Human beta-defensin 3 is up-regulated in cutaneous leprosy type 1 reactions.

<h4>Background</h4>Leprosy, a chronic granulomatous disease affecting the skin and nerves, is caused by Mycobacterium leprae (M. leprae). The type of leprosy developed depends upon the host immune response. Type 1 reactions (T1Rs), that complicate borderline and lepromatous leprosy, are...

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Main Authors: Anna L Cogen, Stephen L Walker, Chrissy H Roberts, Deanna A Hagge, Kapil D Neupane, Saraswoti Khadge, Diana N J Lockwood
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2012-01-01
Series:PLoS Neglected Tropical Diseases
Online Access:https://journals.plos.org/plosntds/article/file?id=10.1371/journal.pntd.0001869&type=printable
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author Anna L Cogen
Stephen L Walker
Chrissy H Roberts
Deanna A Hagge
Kapil D Neupane
Saraswoti Khadge
Diana N J Lockwood
author_facet Anna L Cogen
Stephen L Walker
Chrissy H Roberts
Deanna A Hagge
Kapil D Neupane
Saraswoti Khadge
Diana N J Lockwood
author_sort Anna L Cogen
collection DOAJ
description <h4>Background</h4>Leprosy, a chronic granulomatous disease affecting the skin and nerves, is caused by Mycobacterium leprae (M. leprae). The type of leprosy developed depends upon the host immune response. Type 1 reactions (T1Rs), that complicate borderline and lepromatous leprosy, are due to an increase in cell-mediated immunity and manifest as nerve damage and skin inflammation. Owing to the increase in inflammation in the skin of patients with T1Rs, we sought to investigate the activation of the innate immune system during reactionary events. Specifically, we investigated the expression levels of human beta-defensins (hBDs) 2 and 3 in the skin of patients with T1Rs, in keratinocytes, and in macrophages stimulated with M. leprae and corticosteroids.<h4>Results</h4>Skin biopsies from twenty-three patients with Type 1 reactions were found to have higher transcript levels of hBD3 as compared to fifteen leprosy patients without Type 1 reactions, as measured by qPCR. Moreover, we observed that keratinocytes but not macrophages up-regulated hBD2 and hBD3 in response to M. leprae stimulation in vitro. Corticosteroid treatment of patients with T1Rs caused a suppression of hBD2 and hBD3 in skin biopsies, as measured by qPCR. In vitro, corticosteroids suppressed M. leprae-dependent induction of hBD2 and hBD3 in keratinocytes.<h4>Conclusions</h4>This study demonstrates that hBD3 is induced in leprosy Type 1 Reactions and suppressed by corticosteroids. Furthermore, our findings demonstrate that keratinocytes are responsive to M. leprae and lend support for additional studies on keratinocyte innate immunity in leprosy and T1Rs.<h4>Trial registration</h4>Controlled-Trials.com ISRCTN31894035.
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spelling doaj-art-e2a50e6795644c7bb418591eb87bb2c62025-08-20T03:01:13ZengPublic Library of Science (PLoS)PLoS Neglected Tropical Diseases1935-27271935-27352012-01-01611e186910.1371/journal.pntd.0001869Human beta-defensin 3 is up-regulated in cutaneous leprosy type 1 reactions.Anna L CogenStephen L WalkerChrissy H RobertsDeanna A HaggeKapil D NeupaneSaraswoti KhadgeDiana N J Lockwood<h4>Background</h4>Leprosy, a chronic granulomatous disease affecting the skin and nerves, is caused by Mycobacterium leprae (M. leprae). The type of leprosy developed depends upon the host immune response. Type 1 reactions (T1Rs), that complicate borderline and lepromatous leprosy, are due to an increase in cell-mediated immunity and manifest as nerve damage and skin inflammation. Owing to the increase in inflammation in the skin of patients with T1Rs, we sought to investigate the activation of the innate immune system during reactionary events. Specifically, we investigated the expression levels of human beta-defensins (hBDs) 2 and 3 in the skin of patients with T1Rs, in keratinocytes, and in macrophages stimulated with M. leprae and corticosteroids.<h4>Results</h4>Skin biopsies from twenty-three patients with Type 1 reactions were found to have higher transcript levels of hBD3 as compared to fifteen leprosy patients without Type 1 reactions, as measured by qPCR. Moreover, we observed that keratinocytes but not macrophages up-regulated hBD2 and hBD3 in response to M. leprae stimulation in vitro. Corticosteroid treatment of patients with T1Rs caused a suppression of hBD2 and hBD3 in skin biopsies, as measured by qPCR. In vitro, corticosteroids suppressed M. leprae-dependent induction of hBD2 and hBD3 in keratinocytes.<h4>Conclusions</h4>This study demonstrates that hBD3 is induced in leprosy Type 1 Reactions and suppressed by corticosteroids. Furthermore, our findings demonstrate that keratinocytes are responsive to M. leprae and lend support for additional studies on keratinocyte innate immunity in leprosy and T1Rs.<h4>Trial registration</h4>Controlled-Trials.com ISRCTN31894035.https://journals.plos.org/plosntds/article/file?id=10.1371/journal.pntd.0001869&type=printable
spellingShingle Anna L Cogen
Stephen L Walker
Chrissy H Roberts
Deanna A Hagge
Kapil D Neupane
Saraswoti Khadge
Diana N J Lockwood
Human beta-defensin 3 is up-regulated in cutaneous leprosy type 1 reactions.
PLoS Neglected Tropical Diseases
title Human beta-defensin 3 is up-regulated in cutaneous leprosy type 1 reactions.
title_full Human beta-defensin 3 is up-regulated in cutaneous leprosy type 1 reactions.
title_fullStr Human beta-defensin 3 is up-regulated in cutaneous leprosy type 1 reactions.
title_full_unstemmed Human beta-defensin 3 is up-regulated in cutaneous leprosy type 1 reactions.
title_short Human beta-defensin 3 is up-regulated in cutaneous leprosy type 1 reactions.
title_sort human beta defensin 3 is up regulated in cutaneous leprosy type 1 reactions
url https://journals.plos.org/plosntds/article/file?id=10.1371/journal.pntd.0001869&type=printable
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