial care products reduces the synthesis of the tryptophan light product 6-formylindolo [3,2-b] carbazole (FICZ), which is a potent endogenous ligand of AHR, from the photooxidation of the essential amino acid L-tryptophan. It shows proinflammatory effects at lower concentrations and anti-inflammatory effects at higher concentrations ( 51 ). However, there is no definitive evidence of a causal relationship between sunscreens or environmental factors and FFA.…”

Section: Environmental Factorsmentioning

confidence: 99%

Frontal fibrosing alopecia: A review of disease pathogenesis

Miao

Jing

et al. 2022

Front. Med.

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Frontal fibrosing alopecia (FFA) is a primary patterned cicatricial alopecia that mostly affects postmenopausal women and causes frontotemporal hairline regression and eyebrow loss. Although the incidence of FFA has increased worldwide over the last decade, its etiology and pathology are still unclear. We cover the latest findings on its pathophysiology, including immunomodulation, neurogenic inflammation, and genetic regulation, to provide more alternatives for current clinical treatment. A persistent inflammatory response and immune privilege (IP) collapse develop and lead to epithelial hair follicle stem cells (eHFSCs) destruction and epithelial-mesenchymal transition (EMT) in the bulge area, which is the key process in FFA pathogenesis. Eventually, fibrous tissue replaces normal epithelial tissue and fills the entire hair follicle (HF). In addition, some familial reports and genome-wide association studies suggest a genetic susceptibility or epigenetic mechanism for the onset of FFA. The incidence of FFA increases sharply in postmenopausal women, and many FFA patients also suffer from female pattern hair loss in clinical observation, which suggests a potential association between FFA and steroid hormones. Sun exposure and topical allergens may also be triggers of FFA, but this conjecture has not been proven. More evidence and cohort studies are needed to help us understand the pathogenesis of this disease.

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<p>Frontal Fibrosing Alopecia. An Example of Disrupted Aryl Hydrocarbon Receptor-Mediated Immunological Homeostasis in the Skin?</p>

Cited by 12 publications

References 41 publications

Involvement of kynurenine pathway between inflammation and glutamate in the underlying etiopathology of CUMS-induced depression mouse model

Involvement of kynurenine pathway between inflammation and glutamate in the underlying etiopathology of CUMS-induced depression mouse model

Frontal Fibrosing Alopecia: A Review

Frontal fibrosing alopecia: A review of disease pathogenesis

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