Lactobacillus salivarius LA307 and Lactobacillus rhamnosus LA305 attenuate skin inflammation in mice

2018 ◽  
Vol 9 (2) ◽  
pp. 299-309 ◽  
Author(s):  
S. Holowacz ◽  
C. Blondeau ◽  
I. Guinobert ◽  
A. Guilbot ◽  
S. Hidalgo ◽  
...  
Keyword(s):  
Skin Diseases ◽  
Oral Treatment ◽  
Lactobacillus Rhamnosus ◽  
Skin Inflammation ◽  
Serum Levels ◽  
Skin Lesions ◽  
Lactobacillus Salivarius ◽  
Tnf Α ◽  
Microscopic Evaluation ◽  
Chronic Skin

Oral probiotics potential for the management of dermatological diseases is vast. However, results of available studies in skin diseases, such as atopic dermatitis (AD), are inconsistent, partly because probiotic effects are strain specific. Careful selection of probiotic strains is therefore indispensable to ensure efficacy of treatment. In this study, Lactobacillus salivarius LA307, Lactobacillus rhamnosus LA305 and Bifidobacterium bifidum PI22, three strains that were previously identified for their interesting immunomodulatory properties in allergy and/or colitis models, were assessed in the prevention of chronic skin inflammation induced by repeated applications of 12-O-tetradecanoylphorbol-13-acetate in hairless SKH-1 mice. Macroscopic and microscopic evaluation of skin lesions was performed together with measurements of serum levels of interleukin (IL)-1β, IL-6, tumour necrosis factor alpha (TNF-α), IL-17, IL-22, IL-10 and IL-4. Daily oral treatment with the three strains at the dose of 1×109 cfu/day for 3 weeks limited the development of chronic skin inflammation, the effects being strain dependent. Indeed the two Lactobacillus strains significantly limited the intensity of skin inflammation both at the macroscopic and microscopic levels. Macroscopic observations were correlated to the histological observations and the resulting microscopic score. This limitation of the development of AD-like skin lesions involved the modulation of cytokine production. Treatment with the two Lactobacillus strains induced a decrease in the serum levels of pro-inflammatory cytokines IL-1β, IL-6, TNF-α, IL-17, IL-22 and at the opposite an increase in the production of the anti-inflammatory cytokine IL-10 and also of IL-4. Globally, B. bifidum PI22 had lower benefits. These results obtained in mice suggest that L. salivarius LA307 and L. rhamnosus LA305 could be good candidates for preserving skin integrity and homeostasis via the modulation of the gut microbiota and that their use could be beneficial in dermatological conditions such as AD.

scholarly journals Anti-Inflammatory Activity of a Medicinal Herb Extract Mixture, HM-V, on an Animal Model of DNCB-Induced Chronic Skin Inflammation

Plants ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1546
Author(s):  
Sungbae Park ◽  
Sangmin Lee ◽  
Youngho Weon ◽  
Taewook Kim ◽  
Hakwon Kim ◽  
...  
Keyword(s):  
Animal Model ◽  
Inflammatory Cytokines ◽  
Skin Diseases ◽  
Skin Inflammation ◽  
Medicinal Herb ◽  
Inflammatory Skin Diseases ◽  
Tnf Α ◽  
Ifn Γ ◽  
Chronic Skin ◽  
Pro Inflammatory Cytokines

Chronic inflammatory skin diseases, such as atopic dermatitis, are caused by the accumulation of immune cells and the overproduction of chemokines, including CCL17 and CCL22, due to the activation of pro-inflammatory cytokines secreted from keratinocytes. In the present study, the inhibitory activity of HM-V on tumor necrosis factor alpha (TNF-α)/interferon gamma (IFN-γ)-induced pro-inflammatory cytokines was examined in human keratinocytes (HaCaTs) and 2,4-dinitrofluorobenzene (DNCB)-induced chronic skin contact dermatitis animal models. Traditional Asian medicinal herb extracts mixture (HM-V), which have been extensively used in Asian medicine, were utilized. In TNF-α/IFN-γ-induced HaCaTs, HM-V strongly inhibited mRNA and protein expression of CCL17 and CCL22 in a concentration-dependent manner. The expression of pro-inflammatory cytokines such as TNF-α, IL-1β, and IL-6 was also inhibited. Therefore, localized administration of HM-V in the DNCB-induced animal model alleviated immune cell deposition and skin inflammation. The results indicate that HM-V exerts inhibitory effects on keratinocyte production of CCL17 and CCL22. Furthermore, HM-V may be a useful anti-inflammatory agent for the prevention and treatment of inflammatory skin diseases.

