scholarly journals Skin Microbiota in Atopic Dermatitis

2020 ◽  
Vol 13 (4) ◽  
pp. 374-382
Author(s):  
Jessica Herlianez Saiful ◽  
Satya Wydya Yenny
Keyword(s):  
Immune Response ◽  
Atopic Dermatitis ◽  
Microbial Community ◽  
Immune Responses ◽  
Skin Diseases ◽  
Major Influence ◽  
First Line ◽  
Skin Microbiota ◽  
Immune Mediators

In human body, the skin is the largest organ that has the function of mediating contact with the outside world and providing our body first line of defense against all kinds of pathogens, poisons and dangerous environments. The role of skin which are physical and immunological, supported by the microbial community that inhabits the skin. Skin microbiota contributes to barrier function by competing with pathogens and dealing with immune cells in the skin, to modulate local and systemic immune responses. Skin microbiota and immune mediators, for example complement system, have two-way interactions, and this shows that commensal microbes must be considered an important part of healthy skin. Many evidence shows that the composition of microbiota, especially in the intestines and also on the skin, can have a major influence on an individual's health. The influence of gut microbiota and its influence on the immune response has been widely studied, but the link of skin microbiota, immune response and certain skin diseases has not been widely discussed in the literature. Skin microbiota is expected to be affected in certain dermatological conditions, such as in psoriasis and in atopic dermatitis, which further shows the importance of the skin microbial community for human health. Understanding of skin microbiota role in pathogenesis of atopic dermatitis is still needed.

scholarly journals Pathogens MenTORing Macrophages and Dendritic Cells: Manipulation of mTOR and Cellular Metabolism to Promote Immune Escape

Cells ◽  
2020 ◽  
Vol 9 (1) ◽  
pp. 161 ◽  
Author(s):  
Lonneke V. Nouwen ◽  
Bart Everts
Keyword(s):  
Immune Response ◽  
Dendritic Cells ◽  
Amino Acid ◽  
Immune Responses ◽  
Metabolic Pathways ◽  
Immune Escape ◽  
Mammalian Target Of Rapamycin ◽  
Metabolic Reprogramming ◽  
First Line

Myeloid cells, including macrophages and dendritic cells, represent an important first line of defense against infections. Upon recognition of pathogens, these cells undergo a metabolic reprogramming that supports their activation and ability to respond to the invading pathogens. An important metabolic regulator of these cells is mammalian target of rapamycin (mTOR). During infection, pathogens use host metabolic pathways to scavenge host nutrients, as well as target metabolic pathways for subversion of the host immune response that together facilitate pathogen survival. Given the pivotal role of mTOR in controlling metabolism and DC and macrophage function, pathogens have evolved strategies to target this pathway to manipulate these cells. This review seeks to discuss the most recent insights into how pathogens target DC and macrophage metabolism to subvert potential deleterious immune responses against them, by focusing on the metabolic pathways that are known to regulate and to be regulated by mTOR signaling including amino acid, lipid and carbohydrate metabolism, and autophagy.

scholarly journals The Implications of Pruritogens in the Pathogenesis of Atopic Dermatitis

2021 ◽  
Vol 22 (13) ◽  
pp. 7227
Author(s):  
Lai-San Wong ◽  
Yu-Ta Yen ◽  
Chih-Hung Lee
Keyword(s):  
Atopic Dermatitis ◽  
Environmental Factors ◽  
Immune Responses ◽  
Immune Cells ◽  
Inflammatory Disease ◽  
Targeted Therapies ◽  
Skin Barrier ◽  
Skin Barrier Function ◽  
Inflammatory Molecules

Atopic dermatitis (AD) is a prototypic inflammatory disease that presents with intense itching. The pathophysiology of AD is multifactorial, involving environmental factors, genetic susceptibility, skin barrier function, and immune responses. A recent understanding of pruritus transmission provides more information about the role of pruritogens in the pathogenesis of AD. There is evidence that pruritogens are not only responsible for eliciting pruritus, but also interact with immune cells and act as inflammatory mediators, which exacerbate the severity of AD. In this review, we discuss the interaction between pruritogens and inflammatory molecules and summarize the targeted therapies for AD.

scholarly journals Ubiquitous Overexpression of Chromatin Remodeling Factor SRG3 Exacerbates Atopic Dermatitis in NC/Nga Mice by Enhancing Th2 Immune Responses

