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Role of Intestinal Myofibroblasts in HIV-Associated Intestinal Collagen Deposition and Immune Reconstitution following Combination Antiretroviral Therapy #MMPMID25784439
Asmuth DM; Pinchuk IV; Wu J; Vargas G; Chen X; Mann S; Albanese A; Ma ZM; Saroufeem R; Melcher GP; Troia-Cancio P; Torok NJ; Miller CJ; Powell DW
AIDS 2015[May]; 29 (8): 877-88 PMID25784439show ga
Objective: To investigate the potential role of mucosal intestinal myofibroblasts (IMFs) in HIV and associated fibrosis in GALT. Design: Profibrotic changes within the secondary lymphoid organs and mucosa has been implicated in failed immune reconstitution following effective cART. Microbial translocation is believed to be sustaining these systemic inflammatory pathways. IMFs are non-professional antigen-presenting cells with both immunoregulatory and mesenchymal functions that are ideally positioned to respond to translocating microbial antigen. Methods: Duodenal biopsies obtained from patients naïve to cART underwent trichrome staining and examined for TGF-? expression. Combined immunostaining and second harmonic generation-analysis was used to determine IMF activation and collagen deposition. Confocal microscopy was performed to examine for IMF activation and TLR4 expression. Finally, primary IMF cultures were stimulated with LPS to demonstrate expression of inflammatory biomarkers. Results: The expression of the fibrosis-promoting molecule, TGF-?1, is significantly increased in duodenal biopsies from HIV patients naïve to cART and negatively correlated with subsequent peripheral CD4 recovery. The TGF?1 increases coincided with an increase in collagen deposition in duodenal mucosa in tissue area adjacent to IMFs. We also observed that IMFs expressed TLR4 and had an activated phenotype since they were positive for fibroblast activation protein. Finally, stimulation of IMFs from HIV patients with TLR4 resulted in significantly increased expression of profibrotic molecules, TGF-?1 and IL-6. Conclusions: Our data support the hypothesis that activated IMFs may be among the major cells contributing to the profibrotic changes and thus, the establishment and maintenance of systemic inflammation interfering with immune reconstitution in HIV patients.
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AIDS 2015 ; 29 (8): 877-88
