Cytokine expression patterns distinguish HIV associated skin diseases

Abstract

AIDS is known to cause a shift of cytokines in the periphery. However, predominant cytokines in skin of patients with HIV-associated skin diseases have not been clearly defined. We hypothesized that there are distinct cytokine profiles that distinguish among the different clinical manifestations of AIDS-related skin diseases. To test this hypothesis, lesional and non-lesional skin was biopsied from 53 HIV+ patients with Kaposi's sarcoma (KS), psoriasis, and pruritus due to eosinophilic folliculitis, and from HIV negative controls with psoriasis or KS prior to therapy. Immunohistochemistry was performed with antibodies to tumor necrosis factor (TNF)-alpha, interleukin (IL)-10, interferon (IFN)-gamma, and interferon-inducible protein (IP)-10. HIV positive individuals included 10 with psoriasis, 14 with pruritus, and 15 with Kaposi's sarcoma. HIV negative controls included 12 with psoriasis and two with KS. Semi-quantitative analysis of cytokine staining was confirmed by optical density using a digital imaging system on four representative skin sections from each disease. Optical density analyses were conducted using ANOVA and t-tests. We found that epidermis overlying HIV+ Kaposi's sarcoma was hyperproliferative and was highest in IP-10, IFN-gamma, and IL-10 (P=0.0001). HIV+ pruritus was significantly highest in TNF-alpha (P=0.0001) staining. HIV+ psoriasis represented an intermediate state for all four cytokines. Normal skin adjacent to lesions showed the same relative patterns, with lower intensities. Skin diseases seen frequently in the setting of HIV and immunodeficiency have relatively distinct levels and patterns of cytokine expression that may reflect immune dysfunction, reactivity to HIV and to opportunistic infections.

Antimicrobial Peptides Human β-Defensins and Cathelicidin LL-37 Induce the Secretion of a Pruritogenic Cytokine IL-31 by Human Mast Cells

“…Apart from the secretion of IL-31, hBDs and LL-37 also enhanced the release of numerous cytokines, including IL-2, IL-4, IL-6, IL-8, GM-CSF, and TNF-a, which are known to play a role in the elicitation of itching (52)(53)(54)(55)(56)(57). However, several experimental studies have suggested an indirect pruritogenic effect of above cytokines via other mediators (55,58).…”

Skin symptoms associated with human immunodeficiency virus infection

“…Az immunológiai funckiók HIV okozta folyamatos romlása következtében fellépő opportunista fertőzések és fokozott karcinogenezis jól ismert folyamatok, azonban a primer HIV-bőrtünetek közé sorolt, nagyrészt klasszikus bőrbetegségek (például psoriasis vulgaris, atopiás dermatitis, seborrhoeás dermatitis) atípusos és terápiarezisztens megjelenése HIV-fertőzötteken intenzív kutatások tárgya. A bőrtünetek kialakulásában -az epidermisben jelen levő antigénpre-zentáló sejtek számbeli és funkcióbeli csökkenése mellett -szerepet tulajdonítanak a CD4-lymphocyta-szám csök-kenésének, a HIV okozta komplex immundiszreguláció-nak, de a szuperantigén-és citokinhatásoknak is [8,9].…”

“…A klinikai különbségek hátterében több mechanizmust is feltételeznek. A HIV mint cutan gyulladást provokáló ágens és a HIV okozta immundiszreguláció, ami módosítja a cutan citokinmiliőt, magyarázhatja a psoriasis súlyosabb lefolyását [9,15]. Az utób-bi időben a fi gyelem a retrovírusok autoimmun és autoinfl ammatorikus betegségeket kiváltó tulajdonsága felé fordult.…”

Pruritic papular eruption and eosinophilic folliculitis associated with human immunodeficiency virus (HIV) infection: A histopathological and immunohistochemical comparative study

“…Several reviews reported the clinical, histological, and immunohistochemical findings that distinguish HIV-PPE from HIV-EF. [8][9][10][11][12][13][14] The impact of histopathological differentiation on therapy choice was proposed by Holmes, Martins, and Horn, 15 but differential diagnosis criteria distinguishing between these two entities have not been established.…”