Abstract
Psoriasis is a chronic, inflammatory, complex and multifactorial lifelong condition of the skin with Munro microabscesses and spongiform pustules of Kogoj as morphological diagnostic criteria and red, scaly, indurated plaques clinically. Psoriasis patients have altered innate immune system and changes of antimicrobial peptide expression can play an important role in pathogenesis of psoriasis. The aim of the study was to evaluate the expression of human beta defensin 2 (HBD2), tumour necrosis factoralpha (TNF-alpha), calcitonin gene related peptide (CGRP) and protein gene product 9.5 (PGP 9.5) and subsequent morphological events – inflammation, local immune response and neuropeptides-containing innervation in skin biopsies of psoriatic lesions.
We evaluated 40 Psoriasis vulgaris patients’ skin samples obtained using routine punch method.
All tissue specimens were stained with hematoxylin and eosin and by immunohistochemistry for HBD2, TNF-alpha, CGRP and PGP 9.5. The intensity of staining we graded semiquantitatively.
We observed proliferation of basal layer, reduction of granular layer and parakeratosis, marked infiltration of inflammatory cells in subepithelial layer of the skin, presence of epitheloid cells, macrophages and Munro microabscesses. Arteriole sclerosis and sweat gland cell vacuolization were detected. Numerous to abundant epitheliocytes, macrophages and fibroblasts expressed HBD2, with particular increase in sites
of well defined inflammation. TNF-alpha and CGRP positive cells (lymphocytes and macrophages) were found in almost all skin samples – particularly in subepithelium, walls of blood vessels and eccrine sweat glands. A moderate number of neuropeptide-containing nerve fibres (PGP 9.5) was noticed as fine bundles
in subepithelial area with prominent innervation of epithelium and sweat glands.
Psoriatic skin shows compensatory prominent local antimicrobial protein expression and neuropeptides-containing innervation on the basis of moderate inflammation and thus may play a role in
the pathogenesis of psoriasis.
We evaluated 40 Psoriasis vulgaris patients’ skin samples obtained using routine punch method.
All tissue specimens were stained with hematoxylin and eosin and by immunohistochemistry for HBD2, TNF-alpha, CGRP and PGP 9.5. The intensity of staining we graded semiquantitatively.
We observed proliferation of basal layer, reduction of granular layer and parakeratosis, marked infiltration of inflammatory cells in subepithelial layer of the skin, presence of epitheloid cells, macrophages and Munro microabscesses. Arteriole sclerosis and sweat gland cell vacuolization were detected. Numerous to abundant epitheliocytes, macrophages and fibroblasts expressed HBD2, with particular increase in sites
of well defined inflammation. TNF-alpha and CGRP positive cells (lymphocytes and macrophages) were found in almost all skin samples – particularly in subepithelium, walls of blood vessels and eccrine sweat glands. A moderate number of neuropeptide-containing nerve fibres (PGP 9.5) was noticed as fine bundles
in subepithelial area with prominent innervation of epithelium and sweat glands.
Psoriatic skin shows compensatory prominent local antimicrobial protein expression and neuropeptides-containing innervation on the basis of moderate inflammation and thus may play a role in
the pathogenesis of psoriasis.
| Original language | English |
|---|---|
| Title of host publication | Rīga Stradiņš University Collection of Scientific Papers 2013 |
| Subtitle of host publication | Research articles in medicine & pharmacy |
| Place of Publication | Rīga |
| Publisher | Rīgas Stradiņa universitāte |
| Pages | 36-42 |
| ISBN (Print) | 978-9984-793-43-6 |
| Publication status | Published - 2014 |
Publication series
| Name | Collection of Scientific Papers |
|---|---|
| Publisher | Rīga Stradiņš University |
| ISSN (Print) | 1691-497X |
Keywords*
- antimicrobial peptides
- cytokines
- neuropeptides
- psoriasis
Field of Science*
- 3.1 Basic medicine
- 3.2 Clinical medicine
Publication Type*
- 3.2. Articles or chapters in other proceedings other than those included in 3.1., with an ISBN or ISSN code