scholarly journals Inhibitory Effects of a Novel Chrysin-Derivative, CPD 6, on Acute and Chronic Skin Inflammation

2019 ◽  
Vol 20 (11) ◽  
pp. 2607 ◽  
Author(s):  
Chan-Hee Yu ◽  
Beomseon Suh ◽  
Iljin Shin ◽  
Eun-Hye Kim ◽  
Donghyun Kim ◽  
...  
Keyword(s):  
Skin Diseases ◽  
Human Keratinocytes ◽  
Skin Inflammation ◽  
Inflammatory Reactions ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Chronic Skin ◽  
External Stimuli

The skin is an important physiological barrier against external stimuli, such as ultraviolet radiation (UV), xenobiotics, and bacteria. Dermal inflammatory reactions are associated with various skin disorders, including chemical-induced irritation and atopic dermatitis. Modulation of skin inflammatory response is a therapeutic strategy for skin diseases. Here, we synthesized chrysin-derivatives and identified the most potent derivative of Compound 6 (CPD 6). We evaluated its anti-inflammatory effects in vitro cells of macrophages and keratinocytes, and in vivo dermatitis mouse models. In murine macrophages stimulated by lipopolysaccharide (LPS), CPD 6 significantly attenuated the release of inflammatory mediators such as nitric oxide (NO) (IC50 for NO inhibition: 3.613 μM) and other cytokines. In cultured human keratinocytes, CPD 6 significantly attenuated the release of inflammatory cytokines induced by the combination of IFN-γ and TNF-α, UV irradiation, or chemical irritant stimulation. CPD 6 inhibited NFκB and JAK2/STAT1 signaling pathways, and activated Nrf2/HO-1 signaling. In vivo relevancy of anti-inflammatory effects of CPD 6 was observed in acute and chronic skin inflammation models in mice. CPD 6 showed significant anti-inflammatory properties both in vitro cells and in vivo dermatitis animal models, mediated by the inhibition of the NFκB and JAK2-STAT1 pathways and activation of Nrf2/HO-1 signaling. We propose that the novel chrysin-derivative CPD 6 may be a potential therapeutic agent for skin inflammation.

scholarly journals Gomisin M2 Ameliorates Atopic Dermatitis-like Skin Lesions via Inhibition of STAT1 and NF-κB Activation in 2,4-Dinitrochlorobenzene/Dermatophagoides farinae Extract-Induced BALB/c Mice

Molecules ◽  
2021 ◽  
Vol 26 (15) ◽  
pp. 4409
Author(s):  
Jinjoo Kang ◽  
Soyoung Lee ◽  
Namkyung Kim ◽  
Hima Dhakal ◽  
Taeg-Kyu Kwon ◽  
...  
Keyword(s):  
Atopic Dermatitis ◽  
Oral Administration ◽  
Skin Diseases ◽  
Nuclear Translocation ◽  
Skin Lesions ◽  
Biologically Active ◽  
Therapeutic Effects ◽  
Dermatophagoides Farinae ◽  
Tnf Α ◽  
Ifn Γ

