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At least 19 recordsLinked to original sources
PubMed2026

P1D6 inhibits FnBP-induced extracellular proteome remodeling: proteomic evidence for a novel intervention strategy in atopic dermatitis.

Atopic dermatitis (AD) is an inflammatory skin disorder characterized by skin barrier impairment, chronic inflammation, and intense pruritus. Staphylococcus aureus (S. aureus) critically contributes to its pathogenesis; however, the mechanistic role of its virulence factor fibronectin-binding protein (FnBP) in keratinocytes remains poorly understood. This study used bibliometric analysis and quantitative proteomics to examine the relationship. We first performed a bibliometric analysis, revealing a sustained increase in publications on S. aureus and AD, peaking at 99 articles in 2023, with hotspots focused on skin barrier function, immune inflammation, and pediatrics. Quantitative proteomics was employed to investigate how FnBP reshapes the extracellular proteome and whether the anti-α5 integrin antibody P1D6 exerts interventional effects. HaCaT cells were stimulated with recombinant FnBP alone or in combination with P1D6, followed by data-independent acquisition (DIA)-based proteomic analysis of secretome changes. Proteomic analysis identified FnBP-induced differentially expressed proteins enriched in immune- and barrier-related pathways, including cell adhesion, cell junctions, and VEGFA-VEGFR2 signaling. P1D6 intervention significantly inhibited the secretome profile and identified 241 core responsive proteins, of which approximately 52% returned to baseline levels after intervention (P > 0.05). These proteins were primarily enriched in pathways governing protein homeostasis, folding, proteasomal degradation, and interleukin-7 signaling. Notably, P1D6 modulated the downregulation of ATP5F1B and P4HB, key effectors within the interleukin-7 pathway. This study demonstrates that FnBP remodels the keratinocyte secretome by disrupting protein homeostasis, consequently inducing barrier injury and chronic inflammation related to AD, which can be effectively blocked by P1D6. Combined with bibliometric trends and proteomic evidence, this study focuses on FnBP, an underexplored virulence factor, and provides novel insights into AD pathogenesis and therapeutic interventions.

Humans↗
PubMed1978

Immunofluorescence of the skin in allergic diseases: an investigation of patients with contact dermatitis, allergic vasculitis and atopic dermatitis.

Skin biopsies for immunofluorescent studies were taken from patients with contact dermatitis (positive patch tests), atopic dermatitis and allergic vasculitis for comparison with normal-appearing skin from the same patients, and from healthy controls. A variety of deposits of immunoglobulins, complement components and fibrinogen were demonstrated in 6 out of 20 patients with contact dermatitis, 7 out of 10 with atopic dermatitis, 8 out of 10 with allergic vasculitis, and in 4 out of 20 control individuals. No diagnostic pattern of deposits was found. Elevated serum IgE and eosinophilic counts were found in patients with atopic dermatitis, and high serum IgA and fibrinogen levels were found in the allergic vasculitis group.

Adolescent↗
PubMed2026

Single-cell transcriptome revealed the aberrant keratinocytes activation in antigen presentation in atopic dermatitis.

BACKGROUND: Atopic dermatitis (AD), a common chronic inflammatory skin disease, has been extensively studied using single-cell genomics. However, keratinocytes, as key effector cells in AD, have underlying mechanisms remain incompletely understood and require further investigation. METHODS: We integrated single-cell transcriptomic data from skin tissues of healthy controls, chronic active AD patients, spontaneously healed AD (SHAD) patients, and an ovalbumin-induced AD mouse model. The study particularly emphasized the gene expression and cellular dynamics of keratinocytes across the different groups, as well as their interactions with immune cells. RESULTS: Compared to healthy controls, we observed significant changes in the keratinocyte transcriptome, cellular state, and keratinocyte-immune cell ligand-receptor interactions in AD skin, particularly the marked activation of genes involved in antigen processing and presentation. Interestingly, such gene activation was not observed in keratinocytes from the ovalbumin-induced AD mouse model, despite its phenotype closely resembling human AD. Furthermore, in SHAD, we identified a recovery of both the ligand-receptor interaction patterns and antigen processing and presentation genes, accompanied by a notable shift in the transcriptome. This involved a significant downregulation of genes related to cytoplasmic transcription and oxidative phosphorylation. Notably, this pattern was not observed in the self-healing mouse model following the removal of ovalbumin stimulation. CONCLUSION: Our results suggest that the persistent activation of antigen processing and presentation pathways in keratinocytes may be a key driver of chronic inflammation in AD. Therefore, redirecting anti-allergic therapeutic strategies from solely targeting immune cells to targeting of keratinocyte-mediated antigen presentation may offer a more effective approach. Furthermore, we raise concerns about the use of ovalbumin-induced mouse models to recapitulate human chronic AD, as the underlying mechanisms may differ significantly.

