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    Administration of Panobinostat Is Associated with Increased IL-17A mRNA in the Intestinal Epithelium of HIV-1 Patients

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    Author
    Christensen, AB; Dige, A; Vad-Nielsen, J; Brinkmann, CR; Bendix, M; Ostergaard, L; Tolstrup, M; Sogaard, OS; Rasmussen, TA; Nyengaard, JR; ...
    Date
    2015-01-01
    Source Title
    Mediators of Inflammation
    Publisher
    HINDAWI LTD
    University of Melbourne Author/s
    Rasmussen, Thomas
    Affiliation
    Doherty Institute
    Metadata
    Show full item record
    Document Type
    Journal Article
    Citations
    Christensen, A. B., Dige, A., Vad-Nielsen, J., Brinkmann, C. R., Bendix, M., Ostergaard, L., Tolstrup, M., Sogaard, O. S., Rasmussen, T. A., Nyengaard, J. R., Agnholt, J. & Denton, P. W. (2015). Administration of Panobinostat Is Associated with Increased IL-17A mRNA in the Intestinal Epithelium of HIV-1 Patients. MEDIATORS OF INFLAMMATION, 2015, https://doi.org/10.1155/2015/120605.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/255677
    DOI
    10.1155/2015/120605
    Abstract
    Intestinal CD4(+) T cell depletion is rapid and profound during early HIV-1 infection. This leads to a compromised mucosal barrier that prompts chronic systemic inflammation. The preferential loss of intestinal T helper 17 (Th17) cells in HIV-1 disease is a driver of the damage within the mucosal barrier and of disease progression. Thus, understanding the effects of new therapeutic strategies in the intestines has high priority. Histone deacetylase (HDAC) inhibitors (e.g., panobinostat) are actively under investigation as potential latency reversing agents in HIV eradication studies. These drugs have broad effects that go beyond reactivating virus, including modulation of immune pathways. We examined colonic biopsies from ART suppressed HIV-1 infected individuals (clinicaltrials.gov: NCT01680094) for the effects of panobinostat on intestinal T cell activation and on inflammatory cytokine production. We compared biopsy samples that were collected before and during oral panobinostat treatment and observed that panobinostat had a clear biological impact in this anatomical compartment. Specifically, we observed a decrease in CD69(+) intestinal lamina propria T cell frequency and increased IL-17A mRNA expression in the intestinal epithelium. These results suggest that panobinostat therapy may influence the restoration of mucosal barrier function in these patients.

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