The extracts of Schisandra chinensis (Turcz.) Baill. (Schisandraceae) have various therapeutic effects, including inflammation and allergy. In this study, gomisin M2 (GM2) was isolated from S. chinensis and its beneficial effects were assessed against atopic dermatitis (AD). We evaluated the therapeutic effects of GM2 on 2,4-dinitrochlorobenzene (DNCB) and Dermatophagoides farinae extract (DFE)-induced AD-like skin lesions with BALB/c mice ears and within the tumor necrosis factor (TNF)-α and interferon (IFN)-γ-stimulated keratinocytes. The oral administration of GM2 resulted in reduced epidermal and dermal thickness, infiltration of tissue eosinophils, mast cells, and helper T cells in AD-like lesions. GM2 suppressed the expression of IL-1β, IL-4, IL-5, IL-6, IL-12a, and TSLP in ear tissue and the expression of IFN-γ, IL-4, and IL-17A in auricular lymph nodes. GM2 also inhibited STAT1 and NF-κB phosphorylation in DNCB/DFE-induced AD-like lesions. The oral administration of GM2 reduced levels of IgE (DFE-specific and total) and IgG2a in the mice sera, as well as protein levels of IL-4, IL-6, and TSLP in ear tissues. In TNF-α/IFN-γ-stimulated keratinocytes, GM2 significantly inhibited IL-1β, IL-6, CXCL8, and CCL22 through the suppression of STAT1 phosphorylation and the nuclear translocation of NF-κB. Taken together, these results indicate that GM2 is a biologically active compound that exhibits inhibitory effects on skin inflammation and suggests that GM2 might serve as a remedy in inflammatory skin diseases, specifically on AD.

scholarly journals IL-23 induced in keratinocytes by endogenous TLR4 ligands polarizes dendritic cells to drive IL-22 responses to skin immunization

2016 ◽  
Vol 213 (10) ◽  
pp. 2147-2166 ◽  
Author(s):  
Juhan Yoon ◽  
Juan Manuel Leyva-Castillo ◽  
Guoxing Wang ◽  
Claire Galand ◽  
Michiko K. Oyoshi ◽  
...  
Keyword(s):  
T Cells ◽  
Human Skin ◽  
Cd4 T Cells ◽  
Mouse Skin ◽  
Skin Inflammation ◽  
Serum Levels ◽  
Skin Lesions ◽  
Tape Stripping ◽  
Keratinocyte Proliferation ◽  
Th22 Cells

Atopic dermatitis (AD) is a Th2-dominated inflammatory skin disease characterized by epidermal thickening. Serum levels of IL-22, a cytokine known to induce keratinocyte proliferation, are elevated in AD, and Th22 cells infiltrate AD skin lesions. We show that application of antigen to mouse skin subjected to tape stripping, a surrogate for scratching, induces an IL-22 response that drives epidermal hyperplasia and keratinocyte proliferation in a mouse model of skin inflammation that shares many features of AD. DC-derived IL-23 is known to act on CD4+ T cells to induce IL-22 production. However, the mechanisms that drive IL-23 production by skin DCs in response to cutaneous sensitization are not well understood. We demonstrate that IL-23 released by keratinocytes in response to endogenous TLR4 ligands causes skin DCs, which selectively express IL-23R, to up-regulate their endogenous IL-23 production and drive an IL-22 response in naive CD4+ T cells that mediates epidermal thickening. We also show that IL-23 is released in human skin after scratching and polarizes human skin DCs to drive an IL-22 response, supporting the utility of IL-23 and IL-22 blockade in AD.

scholarly journals ZnO NPs delay the recovery of psoriasis-like skin lesions through promoting inflammation and keratinocyte apoptosis via nuclear translocation of phosphorylated NF-κB p65 and cysteine deficiency

2020 ◽  
Author(s):  
Xuan Lai ◽  
Menglei Wang ◽  
Yixia Zhu ◽  
Xiaoli Feng ◽  
Huimin Liang ◽  
...  
Keyword(s):  
Skin Diseases ◽  
Nuclear Translocation ◽  
Normal Skin ◽  
Redox Homeostasis ◽  
Skin Lesions ◽  
Zno Nps ◽  
Inflammatory Skin Diseases ◽  
Tnf Α ◽  
Jnk Inhibitors