Dermatitis, Atopic↗
PubMed2026

Spatial Transcriptomics Identifies Characteristic Immunological Niches in Atopic Dermatitis.

BACKGROUND: Atopic dermatitis (AD) is primarily driven by a Type 2 immune response, with T helper (TH2) cells producing IL-4 and IL-13, thereby promoting inflammation, itch, and a compromised skin barrier. Yet, the spatial organization of pathogenic immune cells and their interactions with stromal and epithelial compartments in human AD skin remain incompletely understood. METHODS: We performed 10× Genomics Visium spatial transcriptomics on FFPE skin biopsies from patients with AD (n = 6), psoriasis (n = 2), and healthy controls (n = 5). Data were integrated with AD single-cell RNA sequencing (scRNA-seq) datasets and complemented by imaging mass cytometry (IMC) and multiplex immunofluorescence (IF) to validate the spatial localization of immune cells. Cell-cell communication analysis revealed putative signaling interactions within immune niches. RESULTS: Spatial clustering resolved tissue compartments and demonstrated transcriptional dysregulation in keratinocytes in AD and psoriasis. AD lesions showed a conserved spatial organization of immune aggregates within the superficial dermis. Integration of scRNA-seq signatures revealed spatially organized co-localization of T cells and mature migratory dendritic cells (mmDCs). We developed a ring-based neighborhood analysis to characterize the cellular organization of the immune-stromal niches, revealing T cell-enriched regions surrounded by inflammatory fibroblasts and activated keratinocytes. Intercellular communication analysis further identified putative signaling within mmDC-T cell niches that may promote pathogenic T cell recruitment and activation. Application of tertiary lymphoid structure (TLS) signatures indicated the presence of TLS-like regions. IMC and IF validated the close spatial proximity between activated TH2 cells and mmDCs. CONCLUSION: AD lesions contain spatially organized TLS-like immune niches at the dermal-epidermal junction, characterized by the close association of T cells and mmDCs and coordinated interactions with surrounding stromal and epithelial compartments. These mmDC-T cell niches may represent potential targets for future therapeutic strategies aimed at disrupting persistent local inflammatory pathways and improving long-term disease control.

atopic dermatitis↗
PubMed1978

Neutrophil chemotaxis in patients with atopic dermatitis without infection.

Atopic dermatitis has been associated with recurrent infection and impaired neutrophil chemotaxis in some patients. In order to determine if dermatitis per se could decrease polymorphonuclear leukocyte (PMN) chemotaxis, we investigated chemotaxis in 13 patients with atopic dermatitis and no clinical or historical evidence of recurrent or severe infections. Most patients had extensive, but mild, disease. Leukocyte chemotaxis was measured by the Boyden chamber and agarose techniques; There was no difference between patient and control neutrophil chemoatactic activity. These findings suggest that atopic dermatitis is not ordinarily associated with impaired PMN chemotaxis in the absence of generalized erythroderma or increased susceptibility to infection.

Adolescent↗
PubMed1976

Atopic dermatitis: etiology and pathogenesis.

Atopic dermatitis is a recognizable phenotype that most likely results from several mechanisms. An increasing number of children with atopic dermatitis are recognized as having immune defects, although the exact incidence of such immunodeficiency states among patients with atopic dermatitis is unknown. Children with atopic dermatitis who suffer recurrent or persistent infections should undergo immunologic evaluation. Ideally, this should include evaluation of cell-mediated immunity as well as neutrophil and monocyte chemotaxis. Further investigation into the beta-blockade theory may enhance our understanding of atopic dermatitis. Careful attention to factors exacerbating atopic dermatitis is essential in understanding this problem. Abnormal sweating, dry skin, sensitivity to contactants, and emotional stress should always be considered in evaluation of children with atopic dermatitis.

Child↗
PubMed1976

Adrenergic mechanisms and the adenyl cyclase system in atopic dermatitis.

Patients with atopic dermatitis have abnormal autonomic responses of the arterioles, pilomotor smooth muscle, and sweat glands. Their lesions have been reported to contain increased amounts of the neurohumors, acetylcholine and norepinephrine, as well as increased activity of acetylcholinesterase and catechol-O-methyltransferase. In vitro studies of epidermis show that beta adrenergic agonists fail to evoke the normal inhibition of mitosis of basal cells of patients with atopic dermatitis. Epidermis removed not only from the lesions, but also from normal-appearing skin, responded abnormally. The increase in intracellular levels of cAMP after exposure to catecholamines was similar in normal and atopic epidermis. Lymphocytes and PMN leukocytes isolated from patients with atopic dermatitis show both a decreased physiologic response (glycogenolysis and inhibition of lysosome enzyme release) and a decreased rise in intracellular levels of cAMP upon incubation with beta agonists, but a normal response to PGE1. Cortisol increases the response of lymphocyte adenyl cyclase to both agonists and, in the case of the patients with atopic disease, more than overcomes the depressed response to beta agonists. Because the leukocytes respond normally to PGE1 and because others have reported normal activities of skin and adenyl cyclase, phosphodiesterase, and protein kinases, we conclude that the step responsible for the diminished beta adrenergic response lies antecedent to the catalytic site of adenyl cyclase.

