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14 pages, 1110 KiB  
Article
COVID-19 Vaccine: A Potential Risk Factor for Accelerating the Onset of Bullous Pemphigoid
by Anna Pira, Feliciana Mariotti, Francesco Moro, Biagio Didona, Giovanni Luca Scaglione, Annarita Panebianco, Damiano Abeni and Giovanni Di Zenzo
Vaccines 2024, 12(9), 1016; https://doi.org/10.3390/vaccines12091016 - 5 Sep 2024
Cited by 1 | Viewed by 1523
Abstract
Bullous pemphigoid (BP) is the most common autoimmune bullous disease, whose main autoantigens are hemidesmosomal components BP180 and BP230. Although recent studies found no association between COVID-19 vaccines and BP, since mass vaccinations started, more than 90 vaccine-associated BP cases have been reported. [...] Read more.
Bullous pemphigoid (BP) is the most common autoimmune bullous disease, whose main autoantigens are hemidesmosomal components BP180 and BP230. Although recent studies found no association between COVID-19 vaccines and BP, since mass vaccinations started, more than 90 vaccine-associated BP cases have been reported. To find an agreement among real-life clinical observations and recent epidemiologic data, we further investigated this topic. A total of 64 patients with BP onset in 2021 were demographically, clinically, and serologically characterized: 14 (21.9%) vaccine-associated patients (VA) developed BP within 5 weeks from the first/second vaccine dose. VA and vaccine-non-associated (VNA) patients had similar demographics and clinical and immunological characteristics. Noteworthy, the monthly distribution of BP onset during mass vaccinations paralleled vaccine administration to the elderly in the same catchment area. Additionally, in 2021, BP onsets in April–May and June–July significantly increased (p = 0.004) and declined (p = 0.027), respectively, compared to the three years before vaccination campaigns (2018–2020). Interestingly, VA and VNA patients showed statistically significant differences in the use of inhalers and diuretics. Our findings suggest that the COVID-19 vaccine may constitute an accelerating factor that, together with other triggering factors, could act in genetically predisposed individuals with possible sub-clinical autoreactivity against BP antigens, slightly accelerating BP onset. Full article
(This article belongs to the Section COVID-19 Vaccines and Vaccination)
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18 pages, 6794 KiB  
Article
Radiofrequency Treatment Attenuates Age-Related Changes in Dermal–Epidermal Junctions of Animal Skin
by Kyung-A Byun, Hyoung Moon Kim, Seyeon Oh, Sosorburam Batsukh, Kuk Hui Son and Kyunghee Byun
Int. J. Mol. Sci. 2024, 25(10), 5178; https://doi.org/10.3390/ijms25105178 - 9 May 2024
Cited by 1 | Viewed by 3881
Abstract
The dermal–epidermal junction (DEJ) is essential for maintaining skin structural integrity and regulating cell survival and proliferation. Thus, DEJ rejuvenation is key for skin revitalization, particularly in age-related DEJ deterioration. Radiofrequency (RF) treatment, known for its ability to enhance collagen fiber production through [...] Read more.