2021 ◽  
Vol 22 (4) ◽  
pp. 1553
Author(s):  
Sung Won Lee ◽  
Hyun Jung Park ◽  
Jungmin Jeon ◽  
Yun Hoo Park ◽  
Tae-Cheol Kim ◽  
...  
Keyword(s):  
Atopic Dermatitis ◽  
Mast Cells ◽  
Immune Responses ◽  
Chromatin Remodeling ◽  
Skin Diseases ◽  
Immunoglobulin E ◽  
Critical Role ◽  
Interleukin 4 ◽  
Inflammatory Skin Diseases ◽  
Immune Disorder

The SWItch (SWI)3-related gene (SRG3) product, a SWI/Sucrose Non-Fermenting (SNF) chromatin remodeling subunit, plays a critical role in regulating immune responses. We have previously shown that ubiquitous SRG3 overexpression attenuates the progression of Th1/Th17-mediated experimental autoimmune encephalomyelitis. However, it is unclear whether SRG3 overexpression can affect the pathogenesis of inflammatory skin diseases such as atopic dermatitis (AD), a Th2-type immune disorder. Thus, to elucidate the effects of SRG3 overexpression in AD development, we bred NC/Nga (NC) mice with transgenic mice where SRG3 expression is driven by the β-actin promoter (SRG3β-actin mice). We found that SRG3β-actin NC mice exhibit increased AD development (e.g., a higher clinical score, immunoglobulin E (IgE) hyperproduction, and an increased number of infiltrated mast cells and basophils in skin lesions) compared with wild-type NC mice. Moreover, the severity of AD pathogenesis in SRG3β-actin NC mice correlated with expansion of interleukin 4 (IL4)-producing basophils and mast cells, and M2 macrophages. Furthermore, this accelerated AD development is strongly associated with Treg cell suppression. Collectively, our results have identified that modulation of SRG3 function can be applied as one of the options to control AD pathogenesis.

scholarly journals Staphylococcal Communities on Skin Are Associated with Atopic Dermatitis and Disease Severity

2021 ◽  
Vol 9 (2) ◽  
pp. 432
Author(s):  
Sofie Marie Edslev ◽  
Caroline Meyer Olesen ◽  
Line Brok Nørreslet ◽  
Anna Cäcilia Ingham ◽  
Søren Iversen ◽  
...  
Keyword(s):  
Atopic Dermatitis ◽  
Alpha Diversity ◽  
Skin Microbiota ◽  
Specific Primers ◽  
Staphylococcus Lugdunensis ◽  
Disease Symptoms ◽  
Lesional Skin ◽  
Staphylococcus Capitis ◽  
Staphylococcus Hominis

The skin microbiota of atopic dermatitis (AD) patients is characterized by increased Staphylococcus aureus colonization, which exacerbates disease symptoms and has been linked to reduced bacterial diversity. Skin bacterial communities in AD patients have mostly been described at family and genus levels, while species-level characterization has been limited. In this study, we investigated the role of the bacteria belonging to the Staphylococcus genus using targeted sequencing of the tuf gene with genus-specific primers. We compared staphylococcal communities on lesional and non-lesional skin of AD patients, as well as AD patients with healthy controls, and determined the absolute abundance of bacteria present at each site. We observed that the staphylococcal community, bacterial alpha diversity, and bacterial densities were similar on lesional and non-lesional skin, whereas AD severity was associated with significant changes in staphylococcal composition. Increased S. aureus, Staphylococcus capitis, and Staphylococcus lugdunensis abundances were correlated with increased severity. Conversely, Staphylococcus hominis abundance was negatively correlated with severity. Furthermore, S. hominis relative abundance was reduced on AD skin compared to healthy skin. In conclusion, various staphylococcal species appear to be important for skin health.

scholarly journals Role of Immune Response and Some Microbial Agents in Atopic Dermatitis

2020 ◽  
Vol 8 (6) ◽  
pp. 7
Author(s):  
Suzan Yousif Jasim ◽  
Mayssaa E. Abdalah ◽  
Bahir Abdul Razzaq Mshimesh
Keyword(s):  
Immune Response ◽  
Atopic Dermatitis ◽  
Microbial Agents

scholarly journals ROLE OF PATHYAPATHYA IN THE MANAGEMENT OF EKA KUSHTHA (PSORIASIS)