Abstract Background This study aimed to confirm the safety and risk of applying zinc oxide nanoparticles (ZnO NPs) to pathological skin, such as psoriasis-like skin. The majority of previous studies confirmed the safety of applying ZnO NPs to normal skin. However, we know very little about the risks of using sunscreen, cosmetics and topical drugs containing ZnO NPs for individuals with skin diseases. In addition, some studies claimed that ZnO NPs can penetrate normal or pathological skin, and ZnO NPs have frequently been reported to have proinflammatory and lethal effects in vitro. Therefore, it is necessary to evaluate the safety of applying ZnO NPs to pathological skin. Results ZnO NPs passed through gaps between keratinocytes and entered stratum basale of epidermis and dermis in imiquimod (IMQ)-induced psoriasis-like skin lesions. Application of a ZnO NP-containing suspension for 3 connective days delayed the healing of the epidermal barrier; increased the expression levels of inflammatory cytokines; promoted keratinocyte apoptosis and disturbed redox homeostasis. In vitro, ZnO NPs promoted TNF-α, IL-1β and IL-6 secretion and apoptosis of recombinant-human-TNF-α-stimulated HaCaT cells. NF-κB, ERK, p38 and JNK inhibitors blocked ZnO NP-induced inflammation. JSH-23, an inhibitor of the nuclear translocation of p-NF-κB p65, and NAC, an acetylated precursor of L-cysteine, not only inhibited the ZnO NP-induced inflammation but also inhibited apoptosis and cysteine deficiency. Neither erastin nor RSL3 induced p-NF-κB p65 nuclear translocation, but they did reduce cysteine biosynthesis. Additionally, ferropstatin-1, an inhibitor of lipid peroxidation, partially rescued ZnO NP-induced decreases in cell viability and cysteine content. Conclusions ZnO NPs delay the recovery of psoriasis-like skin lesions through promoting inflammation and keratinocyte apoptosis via the nuclear translocation of phosphorylated NF-κB p65 and cysteine deficiency. This work reminds the public that ZnO NPs are not safe for pathological skin, especially in inflammatory skin diseases such as psoriasis, and has revealed a partial mechanism by which ZnO NPs delay the recovery of pathological skin, promoting the appropriate use of ZnO NPs.

scholarly journals Lack of Endogenous Annexin A1 Increases Mast Cell Activation and Exacerbates Experimental Atopic Dermatitis

Cells ◽  
2019 ◽  
Vol 8 (1) ◽  
pp. 51 ◽  
Author(s):  
Jéssica Parisi ◽  
Mab Corrêa ◽  
Cristiane Gil
Keyword(s):  
Atopic Dermatitis ◽  
Mast Cell ◽  
Cell Activation ◽  
Skin Diseases ◽  
Skin Inflammation ◽  
Skin Lesions ◽  
Mast Cell Activation ◽  
Skin Thickness ◽  
Annexin A1 ◽  
Inflammatory Skin Diseases

Annexin A1 (AnxA1) is a protein with potent anti-inflammatory actions and an interesting target that has been poorly explored in skin inflammation. This work evaluated the lack of endogenous AnxA1 in the progression of ovalbumin (OVA)-induced atopic dermatitis (AD)-like skin lesions. OVA/Alum-immunized C57BL/6 male wild-type (WT) and AnxA1 null (AnxA1-/-) mice were challenged with drops containing OVA on days 11, 14–18 and 21–24. The AnxA1-/- AD group exhibited skin with intense erythema, erosion and dryness associated with increased skin thickness compared to the AD WT group. The lack of endogenous AnxA1 also increased IgE relative to WT animals, demonstrating exacerbation of the allergic response. Histological analysis revealed intense eosinophilia and mast-cell activation in AD animals, especially in AnxA1-/-. Both AD groups increased skin interleukin (IL)-13 levels, while IL-17A was upregulated in AnxA1-/- lymph nodes and mast cells. High levels of phosphorylated ERK were detected in keratinocytes from AD groups. However, phospho-ERK levels were higher in the AnxA1-/- when compared to the respective control groups. Our results suggest AnxA1 as an important therapeutic target for inflammatory skin diseases.

