A5036366607- Mitochondrial Function and Pathology
- Immune cells in cancer
- interferon and immune responses
- Cytokine Signaling Pathways and Interactions
- Cytomegalovirus and herpesvirus research
- Neuroinflammation and Neurodegeneration Mechanisms
- Immune Cell Function and Interaction
- Antibiotic Resistance in Bacteria
- ATP Synthase and ATPases Research
- Multiple Sclerosis Research Studies
- Systemic Lupus Erythematosus Research
- Herpesvirus Infections and Treatments
- Mycobacterium research and diagnosis
- Cancer, Hypoxia, and Metabolism
- Immune Response and Inflammation
- T-cell and B-cell Immunology
- Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Adipose Tissue and Metabolism
- Vibrio bacteria research studies
- Respiratory viral infections research
- RNA regulation and disease
- Plant Pathogenic Bacteria Studies
- Coenzyme Q10 studies and effects
- Virus-based gene therapy research
- Viral-associated cancers and disorders
Northwestern University
2019-2025
Michigan Medicine
2019
University of Michigan
2007-2018
Pulmonary and Critical Care Associates
2010
Abstract The NLRP3 inflammasome is linked to sterile and pathogen-dependent inflammation, its dysregulation underlies many chronic diseases. Mitochondria have been implicated as regulators of the through several mechanisms including generation mitochondrial reactive oxygen species (ROS). Here, we report that electron transport chain (ETC) complex I, II, III V inhibitors all prevent activation. Ectopic expression Saccharomyces cerevisiae NADH dehydrogenase (NDI1) or Ciona intestinalis...
Mitochondrial electron transport chain (ETC) function modulates macrophage biology; however, mechanisms underlying mitochondria ETC control of immune responses are not fully understood. Here, we report that mutant mice with complex III (CIII)–deficient macrophages exhibit increased susceptibility to influenza A virus (IAV) and LPS-induced endotoxic shock. Cultured bone marrow–derived (BMDMs) isolated from these CIII–deficient released less IL-10 than controls following TLR3 or TLR4...
Pseudomonas aeruginosa is an opportunistic Gram-negative human pathogen that responsible for a broad range of infections in individuals with variety predisposing conditions. After infection, P. induces marked inflammatory response the host. However mechanisms involved bacterium recognition and induction immune responses are poorly understood. Here we report Nod-like receptor family member Ipaf required optimal bacterial clearance vivo model lung infection. Further analysis showed flagellin...
Plasminogen activation to plasmin protects from lung fibrosis, but the mechanism underlying this antifibrotic effect remains unclear. We found that mice lacking plasminogen inhibitor-1 (PAI-1), which are protected bleomycin-induced pulmonary exhibit overproduction of lipid mediator prostaglandin E2 (PGE2). upregulated PGE2 synthesis in alveolar epithelial cells, fibroblasts, and fibrocytes saline- bleomycin-treated mice, as well normal fetal adult primary human fibroblasts. This response was...
Glioma-associated myeloid cells generate polyamines to survive and function within the acidic tumor microenvironment.
The adoptive transfer of myelin-reactive T cells into wild-type hosts results in spinal cord inflammation and ascending paralysis, referred to as conventional experimental autoimmune encephalomyelitis (EAE), opposed brainstem ataxia, which characterize disease IFN-γRKO (atypical EAE). In this article, we show that atypical EAE correlates with preferential upregulation CXCL2 the brainstem, is driven by CXCR2-dependent recruitment neutrophils. contrast, associated CCL2 cord, monocytes via a...
Abstract GM-CSF has been portrayed as a critical cytokine in the pathogenesis of experimental autoimmune encephalomyelitis (EAE) and, ostensibly, multiple sclerosis. C57BL/6 mice deficient are resistant to EAE induced by immunization with myelin oligodendrocyte glycoprotein (MOG)35–55. The mechanism action is poorly understood. In this study, we show that augments accumulation MOG35–55-specific T cells skin draining lymph nodes primed mice, but it not required for development...
Abstract Aging in mammals leads to reduction genes encoding the 45-subunit mitochondrial electron transport chain complex I. It has been hypothesized that normal aging and age-related diseases such as Parkinson’s disease are part due modest decrease expression of I subunits. By contrast, diminishing lower organisms increases lifespan. Furthermore, metformin, a putative inhibitor, healthspan mice humans. In present study, we investigated whether loss one allele Ndufs2 , catalytic subunit I,...
Although γherpesvirus infections are associated with enhanced lung fibrosis in both clinical and animal studies, there is limited understanding about fibrotic effects of γherpesviruses on cell types present the lung, particularly during latent infection. Wild-type mice were intranasally infected a murine (γHV-68) or mock-infected saline. Twenty-eight days postinfection (dpi), ∼14 following clearance lytic infection, alveolar macrophages (AMs), mesenchymal cells, CD19-enriched populations...
We have shown previously that murine gammaherpesvirus 68 (γHV68) infection exacerbates established pulmonary fibrosis. Because Toll-like receptor (TLR)-9 may be important in controlling the immune response to γHV68 infection, we examined how TLR-9 signaling effects exacerbation of fibrosis viral using models bleomycin- and fluorescein isothiocyanate-induced wild-type (Balb/c) TLR-9-/- mice.We found absence signaling, there was a significant increase collagen deposition following This not...
Abstract Systemic inhibition of Notch signaling was previously shown to attenuate experimental autoimmune encephalomyelitis (EAE), a disease model multiple sclerosis in mice. Different studies attributed these effects decreased T-bet and IFN-γ expression, enhanced regulatory T cell function, reduced chemotaxis the CNS, or impaired Th9 differentiation. Interpretation heterogeneous findings is difficult because past strategies did not ensure complete cells many populations could be affected by...
Myelin oligodendrocyte glycoprotein (MOG)-reactive T-helper (Th)1 cells induce conventional experimental autoimmune encephalomyelitis (cEAE), characterized by ascending paralysis and monocyte-predominant spinal cord infiltrates, in C57BL/6 wildtype (WT) hosts. The same T an atypical form of EAE (aEAE), ataxia neutrophil-predominant brainstem syngeneic IFNγ receptor (IFNγR)-deficient Production ELR+ CXC chemokines within the CNS is required for development aEAE, but not cEAE. cellular...
Lymphocyte homing into the intestine is mediated by binding of leukocytes to mucosal addressin cell adhesion molecule 1 (MAdCAM-1), expressed on endothelial cells. Currently, immune system gut considered a major modulator not only inflammatory bowel disease, but also extra-intestinal autoimmune disorders, including multiple sclerosis (MS). Despite intense research in this field, exact role pathogenesis (neuro-)inflammatory disease conditions remains be clarified. This prompted us investigate...
Apolipoprotein E (ApoE) is recognized for its pleiotropic properties that suppress inflammation. We report ApoE serves as a metabolic rheostat regulates microRNA control of glycolytic and mitochondrial activity in myeloid cells hematopoietic stem progenitor (HSPCs). expression increases microRNA-146a, which reduces nuclear factor κB (NF-κB)-driven GLUT1 activity. In contrast, microRNA-142a, carnitine palmitoyltransferase 1a (CPT1A) expression, fatty acid oxidation, oxidative phosphorylation....