The dermal–epidermal junction (DEJ) is essential for maintaining skin structural integrity and regulating cell survival and proliferation. Thus, DEJ rejuvenation is key for skin revitalization, particularly in age-related DEJ deterioration. Radiofrequency (RF) treatment, known for its ability to enhance collagen fiber production through thermal mechanisms and increase heat shock protein (HSP) expression, has emerged as a promising method for skin rejuvenation. Additionally, RF activates Piezo1, an ion channel implicated in macrophage polarization toward an M2 phenotype and enhanced TGF-β production. This study investigated the impact of RF treatment on HSP47 and HSP90 expression, known stimulators of DEJ protein expression. Furthermore, using in vitro and aged animal skin models, we assessed whether RF-induced Piezo1 activation and the subsequent M2 polarization could counter age-related DEJ changes. The RF treatment of H2O2-induced senescent keratinocytes upregulated the expression of HSP47, HSP90, TGF-β, and DEJ proteins, including collagen XVII. Similarly, the RF treatment of senescent macrophages increased Piezo1 and CD206 (M2 marker) expression. Conditioned media from RF-treated senescent macrophages enhanced the expression of TGF-β and DEJ proteins, such as nidogen and collagen IV, in senescent fibroblasts. In aged animal skin, RF treatment increased the expression of HSP47, HSP90, Piezo1, markers associated with M2 polarization, IL-10, and TGF-β. Additionally, RF treatment enhanced DEJ protein expression. Moreover, RF reduced lamina densa replication, disrupted lesions, promoted hemidesmosome formation, and increased epidermal thickness. Overall, RF treatment effectively enhanced DEJ protein expression and mitigated age-related DEJ structural changes by increasing HSP levels and activating Piezo1. Full article
(This article belongs to the Section Molecular Pathology, Diagnostics, and Therapeutics)
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19 pages, 1849 KiB  
Review
Involvement of Vasoactive Intestinal Peptide Family Members in Diabetic Keratopathy
by Grazia Maugeri, Agata Grazia D’Amico, Benedetta Magrì and Velia D’Agata
Appl. Sci. 2024, 14(5), 1754; https://doi.org/10.3390/app14051754 - 21 Feb 2024
Cited by 2 | Viewed by 1597
Abstract
Diabetic keratopathy (DK) is a common ocular complication of diabetes, characterized by alteration of the normal wound-healing mechanism, reduction of epithelial hemidesmosomes, disruption of the basement membrane, impaired barrier function, reduced corneal sensitivity, corneal ulcers, and corneal edema. The limited number of clinical [...] Read more.
Diabetic keratopathy (DK) is a common ocular complication of diabetes, characterized by alteration of the normal wound-healing mechanism, reduction of epithelial hemidesmosomes, disruption of the basement membrane, impaired barrier function, reduced corneal sensitivity, corneal ulcers, and corneal edema. The limited number of clinical studies do not allow a full characterization of the pathophysiology of DK and, until now, effective therapeutic approaches have not been available. However, in recent years, neuropeptides gained great attention for their biochemical characteristics and therapeutic potential. This review focuses on the role of neuropeptides vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase-activating polypeptide (PACAP) in the eye and, in particular, in the cornea, in physiological conditions, or during DK, by providing an overview of this diabetes mellitus complication. Full article
(This article belongs to the Special Issue Recent Advances in Pathogenesis and Management of Eye Diseases)
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15 pages, 16114 KiB  
Article
C. elegans Hemidesmosomes Sense Collagen Damage to Trigger Innate Immune Response in the Epidermis
by Yi Zhu, Wenna Li, Yifang Dong, Chujie Xia and Rong Fu
Cells 2023, 12(18), 2223; https://doi.org/10.3390/cells12182223 - 6 Sep 2023
Cited by 3 | Viewed by 2541
Abstract
The collagens are an enormous family of extracellular matrix proteins that play dominant roles in cell adhesion, migration and tissue remodeling under many physiological and pathological conditions. However, their function mechanisms in regulating innate immunity remain largely undiscovered. Here we use C. elegans [...] Read more.
The collagens are an enormous family of extracellular matrix proteins that play dominant roles in cell adhesion, migration and tissue remodeling under many physiological and pathological conditions. However, their function mechanisms in regulating innate immunity remain largely undiscovered. Here we use C. elegans epidermis as the model to address this question. The C. elegans epidermis is covered with a collagen-rich cuticle exoskeleton and can produce antimicrobial peptides (AMPs) against invading pathogens or physical injury. Through an RNAi screen against collagen-encoding genes, we found that except the previously reported six DPY collagens and the BLI-1 collagen, the majority of collagens tested appear unable to trigger epidermal immune defense when damaged. Further investigation suggests that the six DPY collagens form a specific substructure, which regulates the interaction between BLI-1 and the hemidesmosome receptor MUP-4. The separation of BLI-1 with MUP-4 caused by collagen damage leads to the detachment of the STAT transcription factor-like protein STA-2 from hemidesmosomes and the induction of AMPs. Our findings uncover the mechanism how collagens are organized into a damage sensor and how the epidermis senses collagen damage to mount an immune defense. Full article
(This article belongs to the Special Issue Caenorhabditis elegans: Cell Biology and Physiology)
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12 pages, 4212 KiB  
Article
Human Skin Drug Metabolism: Relationships between Methyl Salicylate Metabolism and Esterase Activities in IVPT Skin Membranes
by Krishna C. Telaprolu, Jeffrey E. Grice, Yousuf H. Mohammed and Michael S. Roberts
Metabolites 2023, 13(8), 934; https://doi.org/10.3390/metabo13080934 - 9 Aug 2023
Cited by 12 | Viewed by 3373
Abstract
The presence of esterase enzymes in human skin and their role in drug metabolism has been reported, but their distribution in the various skin layers and the relative contributions of those layers to metabolism is poorly defined. To gain further insight into esterase [...] Read more.