scholarly journals AYURVEDIC MANAGEMENT OF KITIBHA KUSHTA W.S.R TO PSORIASIS – A SUCCESSFUL CASE STUDY

2021 ◽  
Vol 9 (5) ◽  
pp. 1147-1151
Author(s):  
Shwetambika Shwetambika ◽  
Shaila Borannavar ◽  
Ananta S Desai
Keyword(s):  
Skin Diseases ◽  
Negative Impact ◽  
Proper Time ◽  
Signs And Symptoms ◽  
Skin Lesions ◽  
The Body ◽  
Clinical Feature ◽  
Emotional Wellbeing ◽  
Chronic Skin

Skin being the largest organ of the body is the reason behind the beauty and cause for confidence. Chronic skin conditions adversely affect one’s physical, functional and emotional wellbeing, thereby causing negative impact on one’s own quality of life. Due to altered lifestyle, lack of physical exercise, unhygienic, mental stress, overeating, nutrition deficiency, skin diseases are commonly observed. WHO has classified skin diseases as a Psycho-cutaneous disease. Materials & Methods 29 year old male was diagnosed with a KitibhaKushta with a clinical feature of flaky reddish white elevated skin lesions over a B/L lower limb associated with severe itching sensation and peeling of the skin since 4 years, has been treated with classical Virechanakarma (Purgation) along with Shamanaushadhis (Oral medicines). Results: After the course of treatment the patient noticed significant relief in signs and symptoms and worth documenting. Conclusion: Kitibha Kushta though it is difficult to manage, but if proper diagnosis is made at proper time many complication can be avoided. In this case study, we found significant results in signs and symptoms with Virechana followed by Shamanoushadhi and Rasayana karma. By this we conclude that various Panchakarma procedures especially Virechana Karma and internal medicines can be the best option in its management. Keywords: Virechana Karma, Kitibha Kushta, Psoriasis

scholarly journals The Role of Gut Microbiome in Psoriasis: Oral Administration of Staphylococcus aureus and Streptococcus danieliae Exacerbates Skin Inflammation of Imiquimod-Induced Psoriasis-Like Dermatitis

2020 ◽  
Vol 21 (9) ◽  
pp. 3303 ◽  
Author(s):  
Karin Okada ◽  
Yoshiaki Matsushima ◽  
Kento Mizutani ◽  
Keiichi Yamanaka
Keyword(s):  
Gut Microbiome ◽  
Skin Diseases ◽  
Skin Inflammation ◽  
Gut Bacteria ◽  
Rrna Gene ◽  
Skin Microbiome ◽  
Inflammatory Skin Diseases ◽  
Fecal Microbiome ◽  
Tnf Α ◽  
Inflammatory Skin

Psoriasis is one of the common chronic inflammatory skin diseases in which inflammatory cytokines such as IL-17 and TNF-α play critical roles. Skin microbiome of psoriasis patients is reported to have elevated Staphylococcus and Streptococcus genus. There are controversial reports about gut microbiome of psoriasis patients, and whether the diversity of bacteria in genus level is decreased or not is still unclear. Moreover, it is not yet known if these gut bacteria would be the cause of the inflammation or the result of the inflammation. We analyzed the gut microbiome of the inflammatory skin model mouse (keratinocyte-specific caspase-1 transgenic (Kcasp1Tg) mouse), by analyzing the 16S rRNA gene. Staphylocuccus aureus and Streptococcus danieliae were abundant in Kcasp1Tg mouse fecal microbiome. These dominant bacteria as well as recessive control bacteria were orally administrated to antibiotic-treated wild type mice, and set up imiquimod-induced psoriasis-like skin inflammation model. The skin inflammation including ear thickness and histopathological findings was analyzed. The exacerbated skin lesions with the elevated levels of TNF-α, IL-17A, IL-17F, and IL-22 were observed in Staphylocuccus aureus and Streptococcus danieliae administrated groups. Our finding suggests that there is affinity between skin inflammation severity and certain gut bacteria leading to a vicious cycle: skin inflammation populates certain gut bacteria which itself worsens the skin inflammation. This is the first report on Staphylocuccus aureus and Streptococcuus danieliae effects in vivo. Not only treating the skin lesion but also treating the gut microbiome could be the future key treatment for inflammatory skin disease such as psoriasis.