AYUSHDHARA ◽  
2021 ◽  
pp. 3009-3013
Author(s):  
Chandrakar Srishti ◽  
Diwan Rashmi ◽  
Sahu Jeevan Lal
Keyword(s):  
Skin Diseases ◽  
Medical Science ◽  
Signs And Symptoms ◽  
Lifestyle Changes ◽  
First Line ◽  
Basic Principles ◽  
Complete Treatment ◽  
Exact Etiology ◽  
Busy Schedule

Ayurveda is not merely a medical science. It is a complete life science. In Ayurveda all skin diseases are described under the Kushtha, which are further divided into Maha Kushtha and Kshudra Kushtha. Eka Kushtha is one of the Kshudra Kushtha described in different Ayurvedic classics. It is Vata-Kaphaj disorder. Ekakushtha has signs and symptoms i.e., Aswedanam (absence of sweating), Mahavastu (big size lesions) and Matsyasha kalopamam (scaling) which can be compared with Psoriasis. The exact etiology of Psoriasis is not known but many precipitating factors like genetic, dietary, immunological and psychological has been found. It is spreading fast because of unsuitable lifestyle changes such as dietary pattern, busy schedule and stress. The aim is to find out safe and effective treatment for psoriasis. Ayurveda plays an important role. There are three basic principles to treat any disease in Ayurveda i.e., Shodhana, Shamana and Nidana Parivarjana. Nidana Parivarjana is considered as the first line of treatment in most of the diseases. In Ayurveda diet plays a major role in the prevention and management of the disease. Sometimes Pathya and Apathya are the complete treatment of any diseases. So the main aim of this article is to focus on etiological factors of Ekakushtha and its management by various dietary regimens described in different Ayurvedic texts.

scholarly journals The Keratinocyte as a Crucial Cell in the Predisposition, Onset, Progression, Therapy and Study of the Atopic Dermatitis

2021 ◽  
Vol 22 (19) ◽  
pp. 10661
Author(s):  
Pamela Gallegos-Alcalá ◽  
Mariela Jiménez ◽  
Daniel Cervantes-García ◽  
Eva Salinas
Keyword(s):  
Atopic Dermatitis ◽  
Complex Disease ◽  
Skin Diseases ◽  
Current Knowledge ◽  
Immune Dysregulation ◽  
Chronic Inflammatory Disease ◽  
Skin Microbiota ◽  
External Agents ◽  
Chronic Skin ◽  
Inflammatory Molecules

The keratinocyte (KC) is the main functional and structural component of the epidermis, the most external layer of the skin that is highly specialized in defense against external agents, prevention of leakage of body fluids and retention of internal water within the cells. Altered epidermal barrier and aberrant KC differentiation are involved in the pathophysiology of several skin diseases, such as atopic dermatitis (AD). AD is a chronic inflammatory disease characterized by cutaneous and systemic immune dysregulation and skin microbiota dysbiosis. Nevertheless, the pathological mechanisms of this complex disease remain largely unknown. In this review, we summarize current knowledge about the participation of the KC in different aspects of the AD. We provide an overview of the genetic predisposing and environmental factors, inflammatory molecules and signaling pathways of the KC that participate in the physiopathology of the AD. We also analyze the link among the KC, the microbiota and the inflammatory response underlying acute and chronic skin AD lesions.

scholarly journals Dual Role of Toll-Like Receptor 7 in the Pathogenesis of Rabies Virus in a Mouse Model

2020 ◽  
Vol 94 (9) ◽  
Author(s):  
Zhaochen Luo ◽  
Lei Lv ◽  
Yingying Li ◽  
Baokun Sui ◽  
Qiong Wu ◽  
...  
Keyword(s):  
Immune Response ◽  
Mouse Model ◽  
Immune Responses ◽  
Rabies Virus ◽  
Mouse Brain ◽  
Early Stage ◽  
Toll Like Receptor ◽  
Innate Recognition ◽  
Recognition Receptor

