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Mediators of Inflammation
Volume 2015, Article ID 120605, 11 pages
Clinical Study

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

1Department of Infectious Diseases, Aarhus University Hospital, 8200 Skejby, Denmark
2Department of Hepatology and Gastroenterology, Aarhus University Hospital, 8000 Aarhus, Denmark
3Department of Clinical Medicine, Aarhus University, 8000 Aarhus, Denmark
4Stereology and Electron Microscopy Laboratory, Centre for Stochastic Geometry and Advanced Bioimaging, Aarhus University Hospital, 8000 Aarhus, Denmark
5Aarhus Institute for Advanced Studies, Aarhus University, 8000 Aarhus, Denmark

Received 23 September 2015; Revised 10 November 2015; Accepted 15 November 2015

Academic Editor: Kong Chen

Copyright © 2015 Ane Bjerg Christensen et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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 ( 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.