The presence of esterase enzymes in human skin and their role in drug metabolism has been reported, but their distribution in the various skin layers and the relative contributions of those layers to metabolism is poorly defined. To gain further insight into esterase distribution, we performed in vitro skin permeation of a commercial 28.3% methyl salicylate (MeSA) cream (Metsal™) in Franz diffusion cells, using a range of human skin membranes, all from the same donor. The membranes were viable epidermis separated by a dispase II enzymatic method, heat separated epidermis, dermatomed skin, and dermis separated by a dispase II enzymatic method. Methyl salicylate and its metabolite, salicylic acid (SA), were measured by high-performance liquid chromatography. Alpha naphthyl acetate and Hematoxylin and Eosin staining provided qualitative estimations of esterase distribution in these membranes. The permeation of methyl salicylate after 24 h was similar across all membranes. Salicylic acid formation and permeation were found to be similar in dermatomed skin and dermis, suggesting dermal esterase activity. These results were supported by the staining studies, which showed strong esterase activity in the dermal–epidermal junction region of the dermis. In contrast with high staining of esterase activity in the stratum corneum and viable epidermis, minimal stained and functional esterase activity was found in heat-separated and dispase II-prepared epidermal membranes. The results are consistent with dispase II digesting hemidesmosomes, penetrating the epidermis, and affecting epidermal esterases but not those in the dermis. Accordingly, whilst the resulting dispase II-generated dermal membranes may be used for in vitro permeation tests (IVPT) involving esterase-based metabolic studies, the dispase II-generated epidermal membranes are not suitable for this purpose. Full article
(This article belongs to the Special Issue Skin Metabolism and Cutaneous Disorders)
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12 pages, 6261 KiB  
Article
Loss of ERβ in Aging LXRαβ Knockout Mice Leads to Colitis
by Xiaoyu Song, Wanfu Wu, Yubing Dai, Margaret Warner, Ivan Nalvarte, Per Antonson, Mukesh Varshney and Jan-Åke Gustafsson
Int. J. Mol. Sci. 2023, 24(15), 12461; https://doi.org/10.3390/ijms241512461 - 5 Aug 2023
Cited by 4 | Viewed by 2695
Abstract
Liver X receptors (LXRα and LXRβ) are oxysterol-activated nuclear receptors that play key roles in cholesterol homeostasis, the central nervous system, and the immune system. We have previously reported that LXRαβ-deficient mice are more susceptible to dextran sodium sulfate (DSS)-induced colitis than their [...] Read more.
Liver X receptors (LXRα and LXRβ) are oxysterol-activated nuclear receptors that play key roles in cholesterol homeostasis, the central nervous system, and the immune system. We have previously reported that LXRαβ-deficient mice are more susceptible to dextran sodium sulfate (DSS)-induced colitis than their WT littermates, and that an LXR agonist protects against colitis in mice mainly via the regulation of the immune system in the gut. We now report that both LXRα and LXRβ are expressed in the colonic epithelium and that in aging LXRαβ−/− mice there is a reduction in the intensity of goblet cells, mucin (MUC2), TFF3, and estrogen receptor β (ERβ) levels. The cytoplasmic compartment of the surface epithelial cells was markedly reduced and there was a massive invasion of macrophages in the lamina propria. The expression and localization of β-catenin, α-catenin, and E-cadherin were not changed, but the shrinkage of the cytoplasm led to an appearance of an increase in staining. In the colonic epithelium there was a reduction in the expression of plectin, a hemidesmosome protein whose loss in mice leads to spontaneous colitis, ELOVL1, a fatty acid elongase protein coding gene whose overexpression is found in colorectal cancer, and non-neuronal choline acetyltransferase (ChAT) involved in the regulation of epithelial cell adhesion. We conclude that in aging LXRαβ−/− mice, the phenotype in the colon is due to loss of ERβ expression. Full article
(This article belongs to the Section Molecular Biology)
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13 pages, 704 KiB  
Review
Eosinophils, Basophils, and Neutrophils in Bullous Pemphigoid
by Maren M. Limberg, Tobias Weihrauch, Natalie Gray, Nancy Ernst, Karin Hartmann and Ulrike Raap
Biomolecules 2023, 13(7), 1019; https://doi.org/10.3390/biom13071019 - 21 Jun 2023
Cited by 14 | Viewed by 4313
Abstract
Bullous pemphigoid (BP) is an autoimmune blistering skin disease, of which the incidence has increased in recent years. BP is characterized by circulating IgG and IgE autoantibodies against the hemidesmosomal proteins BP180 and BP230. Although autoantibodies trigger inflammatory cascades that lead to blister [...] Read more.
