scholarly journals Cytokines and Other Mediators in Alopecia Areata

2010 ◽  
Vol 2010 ◽  
pp. 1-5 ◽  
Author(s):  
Stamatis Gregoriou ◽  
Dafni Papafragkaki ◽  
George Kontochristopoulos ◽  
Eustathios Rallis ◽  
Dimitrios Kalogeromitros ◽  
...  

Alopecia areata, a disease of the hair follicles with multifactorial etiology and a strong component of autoimmune origin, has been extensively studied as far as the role of several cytokines is concerned. So far, IFN-, interleukins, TNF-, are cytokines that are well known to play a major role in the pathogenesis of the disease, while several studies have shown that many more pathways exist. Among them, MIG, IP-10, BAFF, HLA antigens, MIG, as well as stress hormones are implicated in disease onset and activity. Within the scope of this paper, the authors attempt to shed light upon the complexity of alopecia areata underlying mechanisms and indicate pathways that may suggest future treatments.

2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Eun Young Lee ◽  
You Jin Nam ◽  
Sangjin Kang ◽  
Eun Ju Choi ◽  
Inbo Han ◽  
...  

Abstract Background Stress is an important cause of skin disease, including hair loss. The hormonal response to stress is due to the HPA axis, which comprises hormones such as corticotropin releasing factor (CRF), adrenocorticotropic hormone (ACTH), and cortisol. Many reports have shown that CRF, a crucial stress hormone, inhibits hair growth and induces hair loss. However, the underlying mechanisms are still unclear. The aim of this study was to examine the effect of CRF on human dermal papilla cells (DPCs) as well as hair follicles and to investigate whether the HPA axis was established in cultured human DPCs. Results CRF inhibited hair shaft elongation and induced early catagen transition in human hair follicles. Hair follicle cells, both human DPCs and human ORSCs, expressed CRF and its receptors and responded to CRF. CRF inhibited the proliferation of human DPCs through cell cycle arrest at G2/M phase and induced the accumulation of reactive oxygen species (ROS). Anagen-related cytokine levels were downregulated in CRF-treated human DPCs. Interestingly, increases in proopiomelanocortin (POMC), ACTH, and cortisol were induced by CRF in human DPCs, and antagonists for the CRF receptor blocked the effects of this hormone. Conclusion The results of this study showed that stress can cause hair loss by acting through stress hormones. Additionally, these results suggested that a fully functional HPA axis exists in human DPCs and that CRF directly affects human DPCs as well as human hair follicles under stress conditions.


2013 ◽  
Vol 168 (1) ◽  
pp. R13-R18 ◽  
Author(s):  
Géraldine Falgarone ◽  
Hassan M Heshmati ◽  
Régis Cohen ◽  
Gérard Reach

The role of stress in the pathophysiology of Graves' disease is suggested by several clinical observations, by recent advances in immunology and by better understanding of autoimmune diseases which provides new insights into potential effects of stress hormones on T helper cell imbalance involved in the pathogenesis of autoimmune diseases. Stress management should therefore be an important part of the treatment of Graves' disease, as stress reduction may improve the effect of therapy. However, this field still requires interventional data to support stress management in the treatment of Graves' disease.


2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Agnieszka Gerkowicz ◽  
Dorota Krasowska ◽  
Aldona Pietrzak ◽  
Anna Michalak-Stoma ◽  
Joanna Bartosińska ◽  
...  

Alopecia areata (AA) is a common hair disorder observed in dermatological practice; however, the exact mechanisms that lead to the hair loss are still unknown. Disturbances in the blood supply of hair follicles may be one of the elements in the complex pathogenesis of AA. Nailfold videocapillaroscopy is a noninvasive technique that allows analysis of skin microcirculation in vivo. The aim of the study was the videocapillaroscopic assessment of skin microcirculation in AA patients. The study included 44 patients with patchy alopecia areata, 27 with alopecia universalis or totalis, and 40 healthy volunteers. Nailfold videocapillaroscopy was performed in all participants according to a standard protocol. Obtained images were assessed qualitatively and quantitatively. Two types of videocapillaroscopic images were distinguished in the study. Abnormal videocapillaroscopic images were found in 42% of patients. Tortuous and branching capillaries (, ), decreased density of capillaries (), enlargement of the efferent limb (), or top part of the loop () were observed significantly more often than in the control group. Only some patients with AA presented with microvascular abnormalities characterised by altered videocapillaroscopic images. More studies, including larger group of patients with AA, are required to determine the role of observed videocapillaroscopic alterations in AA.


