Effect of acute and regular exercise on growth hormone secretagogue receptor-1a expression in human lymphocytes, T cell subpopulation and monocytes

Bishop, Nicolette C.; Hayashida, Harumi; Clark, Megan L.; Coombs, Chelsey; Miller, Sean; Stensel, David J.

doi:10.1016/j.bbi.2013.09.017

Cited by 14 publications

(13 citation statements)

References 36 publications

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“…However, the mechanisms and cure for contact dermatitis and psoriasis remain unknown 4,57–59 . Many cell types, including epidermal cells 60 , lymphocytes 61 , macrophages 62 , fibroblasts 63 and dendritic cells 64 , secrete ghrelin, and these cells have been reported to mediate effects on skin inflammation, including contact dermatitis and psoriasis 65–67 , indicating the possibility that ghrelin may affect contact dermatitis and psoriasis. However, the effectiveness and mechanism of ghrelin on these skin inflammatory diseases have not been explored.…”

Section: Discussionmentioning

confidence: 99%

Ghrelin protects against contact dermatitis and psoriasiform skin inflammation by antagonizing TNF-α/NF-κB signaling pathways

Chen

et al. 2019

Sci Rep

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Contact dermatitis and psoriasis are skin disorders caused by immune dysregulation, yet much remains unknown about their underlying mechanisms. Ghrelin, a recently discovered novel peptide and potential endogenous anti-inflammatory factor expressed in the epidermis, is involved in skin repair and disease. In this study, we investigated the expression pattern and therapeutic effect of ghrelin in both contact dermatitis and psoriasis mouse models induced by oxazolone (OXA) and imiquimod (IMQ), respectively, and in TNF-α-stimulated RAW264.7 macrophages, NHEKs and skin fibroblasts. Ghrelin expression was reduced in both the OXA-induced contact dermatitis and IMQ-induced psoriasis mouse models. Furthermore, treatment with ghrelin attenuated skin inflammation in both the contact dermatitis and psoriasis mouse models. Mice administered PBS after OXA- or IMQ-induced model generation exhibited typical skin inflammation, whereas ghrelin treatment in these mouse models substantially decreased the dermatitis phenotype. In addition, exogenous ghrelin attenuated the inflammatory reaction induced by TNF-α in RAW264.7 cells. Moreover, ghrelin administration limited activation of NF-κB signaling. In summary, ghrelin may represent a potential molecular target for the prevention and treatment of inflammatory skin diseases, including contact dermatitis and psoriasis.

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Section: Discussionmentioning

confidence: 99%

Ghrelin protects against contact dermatitis and psoriasiform skin inflammation by antagonizing TNF-α/NF-κB signaling pathways

Chen

et al. 2019

Sci Rep

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“…In addition, Ghr can pass through the blood brain barrier and bind to GHSR-1a expressed in the hypothalamus and brain stem [19, 52]. GHSR-1a can be detected on human lymphocytes, T cell subpopulations and monocytes [53, 54]. Ghr can redirect leptin-induced T cell differentiation from a predominantly Th1 to a Th2 profile, leading to the production of anti-inflammatory cytokines, an attenuated Th1-type response in Th1-driven autoimmune disease, and enhanced proliferation of murine T cells [17, 53, 55].…”

Section: Discussionmentioning

confidence: 99%

Therapeutic effect of human ghrelin and growth hormone: Attenuation of immunosuppression in septic aged rats

Zhou

Yang

Aziz

et al. 2017

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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Sepsis is a leading cause of mortality in intensive care units, and is more common in the geriatric population. The control of hyperinflammation has been suggested as a therapeutic approach in sepsis, but to date clinical trials utilizing this strategy have not lead to an effective treatment. In addition to hyperinflammation, patients with sepsis often experience a state of immunosuppression, which serves as an important determinant for increased morbidity and mortality. We previously used aged animals to demonstrate the effectiveness of combined treatment with human ghrelin (Ghr) and human growth hormone (GH) in improving organ injury and survival in septic animals. Here, we hypothesized that combined treatment with Ghr and GH could improve immune function in septic aged animals. Male 24-month-old rats were subjected to cecal ligation and puncture (CLP) for sepsis induction. Human Ghr (80 nmol/kg BW) plus GH (50 μg/kg BW) or vehicle (normal saline) was administrated subcutaneously at 5 h after CLP. The ex vivo production of TNF-α, IL-6 and IL-10 to LPS-stimulation, as well as TNF-α, IL-6, IL-10 and INF-γ production to anti-CD3/anti-CD28 antibody-stimulation, in splenocytes isolated 20 h after CLP, was significantly decreased compared to production of these cytokines in splenocytes from sham animals. The production of cytokines from splenocytes isolated from septic animals that received the combined treatment, however, was significantly higher than from those isolated from vehicle-treated septic animals. Combined treatment prevented the loss of splenic CD4+ and CD8+ T cells in septic aged rats, and reduced lymphocyte apoptosis. Combined treatment also inhibited an increase in the regulatory T cell (Treg) population and expression of the immune co-inhibitory molecule PD-1 in the spleens of septic aged rats. In contrast, expression of HLA-DR was increased after combined treatment with Ghr and GH. Based on these findings, we conclude that co-administration of Ghr and GH is a promising therapeutic tool for reversing immunosuppression caused by sepsis in the geriatric population.

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“…In addition, moderate to high intensity training, reduces systemic cytokines (TNF-alpha, IL-6, IL-1beta) in an inflammatory milieu in elderly women [38], and in obesity [39]. Further, CRP is significantly decreased in physically active subjects [40], and growth hormone secretagogue receptor-1a is increased which has high anti-inflammatory properties [41]. These studies suggest that exercise has anti-inflammatory effects.…”

Section: B Exercise and Anti-inflammatory Effectsmentioning

confidence: 98%

Physical and Immunological Aspects of Exercise in Chronic Diseases

et al. 2014

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Physical inactivity and sedentary lifestyles are believed to be independent risk factors for the occurrence of numerous diseases, including, obesity, Type 2 diabetes, metabolic syndrome, cardiovascular disease, cancer and mental health, all leading to substantial morbidity and/or premature death. It has been found that regular exercise, is associated with better quality of life and health outcomes, and reduces the risk of cardiovascular disease and cancer. Here, we review the effects regular exercise has on mental health and well-being, on the immune system and in cancer, cardiovascular disease, autoimmunity and metabolic syndrome. Is exercise the new immunotherapy to treat diseases?

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Effect of acute and regular exercise on growth hormone secretagogue receptor-1a expression in human lymphocytes, T cell subpopulation and monocytes

Cited by 14 publications

References 36 publications

Ghrelin protects against contact dermatitis and psoriasiform skin inflammation by antagonizing TNF-α/NF-κB signaling pathways

Ghrelin protects against contact dermatitis and psoriasiform skin inflammation by antagonizing TNF-α/NF-κB signaling pathways

Therapeutic effect of human ghrelin and growth hormone: Attenuation of immunosuppression in septic aged rats

Physical and Immunological Aspects of Exercise in Chronic Diseases

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