Bullous pemphigoid (BP) is an autoimmune blistering skin disease, of which the incidence has increased in recent years. BP is characterized by circulating IgG and IgE autoantibodies against the hemidesmosomal proteins BP180 and BP230. Although autoantibodies trigger inflammatory cascades that lead to blister formation, effector cells and cell-mediated autoimmunity must also be considered as important factors in the pathogenesis of BP. The aim of this review is to outline the current knowledge on the role of eosinophils, basophils, and neutrophils in BP. Full article
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25 pages, 1320 KiB  
Systematic Review
Role of Hemidesmosomes in Oral Carcinogenesis: A Systematic Review
by Jordan Nguyen, Tze Wei Chong, Hafsa Elmi, Jiani Ma, John Madi, Asha Mamgain, Eileen Melendez, Julian Messina, Nikhil Mongia, Sanjana Nambiar, Tsu Jie Ng, Huy Nguyen, Michael McCullough, Federica Canfora, Lorraine A. O’Reilly, Nicola Cirillo, Rita Paolini and Antonio Celentano
Cancers 2023, 15(9), 2533; https://doi.org/10.3390/cancers15092533 - 28 Apr 2023
Viewed by 4490
Abstract
Background: Oral cancers have limited diagnostic tools to aid clinical management. Current evidence indicates that alterations in hemidesmosomes, the adhesion complexes primarily involved in epithelial attachment to the basement membrane, are correlated to cancer phenotype for multiple cancers. This systematic review aimed to [...] Read more.
Background: Oral cancers have limited diagnostic tools to aid clinical management. Current evidence indicates that alterations in hemidesmosomes, the adhesion complexes primarily involved in epithelial attachment to the basement membrane, are correlated to cancer phenotype for multiple cancers. This systematic review aimed to assess the experimental evidence for hemidesmosomal alterations, specifically in relation to oral potentially malignant disorders and oral squamous cell carcinomas. Methods: We conducted a systemic review to summarise the available literature on hemidesmosomal components and their role in oral pre-cancer and cancer. Relevant studies were retrieved from a comprehensive search of Scopus, Ovid MEDLINE, Ovid Embase and Web of Science. Results: 26 articles met the inclusion criteria, of which 19 were in vitro studies, 4 in vivo studies, 1 in vitro and in vivo study, and 2 in vitro and cohort studies. Among them, 15 studies discussed individual alpha-6 and/or beta-4 subunits, 12 studies discussed the alpha-6 beta-4 heterodimers, 6 studies discussed the entire hemidesmosome complex, 5 studies discussed bullous pemphigoid-180, 3 studies discussed plectin, 3 studies discussed bullous pemphigoid antigen-1 and 1 study discussed tetraspanin. Conclusion: Heterogeneity in cell type, experimental models, and methods were observed. Alterations in hemidesmosomal components were shown to contribute to oral pre-cancer and cancer. We conclude that there is sufficient evidence for hemidesmosomes and their components to be potential biomarkers for evaluating oral carcinogenesis. Full article
(This article belongs to the Special Issue Advances in Oral Cancers and Precancers)
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21 pages, 2242 KiB  
Review
Regulation of Kinase Signaling Pathways by α6β4-Integrins and Plectin in Prostate Cancer
by Saara Koivusalo, Anette Schmidt, Aki Manninen and Tomasz Wenta
Cancers 2023, 15(1), 149; https://doi.org/10.3390/cancers15010149 - 27 Dec 2022
Cited by 10 | Viewed by 3732
Abstract
Hemidesmosomes (HDs) are adhesive structures that ensure stable anchorage of cells to the basement membrane. They are formed by α6β4-integrin heterodimers and linked to intermediate filaments via plectin. It has been reported that one of the most common events during the pathogenesis of [...] Read more.
