IL-1R1 Signaling Facilitates Munro’s Microabscess Formation in Psoriasiform Imiquimod-Induced Skin Inflammation
Autor: | Mireia Uribe-Herranz, Liselotte E. Jensen, Katelynn A. Milora, Li-Hua Lian, Kirsten M. Hooper |
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Rok vydání: | 2013 |
Předmět: |
Keratinocytes
Chemokine Neutrophils Chemokine CXCL1 Chemokine CXCL2 Interleukin-1beta Primary Cell Culture Inflammation Imiquimod Acanthosis Dermatology Biochemistry Article Mice Adjuvants Immunologic Interleukin-1alpha medicine Animals Humans Psoriasis Microabscess Molecular Biology Mice Knockout Receptors Interleukin-1 Type I biology Epidermis (botany) Dermis Cell Biology medicine.disease Abscess medicine.anatomical_structure Animals Newborn Epidermal Cells Immunology Aminoquinolines biology.protein Drug Eruptions medicine.symptom Signal transduction Keratinocyte Signal Transduction medicine.drug |
Zdroj: | The Journal of investigative dermatology |
ISSN: | 0022-202X |
DOI: | 10.1038/jid.2012.512 |
Popis: | Munro’s microabscesses contain polymorphonuclear leukocytes and form specifically in the epidermis of psoriasis patients. The mechanism whereby the neutrophils are recruited into the epidermis is poorly understood. Using a combination of human and mouse primary keratinocyte cell cultures and the imiquimod-induced psoriasis-like mouse model of skin inflammation we explored the role of interleukin-1 (IL-1) signaling in microabscess formation. In vitro imiquimod stimulated production of IL-1α and neutrophil recruiting chemokines. Imiquimod activated chemokine expression was dependent upon adenosine signaling and independent of IL-1α and IL-1 receptor type 1 (IL-1R1); nevertheless, IL-1α could enhance chemokine expression initiated by imiquimod. Topical application of imiquimod in vivo led to epidermal microabscess formation, acanthosis and increased IL-1α and chemokine expression in the skin of wild type mice. However, in IL-1R1 deficient mice these responses were either absent or dramatically reduced. These results demonstrate that IL-1α and IL-1R1 signaling is essential for microabscess formation, neutrophil recruiting chemokine expression and acanthosis in psoriasis-like skin inflammation induced by imiquimod. |
Databáze: | OpenAIRE |
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