2020 ◽  
Author(s):  
Eun Young Lee ◽  
You Jin Nam ◽  
Sangjin Kang ◽  
Eun Ju Choi ◽  
Inbo Han ◽  
...  

Abstract Background: Stress is an important cause of skin disease, including hair loss. The hormonal response to stress is due to the HPA axis, which comprises hormones such as corticotropin releasing factor (CRF) , adrenocorticotropic hormone (ACTH) , and cortisol. Many reports have shown that CRF, a crucial stress hormone, inhibits hair growth and induces hair loss. However, the underlying mechanisms are still unclear. The aim of this study was to examine the effect of CRF on human dermal papilla cells (DPCs) as well as hair follicles and to investigate whether the HPA axis was established in cultured human DPCs.Results: CRF inhibited hair shaft elongation and induced early catagen transition in human hair follicles. Hair follicle cells, both human DPCs and human ORSCs, expressed CRF and its receptors and responded to CRF. CRF inhibited the proliferation of human DPCs through cell cycle arrest at G2/M phase and induced the accumulation of reactive oxygen species (ROS) . Anagen-related cytokine levels were downregulated in CRF-treated human DPCs. Interestingly, increases in proopiomelanocortin (POMC) , ACTH, and cortisol were induced by CRF in human DPCs, and antagonists for the CRF receptor blocked the effects of this hormone. Conclusion: The results of this study showed that stress can cause hair loss by acting through stress hormones. Additionally, these results suggested that a fully functional HPA axis exists in human DPCs and that CRF directly affects human DPCs as well as human hair follicles under stress conditions.


PLoS ONE ◽  
2021 ◽  
Vol 16 (3) ◽  
pp. e0247506
Author(s):  
Alice Napias ◽  
Emilie Denechere ◽  
Willy Mayo ◽  
Imad Ghorayeb

Focusing on a specific population when studying dream characteristics can shed light on underlying mechanisms and correlates of dreaming. The aim of this study is to establish a clearer description of specific dream aspects and beliefs in a large cohort of students using a validated questionnaire, and to further investigate the role of sociodemographic variables such as age, gender and field of study. Participants were 1137 students aged from 18 to 34 (mean age: 22.2) who responded to an online version of the questionnaire. Our results showed a difference between humanities and science students, and a differential effect of gender on dream variables. Our results are discussed in light of previous investigations using the same questionnaire or focusing on the same population.


2020 ◽  
Author(s):  
Eun Young Lee ◽  
You Jin Nam ◽  
Sangjin Kang ◽  
Eun Ju Choi ◽  
Inbo Han ◽  
...  

Abstract Background: Stress is an important cause of skin disease, including hair loss. The hormonal response to stress is due to the HPA axis, which comprises hormones such as corticotropin releasing factor (CRF) , adrenocorticotropic hormone (ACTH) , and cortisol. Many reports have shown that CRF, a crucial stress hormone, inhibits hair growth and induces hair loss. However, the underlying mechanisms are still unclear. The aim of this study was to examine the effect of CRF on human dermal papilla cells (DPCs) as well as hair follicles and to investigate whether the HPA axis was established in cultured human DPCs. Results: CRF inhibited hair shaft elongation and induced early catagen transition in human hair follicles. Hair follicle cells, both human DPCs and human ORSCs, expressed CRF and its receptors and responded to CRF. CRF inhibited the proliferation of human DPCs through cell cycle arrest at G2/M phase and induced the accumulation of reactive oxygen species (ROS) . Anagen-related cytokine levels were downregulated in CRF-treated human DPCs. Interestingly, increases in proopiomelanocortin (POMC) , ACTH, and cortisol were induced by CRF in human DPCs, and antagonists for the CRF receptor blocked the effects of this hormone. Conclusion: The results of this study showed that stress can cause hair loss by acting through stress hormones. Additionally, these results suggested that a fully functional HPA axis exists in human DPCs and that CRF directly affects human DPCs as well as human hair follicles under stress conditions.