Hemidesmosomes (HDs) are adhesive structures that ensure stable anchorage of cells to the basement membrane. They are formed by α6β4-integrin heterodimers and linked to intermediate filaments via plectin. It has been reported that one of the most common events during the pathogenesis of prostate cancer (PCa) is the loss of HD organization. While the expression levels of β4-integrins are strongly reduced, the expression levels of α6-integrins and plectin are maintained or even elevated, and seem to promote tumorigenic properties of PCa cells, such as proliferation, invasion, metastasis, apoptosis- and drug-resistance. In this review, we discuss the potential mechanisms of how HD components might contribute to various cellular signaling pathways to promote prostate carcinogenesis. Moreover, we summarize the current knowledge on the involvement of α6β4-integrins and plectin in PCa initiation and progression. Full article
(This article belongs to the Special Issue Kinase Signaling in Cancer)
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Graphical abstract

20 pages, 1615 KiB  
Review
Invasion-Associated Reorganization of Laminin 332 in Oral Squamous Cell Carcinomas: The Role of the Laminin γ2 Chain in Tumor Biology, Diagnosis, and Therapy
by Alexander Berndt, Nikolaus Gaßler and Marcus Franz
Cancers 2022, 14(19), 4903; https://doi.org/10.3390/cancers14194903 - 7 Oct 2022
Cited by 8 | Viewed by 3319
Abstract
Invasion of the connective tissue by carcinoma cells is accompanied by disintegration and reorganization of the hemidesmosomes, which connect the basement membrane to the basal epithelial cells. In terms of mediating the basement membrane, i.e., basal cell interactions, the heterotrimeric laminin 332 is [...] Read more.
Invasion of the connective tissue by carcinoma cells is accompanied by disintegration and reorganization of the hemidesmosomes, which connect the basement membrane to the basal epithelial cells. In terms of mediating the basement membrane, i.e., basal cell interactions, the heterotrimeric laminin 332 is the most important bridging molecule. Due to this distinct function, laminin 332, especially its gamma 2 chain, came into the focus of cancer research. Specific de novo synthesis and deposition patterns of laminin 332 are evident upon development and progression of oral squamous cell carcinomas (OSCCs). Loss from the basement membrane, cytoplasmic accumulation, and extracellular deposition are associated with crucial processes such as stromal activation and immune response, epithelial to mesenchymal transition, and tumor cell budding. In networks with components of the tumor microenvironment, altered expression of laminin 332 chains, proteolytic processing, and interaction with integrin receptors seem to promote cancer cell migration. Indeed, reorganization patterns are shown to have a high diagnostic and prognostic value. Here, we summarize the current knowledge on laminin 332 reorganization in OSCCs with special focus on its gamma 2 chain and provide, based on the current literature, evidence on its promising role as a grading and monitoring parameter and as a potential therapeutic target. Full article
(This article belongs to the Special Issue Study and Treatment of Oral Squamous Cell Carcinoma)
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14 pages, 1974 KiB  
Review
Cross Talk between Synthetic Food Colors (Azo Dyes), Oral Flora, and Cardiovascular Disorders
by Arooba John, Hsi-Hsien Yang, Sohaib Muhammad, Zafar Iqbal Khan, Haiyang Yu, Muhammad Luqman, Matiba Tofail, Muhammad Iftikhar Hussain and Muhammad Umer Farooq Awan
Appl. Sci. 2022, 12(14), 7084; https://doi.org/10.3390/app12147084 - 13 Jul 2022
Cited by 25 | Viewed by 5971
Abstract
Synthetic food colors are important ingredients in the food industry. These synthetic food colorants are azo dyes, majorly acidic in nature such as Allura red and Tartrazine. They are present in sweets, carbonated drinks, meat products, and candies to attract the consumers. This [...] Read more.
