Person: Amouzegar, Afsaneh
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Amouzegar
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Afsaneh
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Amouzegar, Afsaneh
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Publication Kinetics of Corneal Antigen Presenting Cells in Experimental Dry Eye Disease(BMJ Publishing Group, 2017) Lee, Hyun Soo; Amouzegar, Afsaneh; Dana, RezaObjective: To evaluate dry eye disease (DED)-induced alterations in subsets of corneal antigen presenting cells (APCs) in a mouse model of experimental DED. Methods and Analysis Seven to 8-week-old female C57BL/6 mice were housed in a controlled environment chamber and were treated with subcutaneous scopolamine to induce DED. Normal mice were used as controls. The frequencies of different subsets of dendritic cells (DCs) and macrophages in the cornea were evaluated using immunohistochemistry and flow cytometry at days 2, 7 and 14 after DED induction. Real-time PCR was used to assess the functional phenotype of macrophages in the cornea of DED mice. Results: Our results demonstrated significant corneal infiltration of CD11b+ and CD11c+ cells on days 7 and 14. Further analysis of different DC subsets revealed non-significant changes in the frequencies of total CD11b+CD11c+ cells at different time points. However, frequencies of CD11c+CD11b- DCs, CD11c+ Langerin (CD207)+ DCs and macrophages were significantly increased on both days 7 and 14 after DED induction. Real-time PCR data demonstrated increased expression of M1 macrophage markers, iNOS and TNF-α, and reduced expression of M2 macrophage markers, Arg1 and IL-10, by corneal F4/80+ macrophages at day 7. Conclusion: Although the frequencies of total CD11b+CD11c+ cells do not significantly change in the course of DED, CD11c+CD11b- DCs and Langerin+ DCs do show a significant increase. Interestingly, macrophages exhibit a predominant inflammatory M1 phenotype and suppressed anti-inflammatory M2 phenotype early after induction of DED, which are restored to near baseline levels in later stages of the disease.Publication Mesenchymal Stromal Cells Inhibit Neutrophil Effector Functions in a Murine Model of Ocular Inflammation(The Association for Research in Vision and Ophthalmology, 2018) Mittal, Sharad; Mashaghi, Alireza; Amouzegar, Afsaneh; Li, Mingshun; Foulsham, William; Sahu, Srikant K.; Chauhan, SunilPurpose Neutrophil-secreted effector molecules are one of the primary causes of tissue damage during corneal inflammation. In the present study, we have investigated the effect of stromal cells in regulating neutrophil expression of tissue-damaging enzymes, myeloperoxidase (MPO), and N-elastase (ELANE). Methods: Bone marrow–purified nonhematopoietic mesenchymal stromal cells and formyl-methionyl-leucyl-phenylalanine–activated neutrophils were cocultured in the presence or absence of Transwell inserts for 1 hour. Neutrophil effector molecules, MPO and ELANE, were quantified using ELISA. In mice, corneal injury was created by mechanical removal of the corneal epithelium and anterior stroma approximating one third of total corneal thickness, and mesenchymal stromal cells were then intravenously injected 1 hour post injury. Corneas were harvested to evaluate MPO expression and infiltration of CD11b+Ly6G+ neutrophils. Results: Activated neutrophils cocultured with mesenchymal stromal cells showed a significant 2-fold decrease in secretion of MPO and ELANE compared to neutrophils activated alone (P < 0.05). This suppressive effect was cell–cell contact dependent, as stromal cells cocultured with neutrophils in the presence of Transwell failed to suppress the secretion of neutrophil effector molecules. Following corneal injury, stromal cell–treated mice showed a significant 40% decrease in MPO expression by neutrophils and lower neutrophil frequencies compared to untreated injured controls (P < 0.05). Reduced MPO expression by neutrophils was also accompanied by normalization of corneal tissue structure following stromal cell treatment. Conclusions: Mesenchymal stromal cells inhibit neutrophil effector functions via direct cell–cell contact interaction during inflammation. The current findings could have implications for the treatment of inflammatory ocular disorders caused by excessive neutrophil activation.Publication Restoration of Corneal Transparency by Mesenchymal Stem Cells(Elsevier, 2016) Mittal, Sharad K.; Omoto, Masahiro; Amouzegar, Afsaneh; Sahu, Anuradha; Rezazadeh, Alexandra; Katikireddy, Kishore R.; Shah, Dhvanit I.; Sahu, Srikant K.; Chauhan, Sunil K.Summary Transparency of the cornea is indispensable for optimal vision. Ocular trauma is a leading cause of corneal opacity, leading to 25 million cases of blindness annually. Recently, mesenchymal stem cells (MSCs) have gained prominence due to their inflammation-suppressing and tissue repair functions. Here, we investigate the potential of MSCs to restore corneal transparency following ocular injury. Using an in vivo mouse model of ocular injury, we report that MSCs have the capacity to restore corneal transparency by secreting high levels of hepatocyte growth factor (HGF). Interestingly, our data also show that HGF alone can restore corneal transparency, an observation that has translational implications for the development of HGF-based therapy.Publication Effector and Regulatory T Cell Trafficking in Corneal Allograft Rejection(Hindawi, 2017) Amouzegar, Afsaneh; Chauhan, SunilCorneal transplantation is among the most prevalent and successful forms of solid tissue transplantation in humans. Failure of corneal allograft is mainly due to immune-mediated destruction of the graft, a complex and highly coordinated process that involves elaborate interactions between cells of innate and adaptive immunity. The migration of immune cells to regional lymphoid tissues and to the site of graft plays a central role in the immunopathogenesis of graft rejection. Intricate interactions between adhesion molecules and their counter receptors on immune cells in conjunction with tissue-specific chemokines guide the trafficking of these cells to the draining lymph nodes and ultimately to the site of graft. In this review, we discuss the cascade of chemokines and adhesion molecules that mediate the trafficking of effector and regulatory T cells during corneal allograft rejection.Publication Alloimmunity and Tolerance in Corneal Transplantation(The American Association of Immunologists, 2016) Amouzegar, Afsaneh; Chauhan, Sunil; Dana, RezaCorneal transplantation is one of the most prevalent and successful forms of solid tissue transplantation. Despite favorable outcomes, immune-mediated graft rejection still remains the major cause of corneal allograft failure. While ‘low risk’ graft recipients with uninflamed graft beds enjoy a success rate of approximately 90%, the rejection rates in inflamed graft beds or ‘high risk’ recipients often exceed 50% despite maximal immune suppression. In this review we discuss the critical facets of corneal alloimmunity, including immune and angiogenic privilege, mechanisms of allosensitization, cellular and molecular mediators of graft rejection, and allotolerance induction.