2009 ◽  
Vol 101 (6) ◽  
pp. 3192-3198 ◽  
Author(s):  
Matthew R. Campioni ◽  
Ming Xu ◽  
Daniel S. McGehee

Stress hormones released in the CNS following exposure to unavoidable, aversive stimuli have been shown to alter the physiology of neurons in multiple brain regions including hippocampus, amygdala, prefrontal cortex, and ventral tegmental area. The nucleus accumbens (NAc), a motor-limbic interface linked to motivation and reward, receives inputs from each of these stress-affected brain regions, raising the possibility that its function might also be altered in response to stress. To assess potential stress-induced plasticity in the NAc, we exposed adult mice to daily cold water forced swim for 2 consecutive days and conducted electrophysiological experiments assessing glutamate receptor function in brain slices taken 18–24 h following the second swim. We found that AMPA receptor (AMPAR)/ N-methyl-d-aspartate receptor (NMDAR) ratios, a measure of synaptic strength, were increased in the NAc shell but not core medium spiny neurons (MSNs) in stressed animals relative to controls. This effect was blocked by preadministration of glucocorticoid receptor (GR) antagonist RU486, suggesting that the observed changes are dependent on corticosteroid signaling. The role of corticosterone (CORT) in the observed plasticity was confirmed, because exogenous administration of 10 mg/kg CORT also enhanced AMPAR/NMDAR ratios in the NAc shell. The synaptic changes in NAc shell MSNs reflect an enhancement of AMPAR-mediated currents, as we observed increased AMPAR miniature postsynaptic current (mEPSC) amplitude following stress but no change in NMDAR mEPSCs. We hypothesize that altered information processing via plasticity of excitatory inputs might contribute to reward-related behaviors such as stress-induced reinstatement of drug seeking in animals and relapse in humans.


2019 ◽  
Vol 21 (4) ◽  
pp. 389-396 ◽  

Psychosocial stress—especially when chronic, excessive, or occurring early in life—has been associated with accelerated aging and increased disease risk. With rapid aging of the world population, the need to elucidate the underlying mechanisms is pressing, now more so than ever. Among molecular mechanisms linking stress and aging, the present article reviews evidence on the role of epigenetics, biochemical processes that can be set into motion by stressors and in turn influence genomic function and complex phenotypes, including aging-related outcomes. The article further provides a conceptual mechanistic framework on how stress may drive epigenetic changes at susceptible genomic sites, thereby exerting systems level effects on the aging epigenome while also regulating the expression of molecules implicated in aging-related processes. This emerging evidence, together with work examining related biological processes, begins to shed light on the epigenetic and, more broadly, molecular underpinnings of the long-hypothesized connection between stress and aging.


2021 ◽  
Vol 7 (4) ◽  
pp. 363-366
Author(s):  
Kashish Tyagi ◽  
Sheilly Kapoor ◽  
Ishani Mohapatra ◽  
Komal Sharma

Alopecia areata, an auto-immune disorder characterised by the appearance of non-scarring bald patches affecting the hair bearing areas of the body, it can be extremely difficult to treat and has a poor prognosis despite many therapeutic options. Platelet Rich Plasma (PRP) has been previously used to treat variety of alopecia including alopecia areata. A 21-year old girl presented with asymptomatic loss of hair from the scalp for the last more than two years. On examination, there was diffuse loss of hair all over the scalp with few small, thin light-coloured hair in the occipital region. Histopathological examination showed miniaturised hair follicles surrounded by variable inflammatory lymphohistiocytic infiltrate with a marked reduction in terminal-vellus hair ratio to 1:1.The response to previous treatments was poor at the end of 1 year. A trial of PRP was given with no adjuvant treatment with a total of eight sessions of PRP. Dramatic response was noted after 2 sessions in the form of improvement in hair diameter and total volume. Resistant areas also started showing hair growth. There are a few studies assessing the role of PRP therapy in AA. First report to establish the efficacy of PRP as a treatment modality in AA, showed PRP therapy to be superior to TCA and Placebo in growing pigmented hair in AA patches. A case report with ophiasis type AA resistant to intralesional steroid injections showed excellent response to PRP therapy. Previous studies have demonstrated beneficial role of PRP therapy in cases of patchy alopecia areata, in contrast ours was a case of chronic diffuse AA. Inspite of many treatment modalities tried for more than a year, the response was unsatisfactory. PRP therapy yielded amazing results in the form of hair growth over resistant areas and overall increase in pigmented hair which were sustained at one and a half year follow up. Our case was unique in the way that excellent response to PRP treatment was noted (a) In a case of diffuse alopecia areata. (b) In a case non- responsive to standard modalities. (c) In a case with no other supportive treatment.


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