A5102766653- Transplantation: Methods and Outcomes
- Organ Transplantation Techniques and Outcomes
- Complement system in diseases
- Phagocytosis and Immune Regulation
- MicroRNA in disease regulation
- RNA modifications and cancer
- Pneumonia and Respiratory Infections
- Immune Response and Inflammation
- Immune cells in cancer
- Organ and Tissue Transplantation Research
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Cancer-related molecular mechanisms research
- Adenosine and Purinergic Signaling
- Head and Neck Surgical Oncology
- Intracerebral and Subarachnoid Hemorrhage Research
- Mitochondrial Function and Pathology
- Renal Transplantation Outcomes and Treatments
- Bacterial Infections and Vaccines
- Neuroinflammation and Neurodegeneration Mechanisms
- Cardiac Ischemia and Reperfusion
- Cell Adhesion Molecules Research
- Advanced Glycation End Products research
- Nasolacrimal Duct Obstruction Treatments
- COVID-19 Impact on Reproduction
- Sinusitis and nasal conditions
University of Florida
2021-2024
Medical University of South Carolina
2018-2021
Huazhong University of Science and Technology
2017-2021
Tongji Hospital
2017-2021
ABSTRACT Post‐lung transplant (LTx) injury can involve sterile inflammation due to ischemia–reperfusion (IRI) that contributes allograft dysfunction. In this study, we investigated the cell‐specific role of ferroptosis (excessive iron‐mediated cell death) in mediating lung IRI and if specialized pro‐resolving mediators such as Lipoxin A4 (LxA 4 ) protect against IRI. Single‐cell RNA sequencing analysis tissue from post‐LTx patients was performed, evaluated C57BL/6 (WT), formyl peptide...
Patients with end stage lung diseases require transplantation (LTx) that can be impeded by ischemia-reperfusion injury (IRI) leading to subsequent chronic allograft dysfunction (CLAD) and inadequate outcomes.
Complement is known to play a role in ischemia and reperfusion injury (IRI). A general paradigm that complement activated by self-reactive natural IgM antibodies (nAbs), after they engage postischemic neoepitopes. However, for nAbs lung transplantation (LTx) has not been explored. Using mouse models of LTx, we investigated the two neoepitopes, modified annexin IV (B4) subset phospholipids (C2), LTx. Antibody deficient Rag1-/- recipient mice were protected from LTx IRI. Reconstitution with...
Early insults associated with cardiac transplantation increase the immunogenicity of donor microvascular endothelial cells (ECs), which interact recipient alloreactive memory T and promote responses leading to allograft rejection. Thus, modulating EC could potentially alter cell responses. Recent studies have shown mitochondrial fusion/fission alters immune phenotype. Here, we assess whether reduces EC-T interactions. By knocking down DRP1, a fission protein, or by using small molecules M1,...
ABSTRACT BACKGROUND Post-lung transplantation (LTx) injury can involve sterile inflammation due to ischemia-reperfusion (IRI). We investigated the cell-specific role of ferroptosis (excessive iron-mediated cell death) in mediating lung IRI and determined if specialized pro-resolving mediators such as Lipoxin A4 (LxA 4 ) protect against IRI. METHODS Single-cell RNA sequencing tissue from post-LTx patients was analyzed. Lung evaluated C57BL/6 (WT), formyl peptide receptor 2 knockout ( Fpr2 −/−...
Donor brain death (BD) is an unavoidable component of vascularized composite allograft (VCA) transplantation and a key contributor to ischemia-reperfusion injury (IRI). Complement activated deposited within solid organ grafts as consequence BD has been shown exacerbate IRI, although the role complement in VCA it plays IRI rejection not studied. was induced Balb/c donors, perfused prior graft procurement with UW solution supplemented or without CR2-Crry, C3 convertase inhibitor that binds at...
Lung transplantation (LTx) outcomes are impeded by ischemia/reperfusion injury (IRI) and subsequent chronic lung allograft dysfunction (CLAD). We examined the undefined role of receptor Mer tyrosine kinase (MerTK) on monocytic myeloid-derived suppressor cells (M-MDSCs) in efferocytosis to facilitate resolution IRI. Single-cell RNA sequencing tissue bronchoalveolar lavage (BAL) from patients after LTx were analyzed. Murine hilar ligation allogeneic orthotopic models IRI used with BALB/c (WT),...
Donor brain death (BD) is an inherent component of vascularized composite allograft (VCA) transplantation and thought to be a key contributor ischemia-reperfusion injury (IRI). Complement activated deposited within solid organ grafts as consequence BD has been shown exacerbate IRI, although the role complement in VCA it plays IRI graft rejection not studied. Here we investigate context therapeutic clinically relevant paradigm involving delivery inhibitor pre-transplant. was induced Balb/c...
Abstract Ischemia-reperfusion injury (IRI) after lung transplantation results in primary graft dysfunction leading to acute and chronic rejection. We investigated the role of monocytic myeloid-derived suppressor cells (M-MDSCs) mediate inflammation-resolution IRI. A murine model hilar ligation was used Balb/c (WT) cebpβ −/−(M-MDSC deficient) mice. Lung function, inflammation M-MDSC infiltration were assessed 6- or 24hrs mice undergoing sham control IRI surgeries. CD11b +Ly6G −Ly6C +iNOS...
Purpose: Chronic obstructive pulmonary disease is characterized by chronic inflammation and severe lung parenchyma damage that in part driven autoimmunity. Lung specific autoreactive antibodies (AAb) are indicative of progression severity. Our goal was to elucidate how pre-existing AAb contribute ischemia reperfusion injury (IRI) graft rejection following transplant (LTx). We hypothesize bind cryptic antigens exposed during IRI which exacerbates a complement (C)-dependent pathway. Methods...
Abstract Ischemia-reperfusion injury (IRI) after lung transplantation entails dysregulation of inflammation-resolution pathways leading to primary graft dysfunction. We investigated the role ω-3-derived specialized pro-resolving lipid mediators, i.e. Lipoxin A4 (LxA4), and formyl peptide receptor (FPR2) signaling in resolution IRI. used an established murine model hilar ligation for IRI using C57BL/6 wild-type (WT) FPR2−/− mice that underwent sham surgery or (1hr left ischemia followed by 6-...