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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

M2 macrophages or IL-33 treatment attenuate ongoing Mycobacterium tuberculosis infection

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Author(s):
Pineros, A. R. ; Campos, L. W. ; Fonseca, D. M. ; Bertolini, T. B. ; Gembre, A. F. ; Prado, R. Q. ; Alves-Filho, J. C. ; Ramos, S. G. ; Russo, M. ; Bonato, V. L. D.
Total Authors: 10
Document type: Journal article
Source: SCIENTIFIC REPORTS; v. 7, JAN 27 2017.
Web of Science Citations: 6
Abstract

The protective effects of mycobacterial infections on lung allergy are well documented. However, the inverse relationship between tuberculosis and type 2 immunity is still elusive. Although type 1 immunity is essential to protection against Mycobacterium tuberculosis it might be also detrimental to the host due to the induction of extensive tissue damage. Here, we determined whether lung type 2 immunity induced by allergen sensitization and challenge could affect the outcome of M. tuberculosis infection. We used two different protocols in which sensitization and allergen challenge were performed before or after M. tuberculosis infection. We found an increased resistance to M. tuberculosis only when allergen exposure was given after, but not before infection. Infected mice exposed to allergen exhibited lower bacterial load and cellular infiltrates in the lungs. Enhanced resistance to infection after allergen challenge was associated with increased gene expression of alternatively activated macrophages (M2 macrophages) and IL-33 levels. Accordingly, either adoptive transfer of M2 macrophages or systemic IL-33 treatment was effective in attenuating M. tuberculosis infection. Notably, the enhanced resistance induced by allergen exposure was dependent on IL-33 receptor ST2. Our work indicates that IL-33 might be an alternative therapeutic treatment for severe tuberculosis. (AU)

FAPESP's process: 08/07861-3 - EVALUATION OF THE MECHANISMS IMPLICATED IN THE MODULATION OF IMMUNE RESPONSE IN A CO-INFLAMMATION MODEL OF TUBERCULOSIS X ALLERGY
Grantee:Lívia Weijenborg Campos
Support Opportunities: Scholarships in Brazil - Master
FAPESP's process: 09/13689-1 - Evaluation of mechanisms involved in the modulation of immune response in a model of co-inflammation tuberculosis and allergy
Grantee:Vânia Luiza Deperon Bonato
Support Opportunities: Regular Research Grants