Acetylcholine↗
PubMed1979

On the significance of the trichophytin reactivity in atopic dermatitis.

Patients with pure atopic dermatitis with and without tinea infection were investigated and compared with patients with long-lasting tinea infections and with controls, for presence of intracutaneous reactivity to trichoptin, Penicillium, Cladosporium and Alternaria antigens. RAST to Penicillium and Cladosporium was also performed. The results showed a lack of delayed reactivity, but an immediate reactivity to trichophytin in 50%/40% of atopic patients with/without tinea infection. Non-atopics infected with tinea showed 66% immediate and 33% delayed response to trichophytin. The reactivities in atopic dermatitis (but not in the non-atopic group) went general parallel with mould reactions tested intracutaneously or by RAST. It is assumed that a positive trichophytin reaction in atopic dermatitis does not necessarily mean sensitisation to dermatophytes, but is primarily the sign of a cross sensitivity to moulds.

Adult↗
PubMed2025

Shared Genetic Architecture Between Atopic Dermatitis and Autoimmune Diseases.

Atopic dermatitis (AD) and autoimmune diseases exhibit epidemiological comorbidity, yet the shared genetic architecture remains incompletely understood. We investigated the genetic overlap between AD and three autoimmune disorders including inflammatory bowel disease (IBD), rheumatoid arthritis (RA), and vitiligo, leveraging genome-wide association data. Despite modest evidence for global genetic correlations, we found 113 independent pleiotropic loci shared among AD and autoimmune diseases, with 11 displaying a concordant effect across all 3 pairwise comparisons. Gene-set and tissue enrichment analyses evidenced the inflammatory background of pleiotropic associations. Multi-trait colocalization analysis prioritized 22 loci, linking the tissue-specific expression of DOK2, GPR132, RERE, RERE-AS1, SUOX, TNFRSF11A, and TRAF1 pleiotropic genes with AD risk. Mendelian randomization revealed no causal effect of genetic liability to AD on autoimmune diseases. Nevertheless, genetic liability to IBD increased AD risk, while vitiligo exhibited a protective effect post outlier correction. Our findings provide mechanistic insights into the multimorbidity of atopic dermatitis (AD) and autoimmune diseases, offering additional evidence for the pleiotropic genetic architecture of AD that contributes to systemic immune dysregulation across multiple organ systems.

Humans↗
PubMed1979

Plasma complement and histamine changes in atopic dermatitis.

Fifteen patients with atopic dermatitis were investigated to evaluate the total of complement and histamine. In five patients total serum complement haemolytic activity (CH50) was significantly decreased as was the haemolytic activity of complement components C2 (C2H50) and C3 (C3H50). By counter immunoelectrophoresis split products of C3 were detected. There was no evidence for alternative pathway activation or the presence of an activator of the alternative pathway. In three patients plasma histamine concentrations were elevated. The intensity of the complement and histamine changes observed seemed to be correlated to the severity of the disease.

Adolescent↗
PubMed1978

Serum IgE in atopic dermatitis: relationship to severity of cutaneous involvement and course of disease as well as coexistence of atopic respiratory diseases.

Serum IgE concentrations were determined according to the radioimmunosorbent technique (RIST, Phadebas) on 116 adult patients with atopic dermatitis of varying severity and activity. Geometric mean IgE levels of patients with atopic dermatitis were significantly higher compared with the mean level of ninety-three non-atopic adult subjects without parasitic infestation. Severity of the atopic dermatitis was highly correlated to the levels of serum IgE. Severe chronic cases with ever-recurrent exacerbations show the most extreme values. In the moderate forms of atopic dermatitis, coexistent bronchial asthma causes a greater increase in the IgE values. Among the mild or abortive forms higher IgE levels were found in cases with allergic rhinitis than in the cases with 'pure' atopic dermatitis. Other findings in connection with IgE in atopic dermatitis are summarized. The pathogenetic significance of IgE in the cutaneous changes is briefly discussed.

Adolescent↗
PubMed1979

In vitro histamine and serotonin release studies in atopic dermatitis.