Synthetic food colors are important ingredients in the food industry. These synthetic food colorants are azo dyes, majorly acidic in nature such as Allura red and Tartrazine. They are present in sweets, carbonated drinks, meat products, and candies to attract the consumers. This review article is an attempt to explain the adverse effects of azo dyes and their association with oral cavities and cardiovascular disorders. These synthetic dyes (azo dyes) have staining effects on dentin. Poor dental care accelerates the bacterial accumulation on the dental crown (Gram-negative bacteria P. gingivalis, T. denticola, and T. forsythia and Gram-positive bacteria Strep. Gordonii), causing the washing of enamel, forming dental plaque. Bacterial pathogens (P. ginigivalis and F. nacleatum) release different chemicals (FadA and Fap2) that bind to protein on the cell by producing an inflammatory response through different line-host defenses, such as Gingival epithelial cells (ECs), Hemi-desmosomes, and desmosomes, which helps the bacterium migration from the cell–cell junction. This makes the junctions slightly open up and makes the whole vessel permeable, through which the bacterium enters into the blood stream line. This leads to different major arteries, such as the carotid artery, and causes the accumulation of plaque in major cardiac arteries, which causes different cardiovascular disorders. These bacterial species present in gums cause cardiovascular diseases, such as ischemic heart disease, coronary artery disease, heart attacks and strokes, and arrhythmias, which can lead to death. Full article
(This article belongs to the Special Issue Food Microbiology: Contemporary Issues of Food Safety)
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11 pages, 561 KiB  
Review
Deciphering the Contribution of BP230 Autoantibodies in Bullous Pemphigoid
by Connor Cole, Luca Borradori and Kyle T. Amber
Antibodies 2022, 11(3), 44; https://doi.org/10.3390/antib11030044 - 28 Jun 2022
Cited by 13 | Viewed by 6411
Abstract
Bullous pemphigoid (BP) is a subepidermal autoimmune blistering disease predominantly affecting elderly patients and carries significant morbidity and mortality. Patients typically suffer from severe itch with eczematous lesions, urticarial plaques, and/or tense blisters. BP is characterized by the presence of circulating autoantibodies against [...] Read more.
Bullous pemphigoid (BP) is a subepidermal autoimmune blistering disease predominantly affecting elderly patients and carries significant morbidity and mortality. Patients typically suffer from severe itch with eczematous lesions, urticarial plaques, and/or tense blisters. BP is characterized by the presence of circulating autoantibodies against two components of the hemidesmosome, BP180 and BP230. The transmembrane BP180, also known as type XVII collagen or BPAG2, represents the primary pathogenic autoantigen in BP, whereas the intracellular BP230 autoantigen is thought to play a minor role in disease pathogenesis. Although experimental data exist suggesting that anti-BP230 antibodies are secondarily formed following initial tissue damage mediated by antibodies targeting extracellular antigenic regions of BP180, there is emerging evidence that anti-BP230 IgG autoantibodies alone directly contribute to tissue damage. It has been further claimed that a subset of patients has a milder variant of BP driven solely by anti-BP230 autoantibodies. Furthermore, the presence of anti-BP230 autoantibodies might correlate with distinct clinical features. This review summarizes the current understanding of the role of BP230 and anti-BP230 antibodies in BP pathogenesis. Full article
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10 pages, 3433 KiB  
Communication
The Haptomonad Stage of Crithidia acanthocephali in Apis mellifera Hindgut
by María Buendía-Abad, Pilar García-Palencia, Luis Miguel de Pablos, Raquel Martín-Hernández and Mariano Higes
Vet. Sci. 2022, 9(6), 298; https://doi.org/10.3390/vetsci9060298 - 16 Jun 2022
Cited by 7 | Viewed by 2575
Abstract
Crithidia acanthocephali is a trypanosomatid species that was initially described in the digestive tract of Hemiptera. However, this parasite was recently detected in honey bee colonies in Spain, raising the question as to whether bees can act as true hosts for this species. [...] Read more.
