Herpes Simplex Virus 1 Can Bypass Impaired Epidermal Barriers upon
            <i>Ex Vivo</i>
            Infection of Skin from Atopic Dermatitis Patients

Möckel, Maureen; Cruz, Nydia C. De La; Rübsam, Matthias; Wirtz, Lisa; Tantcheva‐Poór, Iliana; Malter, Wolfram; Zinser, Max; Bieber, Thomas; Knebel-Mörsdorf, Dagmar

doi:10.1128/jvi.00864-22

Cited by 12 publications

(16 citation statements)

References 52 publications

(74 reference statements)

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“…Factors such as impaired epidermal barrier function, chronic inflammation, and disturbed skin flora all contribute to increased viral susceptibility in AD patients. [18][19][20] Chronic eczematous lesions also present similar problems. This study found that CD2AP and CD123 specifically expressed in pDC were higher in chronic eczema lesions than in normal lesions, suggesting that pDCs accumulate in chronic eczema lesions, mainly in the superficial dermis and basal layer of the epidermis.…”

Section: Discussionmentioning

confidence: 97%

The Expression of Plasmacytoid Dendritic Cells and TLR7/9-MyD88-IRAKs Pathway in Chronic Eczema Lesions

Wen¹,

Weng²,

Lu³

et al. 2023

CCID

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To investigate the expression of Plasmacytoid Dendritic Cells (pDCs) and TLR7/9-MyD88-IRAKs pathway in chronic eczema lesions. Patients and Methods: Lesional tissues and the surrounding healthy tissues were collected from 25 individuals with chronic eczema, and immunohistochemistry was used to detect and comparatively analyze the expression profile of CD123, CD2AP, toll-like receptor 7 (TLR7), toll-like receptor 9 (TLR9) along with interleukin-1 receptor-associated kinase 1 (IRAK1) and interferon regulatory factor 7 (IRF7) in signaling pathways. Results: The positive rates of CD2AP + pDC and CD123 + pDC in lesional tissues were significantly elevated compared to the surrounding healthy tissues (P < 0.05). They were distributed in both the epidermal and dermal layers of the lesional tissue, but the majority were in the dermal layer. The TLR7, TLR9, IRAK1 and IRF7 were more expressed in dermal layers of the lesional tissue with higher positive rates of expression compared to the surrounding healthy tissues (P < 0.05). IRAK1 and IRF7 were expressed in a small amount in the epidermal layer with higher positive rates of expression than in the surrounding healthy tissues (P < 0.05), while the positive rates of TLR7 and TLR9 expression in the epidermal layer were not statistically different from those in the surrounding healthy tissues (P > 0.05). Conclusion: PDC and TLR7/9-MyD88-IRAKs pathways are actively expressed in chronic eczema lesions and may be involved in pathogenesis and disease progression.

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Section: Discussionmentioning

confidence: 97%

The Expression of Plasmacytoid Dendritic Cells and TLR7/9-MyD88-IRAKs Pathway in Chronic Eczema Lesions

Wen¹,

Weng²,

Lu³

et al. 2023

CCID

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“…Together with the S100A7 gene series, they constitute the bulk of the epidermal differentiation complex (EDC) [25]. Expression of the complex is internally modulated by cytokines (IL-4,13,17A,22) derived from T-helper cells (Th1, 2,17,22). On the other hand, external modulation can occur via microorganisms (Malassezia spp.…”

Section: Genetic Risk Factors and Epigenetic Regulatorsmentioning

confidence: 99%

“…The major medical co-morbidities associated with AD are microbial infections, specifically SA [14][15][16][17][18], affecting > 90% of patients. SA colonization is related to skin barrier disruption, a predominant Th2 immune response, elevated IgE levels specific to staphylococcal enterotoxin, and a reduction in skin microbial diversity.…”

Section: Introductionmentioning

confidence: 99%

Staphylococcus Infection: Relapsing Atopic Dermatitis and Microbial Restoration

Hulme

2023

Antibiotics

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Atopic Dermatitis (AD) skin is susceptible to Staphylococcus aureus (SA) infection, potentially exposing it to a plethora of toxins and virulent determinants, including Panton-Valentine leukocidin (PVL) (a-hemolysin (Hla) and phenol-soluble modulins (PSMs)), and superantigens. Depending on the degree of infection (superficial or invasive), clinical treatments may encompass permanganate (aq) and bleach solutions coupled with intravenous/oral antibiotics such as amoxicillin, vancomycin, doxycycline, clindamycin, daptomycin, telavancin, linezolid, or tigecycline. However, when the skin is significantly traumatized (sheathing of epidermal sections), an SA infection can rapidly ensue, impairing the immune system, and inducing local and systemic AD presentations in susceptible areas. Furthermore, when AD presents systemically, desensitization can be long (years) and intertwined with periods of relapse. In such circumstances, the identification of triggers (stress or infection) and severity of the flare need careful monitoring (preferably in real-time) so that tailored treatments targeting the underlying pathological mechanisms (SA toxins, elevated immunoglobulins, impaired healing) can be modified, permitting rapid resolution of symptoms.

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“…Unexpectedly, the wounded human skin surface does not allow penetration of HSV-1 upon ex vivo infection ( 13 ). However, we observed successful invasion in lesional atopic dermatitis skin, which is characterized by inflammation-induced modifications and dysfunctional physical barriers ( 14 ). Patients with atopic dermatitis can be seriously affected by HSV skin infections termed eczema herpeticum ( 15 , 16 ).…”

Section: Introductionmentioning

confidence: 95%

Ex Vivo Infection of Human Skin Models with Herpes Simplex Virus 1: Accessibility of the Receptor Nectin-1 during Formation or Impairment of Epidermal Barriers Is Restricted by Tight Junctions

Cruz

Möckel

Niehues

et al. 2023

J Virol

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Herpes Simplex Virus 1 Can Bypass Impaired Epidermal Barriers upon Ex Vivo Infection of Skin from Atopic Dermatitis Patients

Cited by 12 publications

References 52 publications

The Expression of Plasmacytoid Dendritic Cells and TLR7/9-MyD88-IRAKs Pathway in Chronic Eczema Lesions

The Expression of Plasmacytoid Dendritic Cells and TLR7/9-MyD88-IRAKs Pathway in Chronic Eczema Lesions

Staphylococcus Infection: Relapsing Atopic Dermatitis and Microbial Restoration

Ex Vivo Infection of Human Skin Models with Herpes Simplex Virus 1: Accessibility of the Receptor Nectin-1 during Formation or Impairment of Epidermal Barriers Is Restricted by Tight Junctions

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