6 patients suffering from severe atopic dermatitis with high serum IgE were investigated. 3 of the patients had elevated plasma histamine levels (1.5-2.0 ng/ml). Compared to 9 nonatopic normal volunteers, the patient showed increased in vitro histamine release from peripheral leukocytes after stimulation with iothalamate and methacholine: while there was no significant histamine release at a methacholine concentration of 10(-4) M in normals, 4 of the patients with atopic dermatitis showed measurable histamine release under these conditions in vitro. The uptake of radiolabeled serotonin by platelets in vitro was decreased in 2 of the patients. There was no significant difference in serotonin release induced in vitro by different concentrations of thrombin, epinephrine and methacholine; 2 patients showed an increased platelet release reaction after iodipamide stimulation. It is concluded that a general tendency to release vasoactive mediators, even after 'nonimmunologic' stimulation, might play a role in the pathogenesis of atopic dermatitis.

Adult↗
PubMed1977

T and B lymphocytes in contact and atopic dermatitis.

Twenty patients with contact dermatitis, eighteen with atopic dermatitis, two with mixed dermatitis, and 20 controls were examined for the number of T and B lymphocytes, and serum concentrations of IgD and IgE. Significantly higher counts of B lymphocytes bearing IgE and high serum IgE values were found in the atopic group. No other significant differences were found. In particular, we found a normal frequency of IgD bearing lymphocytes in contact dermatitis, and normal T lymphocyte counts in both groups of patients.

Adolescent↗
PubMed1979

Beta adrenergic receptor binding on polymorphonuclear leukocytes in atopic dermatitis.

It has been postulated that the patient with atopic dermatitis has defective beta adrenergic receptor function. However, a more generalized defect is suggested by the observation that cyclic AMP generation is diminished in these patients following stimulation with both isoproterenol and PGE1. To determine the nature of this abnormality, we measured beta adrenergic receptor binding directly on polymorphonuclear leukocyte membranes using the radiolabeled beta adrenergic antagonist (-) [3H]dihydroalprenolol (DHA). DHA binding was studied in 6 mild and 9 moderate-to-severe atopic dermatitis patients, and 8 normal controls using a subsaturating concentration of DHA (0.5 nM) to estimate receptor affinity and a saturating concentration of DHA (30 mM) to determine the total number of receptors per cell. No significant differences (p greater than .05) were found in the total number of receptors per PMN between the control population (805 +/- 95) and the mild atopic dermatitis patients (745 +/- 91) or the moderate to severe group (621 +/- 79). In addition, no significant differences in receptor affinity were found among any of the 3 study groups. These findings suggest that beta receptor binding in atopic dermatitis is normal. Reduced cyclic AMP generation in atopic dermatitis PMN leukocytes would appear to be due to a defect distal to the beta adrenergic receptor itself.

Adult↗
PubMed1979

Cell-mediated immunity in vitro in atopic dermatitis.

The function of T cells in atopic dermatitis was studied by leukocyte migration agarose and lymphocyte transformation tests. We found that phytohemagglutinin (PHA)- and PPD-induced release of leukocyte migration inhibition factor (LIF) from lymphocytes is significantly decreased (P less than .001) in patients with atopic dermatitis as compared with healthy controls. Blastogenic response of lymphocytes induced by PPD was also decreased in atopic patients as compared with controls (P less than .01). No differences were found in spontaneous blastogenesis or in blastogenic response of lymphocytes in vitro to PHA, concanavalin A (ConA), or streptokinase-streptodornase (SK-SD) between patients with atopic dermatitis and controls.

Adolescent↗
PubMed1979

A study of HLA antigen distribution in families with atopic dermatitis.

Seventeen children presenting with atopic dermatitis were HLA typed together with their parents and siblings. A total of 89 individuals was studied. No close link between HLA antigen distribution and clinical expression of atopy was demonstrated, and 14 HLA identical but disease-free siblings were identified. An increase in the A1 B8 haplotype was observed in the families as a whole by comparison with a large control series.

Adult↗
PubMed1979

Lymphocyte response to phytohemagglutinin in atopic dermatitis.

Studies of patients with atopic dermatitis (AD) have demonstrated several clinical and laboratory indications of immunity defects, but with frequently contradictory results. We have recently shown that many patients with negative cutaneous delayed type hypersensitivity to candidin and streptokinase-streptodornase may have normal in vitro lymphocyte transformation to the same antigens. We hypothesized that this represents recovery of immunocompetent cells when they are isolated in vitro. This report describes phytohemagglutinin-induced transformation of lymphocytes immediately after isolation and after four days in culture (precultured). Responses of lymphocytes from patients with AD were initially subnormal, but increased to normal levels after the preculture period. Our results suggest that defective immune function in AD is not due to a permanent intrinsic lymphocyte defect, but is more likely due to factors associated with disease activity and severity.

Adolescent↗