Background: Diabetic patients are refractory to allergic inflammatory diseases. In this study, the influence of alloxan-induced diabetes on allergic skin inflammation was investigated.
Methods: Diabetes was induced by intravenous injection of alloxan into male Wistar rats, and the analyses were performed 21 days later. Animals were actively sensitized with a mixture of aluminium hydroxide plus ovalbumin and challenged intradermally with ovalbumin on day 14.
Results: Diabetic sensitized rats exhibited a less pronounced antigen-induced protein extravasation in the dorsal skin when compared with normal animals. Also, fragments of the dorsal subcutaneous tissue from diabetic sensitized rats showed a reduction in histamine release after stimulation with antigen in vitrowhen compared with fragments obtained from nondiabetic sensitized rats. Optical microscopy analysis revealed that the dorsal skin of diabetic rats showed a marked reduction in dermis thickness, as compared with that seen in normal animals. A significant decrease in the number of skin mast cells was also noted, a phenomenon that paralleled with the reduction in the expression of extracellular matrix components laminin, fibronectin and collagen. Administration of insulin into diabetic rats restored basal mast cell numbers as well as the levels of laminin, fibronectin and collagen.
Conclusions: Our findings show that alloxan diabetes induces downregulation of the skin allergic inflammatory response in rats, and this was correlated with reduction in local mast cell numbers and expression of extracellular matrix components. Lastly, these alterations were reversed with insulin treatment.
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http://dx.doi.org/10.1159/000142049 | DOI Listing |
J Invest Dermatol
December 2024
Department of Dermatology, Venereology and Allergology, University Hospital Würzburg, 97080 Würzburg, Germany. Electronic address:
A plethora of data supports a major role of CD4 and CD8 T lymphocytes for the initiation, progression and maintenance of allergic contact dermatitis (ACD). However, in-depth understanding of the molecular mechanisms is still limited. NFATc1 plays an essential role in T cell activation.
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College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, 408 Raymond Stotzer Parkway, College Station, TX 77845, USA. Electronic address:
Canine atopic dermatitis (cAD) and feline atopic skin syndrome are inflammatory and pruritic skin diseases with both environmental and genetic factors. Genetic factors may include barrier defects and a predisposition to mount T helper 2 lymphocyte immune response when allergens are encountered. These diseases have repeatable patterns of skin and ear inflammation and commonly lead to Staphylococcal and Malassezia skin and ear infections.
View Article and Find Full Text PDFVet Clin North Am Small Anim Pract
December 2024
College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, 408 Raymond Stotzer Parkway, College Station, TX 77845, USA. Electronic address:
Alterations in the lipid layer and intercellular corneocyte connections can lead to increased allergen penetration through the skin surface. A normal cutaneous microbiome keeps the opportunistic pathogen Staphylococcus pseudintermedius levels low, but allergic inflammation leads to decreased diversity and increase in S pseudintermedius. Keratinocytes sound the initial allergen alarm via cytokine signaling and promote T-helper 2 (Th-2) inflammation.
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Background: Environmental pollutants have been found to contribute to the development and acute exacerbation of asthma. Microplastics (MPs) have received widespread attention as an emerging global pollutant. Airborne MPs can cause various adverse health effects.
View Article and Find Full Text PDFJ Inflamm (Lond)
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Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, 230022, China.
The chemokine CCL20, a small cytokine that belongs to the C-C chemokine family, interacts with its homologous receptor CCR6, which is expressed on wide range of cell types. According to current research, the CCL20-CCR6 has been established as acritical player in a diverse range of inflammatory, oncogenic, and autoimmune diseases. Within the respiratory system, CCL20-CCR6 demonstrates heightened expression in conditions such as allergic asthma, chronic airway inflammation, non-small cell lung cancer (NSCLC), chronic obstructive pulmonary disease (COPD), and other respiratory diseases, which is conducive to the inflammatory mediators recruitment and tumor microenvironment remodeling.
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