ABSTRACT Rabies, caused by rabies virus (RABV), is a fatal encephalitis in humans and other mammals, which continues to present a public health threat in most parts of the world. Our previous study demonstrated that Toll-like receptor 7 (TLR7) is essential in the induction of anti-RABV antibodies via the facilitation of germinal center formation. In the present study, we investigated the role of TLR7 in the pathogenicity of RABV in a mouse model. Using isolated plasmacytoid dendritic cells (pDCs), we demonstrated that TLR7 is an innate recognition receptor for RABV. When RABV invaded from the periphery, TLR7 detected viral single-stranded RNA and triggered immune responses that limited the virus’s entry into the central nervous system (CNS). When RABV had invaded the CNS, its detection by TLR7 led to the production of cytokines and chemokines and an increase the permeability of the blood-brain barrier. Consequently, peripheral immune cells, including pDCs, macrophages, neutrophils, and B cells infiltrated the CNS. While this immune response, triggered by TLR7, helped to clear viruses, it also increased neuroinflammation and caused immunopathology in the mouse brain. Our results demonstrate that TLR7 is an innate recognition receptor for RABV, which restricts RABV invasion into the CNS in the early stage of viral infection but also contributes to immunopathology by inducing neuroinflammation. IMPORTANCE Developing targeted treatment for RABV requires understanding the innate immune response to the virus because early virus clearance is essential for preventing the fatality when the infection has progressed to the CNS. Previous studies have revealed that TLR7 is involved in the immune response to RABV. Here, we establish that TLR7 recognizes RABV and facilitates the production of some interferon-stimulated genes. We also demonstrated that when RABV invades into the CNS, TLR7 enhances the production of inflammatory cytokines which contribute to immunopathology in the mouse brain. Taken together, our findings suggest that treatments for RABV must consider the balance between the beneficial and harmful effects of TLR7-triggered immune responses.

scholarly journals Crosstalk between Dendritic Cells and Immune Modulatory Agents against Sepsis

Genes ◽  
2020 ◽  
Vol 11 (3) ◽  
pp. 323 ◽  
Author(s):  
Guoying Wang ◽  
Xianghui Li ◽  
Lei Zhang ◽  
Abualgasim Elgaili Abdalla ◽  
Tieshan Teng ◽  
...  
Keyword(s):  
Immune Response ◽  
Dendritic Cells ◽  
Immune Responses ◽  
Critical Role ◽  
Innate Immune ◽  
Adaptive Immune Responses ◽  
Adaptive Immune ◽  
Th2 Responses ◽  
Novel Strategy

Dendritic cells (DCs) play a critical role in the immune system which sense pathogens and present their antigens to prime the adaptive immune responses. As the progression of sepsis occurs, DCs are capable of orchestrating the aberrant innate immune response by sustaining the Th1/Th2 responses that are essential for host survival. Hence, an in-depth understanding of the characteristics of DCs would have a beneficial effect in overcoming the obstacle occurring in sepsis. This paper focuses on the role of DCs in the progression of sepsis and we also discuss the reverse sepsis-induced immunosuppression through manipulating the DC function. In addition, we highlight some potent immunotherapies that could be used as a novel strategy in the early treatment of sepsis.

The rôle of cortisol and β-endorphin in the response of the immune system to weaning in lambs

1998 ◽  
Vol 66 (2) ◽  
pp. 397-402 ◽  
Author(s):  
S. M. Rhind ◽  
H. W. Reid ◽  
S. R. McMillen ◽  
G. Palmarini
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Stress Hormone ◽  
Keyhole Limpet Haemocyanin ◽  
Weaning Stress ◽  
Cell Mediated Immune Response ◽  
Acth Treatment ◽  
Induced Changes ◽  
The Relationship

AbstractThe relationship between weaning stress-induced changes in stress hormone profiles and immune function was investigated in groups of 10 lambs immunized against adrenocorticotrophic hormone (ACTH; treatment A) or fi-endorphin (treatment B) to reduce the circulating concentrations of cortisol and fi-endorphin respectively. Control animals (treatment C) were immunized against a porcine thyroglobulin carrier protein. Application of weaning stress was associated with significantly elevated plasma cortisol concentrations but no significant increase in fi-endorphin concentrations in C lambs. Immunization against ACTH suppressed the post-weaning increase in cortisol concentration. This was associated with a transient reduction in the lymphocyte stimulation response to keyhole limpet haemocyanin (KLH) antigen in the A animals but there was no effect on the antibody response or interferon-y production by antigen stimulated lymphocytes. There were no significant effects of immunization against fi-endorphin on the capacity to mount antibody or cell-mediated immune responses. It is concluded that weaning stress-induced increases in cortisol did not inhibit the immune response. Since cortisol concentrations and the cell mediated immune response at 8 days after immunization were positively associated it is concluded that these indices are not independent measures of stress.

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