scholarly journals Melatonin: clinical prospects in immunology

2020 ◽  
Keyword(s):  
Viral Infections ◽  
Skin Diseases ◽  
Skin Inflammation ◽  
People Living With Hiv ◽  
Long Time ◽  
Chronic Skin ◽  
Living With Hiv ◽  
Drug Provision ◽  
The Relationship

Introduction. For a long time, HIV has been associated with a number of inflammatory, infectious and neoplastic skin diseases. In the era of anti-retroviral therapy researchers have found even more about the relationship between skin disease and chronic immunosuppression. In particular, clinicians continue to face the trend of difficult-to-control viral infections, chronic skin inflammation and itching in people living with HIV. Objectives. This article summarizes the latest updates in immunology, dermatology and HIV, revealing potential of the prospective substance melatonin and its efficacy in treating herpesvirus skin diseases as an alternative immunomodulator. Materials and methods. A comprehensive literature search was carried out in July 2020 using electronic databases PubMed, EMBASE, MEDLINE, U.S. National Library of Medicine Clinical Trials, ResearchGate, and Cocharane Library. Results. This review includes 24 articles, that demonstrated the modulating properties of melatonin and have established its effectiveness in the treatment of diseases associated with immunodeficiency conditions. Melatonin has been shown to have a regulatory effect on the immune system and directly enhance the immune response by improving the proliferation and maturation of natural killers, T and B lymphocytes, granulocytes and monocytes, and activates complement receptors. Conclusions. Currently, the course of dermatological manifestations associated with herpes viruses, unfortunately, remains unfavorable and persists with high mortality coefficients, so the development of new approaches to the provision of medical care to HIV-infected patients is still relevant. Recent scientific studies indicate the high effectiveness of melatonin in the treatment of diseases accompanied by immunodeficiency. Researching of its effects in the dermatological manifestations of herpesvirus infections on the background of HIV is prospective and necessary for expand drug provision, treating comorbid conditions and improving the quality of life of each patient.

scholarly journals Pellino 1 Communicates Intercellular Signaling in Chronic Skin Inflammatory Microenvironment

2018 ◽  
Author(s):  
Suhyeon Kim ◽  
Seoyoon Bae ◽  
Jihyun Park ◽  
Geun-Hyoung Ha ◽  
Kyungrim Hwang ◽  
...  
Keyword(s):  
Skin Inflammation ◽  
Skin Lesions ◽  
Psoriatic Skin ◽  
Intercellular Signaling ◽  
Multisystem Disease ◽  
Signaling Mechanism ◽  
Inflammatory Microenvironment ◽  
Systemic Signaling ◽  
Ubiquitin E3 Ligase ◽  
Chronic Skin

AbstractChronic skin inflammation including psoriasis is a multisystem disease, affecting more than 5% of the general population. Here we show that Pellino 1 (Peli1), a signal-responsive ubiquitin E3 ligase, is highly up-regulated in human psoriatic skin lesions and that increased Peli1 expression correlates with the immunopathogenesis of psoriasis-like chronic skin inflammatory disease. Interestingly, Peli1 directly interacts with interferon regulatory factor 4 (IRF4, a transcription factor that plays pivotal roles in proliferation and cytokine production) and induces lysine 63-mediated ubiquitination. Peli1-mediated IRF4 ubiquitination appears to be a common systemic signaling mechanism shared by lesional keratinocytes, dendritic cells, macrophages, and T cells, generating a feedback relationship between keratinocyte and Th17 cell responses. Conversely, inhibition of Peli1 interferes with IRF4 induction and attenuates immunopathogenic signaling in the psoriasis. In summary, Peli1-mediated ubiquitination is a common immunopathogenic intercellular signaling in psoriasis-like chronic skin inflammatory microenvironment. Thus, targeting Peli1 could be used as a potential strategy for psoriasis treatment.

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