Crithidia acanthocephali is a trypanosomatid species that was initially described in the digestive tract of Hemiptera. However, this parasite was recently detected in honey bee colonies in Spain, raising the question as to whether bees can act as true hosts for this species. To address this issue, worker bees were experimentally infected with choanomastigotes from the early stationary growth phase and after 12 days, their hindgut was extracted for analysis by light microscopy and TEM. Although no cellular lesions were observed in the honey bee’s tissue, trypanosomatids had differentiated and adopted a haptomonad morphology, transforming their flagella into an attachment pad. This structure allows the protozoa to remain attached to the gut walls via hemidesmosomes-such as junctions. The impact of this species on honey bee health, as well as the pathogenic mechanisms involved, remains unknown. Nevertheless, these results suggest that insect trypanosomatids may have a broader range of hosts than initially thought. Full article
(This article belongs to the Special Issue Challenges and Advances in Bee Health and Diseases)
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22 pages, 792 KiB  
Review
Epidermolysis Bullosa—A Different Genetic Approach in Correlation with Genetic Heterogeneity
by Monica-Cristina Pânzaru, Lavinia Caba, Laura Florea, Elena Emanuela Braha and Eusebiu Vlad Gorduza
Diagnostics 2022, 12(6), 1325; https://doi.org/10.3390/diagnostics12061325 - 27 May 2022
Cited by 13 | Viewed by 5582
Abstract
Epidermolysis bullosa is a heterogeneous group of rare genetic disorders characterized by mucocutaneous fragility and blister formation after minor friction or trauma. There are four major epidermolysis bullosa types based on the ultrastructural level of tissue cleavage: simplex, junctional, dystrophic, and Kindler epidermolysis [...] Read more.
Epidermolysis bullosa is a heterogeneous group of rare genetic disorders characterized by mucocutaneous fragility and blister formation after minor friction or trauma. There are four major epidermolysis bullosa types based on the ultrastructural level of tissue cleavage: simplex, junctional, dystrophic, and Kindler epidermolysis bullosa. They are caused by mutations in genes that encode the proteins that are part of the hemidesmosomes and focal adhesion complex. Some of these disorders can be associated with extracutaneous manifestations, which are sometimes fatal. They are inherited in an autosomal recessive or autosomal dominant manner. This review is focused on the phenomena of heterogeneity (locus, allelic, mutational, and clinical) in epidermolysis bullosa, and on the correlation genotype–phenotype. Full article
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17 pages, 1725 KiB  
Review
Leaky Gum: The Revisited Origin of Systemic Diseases
by Do-Young Park, Jin Young Park, Dahye Lee, Inseong Hwang and Hye-Sung Kim
Cells 2022, 11(7), 1079; https://doi.org/10.3390/cells11071079 - 23 Mar 2022
Cited by 18 | Viewed by 7123
Abstract
The oral cavity is the gateway for microorganisms into your body where they disseminate not only to the directly connected respiratory and digestive tracts but also to the many remote organs. Oral microbiota, travelling to the end of the intestine and circulating in [...] Read more.
The oral cavity is the gateway for microorganisms into your body where they disseminate not only to the directly connected respiratory and digestive tracts but also to the many remote organs. Oral microbiota, travelling to the end of the intestine and circulating in our bodies through blood vessels, not only affect a gut microbiome profile but also lead to many systemic diseases. By gathering information accumulated from the era of focal infection theory to the age of revolution in microbiome research, we propose a pivotal role of “leaky gum”, as an analogy of “leaky gut”, to underscore the importance of the oral cavity in systemic health. The oral cavity has unique structures, the gingival sulcus (GS) and the junctional epithelium (JE) below the GS, which are rarely found anywhere else in our body. The JE is attached to the tooth enamel and cementum by hemidesmosome (HD), which is structurally weaker than desmosome and is, thus, vulnerable to microbial infiltration. In the GS, microbial biofilms can build up for life, unlike the biofilms on the skin and intestinal mucosa that fall off by the natural process. Thus, we emphasize that the GS and the JE are the weakest leaky point for microbes to invade the human body, making the leaky gum just as important as, or even more important than, the leaky gut. Full article
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