Matthew V. Russo

ORCID: 0000-0002-3715-8974
Publications
Citations
Views
---
Saved
---
About
Contact & Profiles
Research Areas
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Traumatic Brain Injury and Neurovascular Disturbances
  • Spinal Cord Injury Research
  • S100 Proteins and Annexins
  • Malaria Research and Control
  • Plant Pathogens and Fungal Diseases
  • Neurogenesis and neuroplasticity mechanisms
  • Plant Disease Resistance and Genetics
  • Complement system in diseases
  • Immune Cell Function and Interaction
  • Anesthesia and Neurotoxicity Research
  • Lysosomal Storage Disorders Research
  • Wound Healing and Treatments
  • Acute Lymphoblastic Leukemia research
  • Myxozoan Parasites in Aquatic Species
  • Intracerebral and Subarachnoid Hemorrhage Research
  • Trauma and Emergency Care Studies
  • Immune cells in cancer
  • Renal Diseases and Glomerulopathies
  • Mosquito-borne diseases and control
  • Plant Pathogens and Resistance
  • Bird parasitology and diseases
  • Neonatal and fetal brain pathology
  • Microbial infections and disease research

National Institute of Neurological Disorders and Stroke
2015-2021

National Institutes of Health
2015-2021

Pfizer (United States)
2020

University of Baltimore
2017

Johns Hopkins University
2017

Infiltrating monocyte-derived macrophages (MDMs) and resident microglia dominate central nervous system (CNS) injury sites. Differential roles for these cell populations after are beginning to be uncovered. Here, we show evidence that MDMs directly communicate with one another differentially modulate each other’s functions. Importantly, microglia-mediated phagocytosis inflammation suppressed by infiltrating macrophages. In the context of spinal cord (SCI), preventing such communication...

10.1371/journal.pbio.2005264 article EN public-domain PLoS Biology 2018-10-17

Cerebral malaria (CM) is a severe complication of Plasmodium falciparum infection that results in thousands deaths each year, mostly African children. The vivo mechanisms underlying this fatal condition are not entirely understood. Using the animal model experimental cerebral (ECM), we sought mechanistic insights into pathogenesis CM. Fatal disease was associated with alterations tight junction proteins, vascular breakdown meninges / parenchyma, edema, and ultimately neuronal cell death...

10.1371/journal.ppat.1006022 article EN public-domain PLoS Pathogens 2016-12-01

Abstract Cerebral malaria (CM) is a severe complication of Plasmodium falciparum infection that results in thousands deaths each year, mostly African children. Pathological studies CM victims reveal vascular hemorrhaging and edema within the brain, yet underlying mechanisms lead to this fatal condition are unknown. Using animal model experimental cerebral (ECM), we sought mechanistic insights into factors drive pathogenesis CM. We found ECM associated with large influx immune cells central...

10.4049/jimmunol.196.supp.134.1 article EN The Journal of Immunology 2016-05-01

10.1016/j.jcpa.2009.08.080 article EN Journal of Comparative Pathology 2009-11-01

Abstract Mild traumatic brain injury (mTBI) leads to a robust immune response featuring resident microglia/macrophages and recruitment of peripherally-derived monocytes/macrophages. We sought novel insights into the dynamics function innate myeloid cells following by studying closed-skull focal contusion model mTBI that permits real-time imaging intravital two-photon microscopy (TPM). TPM studies CX3CR1GFP/+ CCR2RFP/+ reporter mice revealed an early microglia followed CCR2+ monocytes CX3CR1+...

10.4049/jimmunol.198.supp.206.28 article EN The Journal of Immunology 2017-05-01

Abstract Mild traumatic brain injury (mTBI) causes severe meningeal cell death and vascular injury, leading to a robust peripheral immune response featuring neutrophils monocytes/macrophages. Complications such as repetitive head injuries or viral infections following mTBI have the potential significantly alter impact wound repair. Using closed-skull compression model of mTBI, we found that vasculature can regenerate within 7 days coinciding with dynamic, bifurcated myeloid response....

10.4049/jimmunol.200.supp.108.10 article EN The Journal of Immunology 2018-05-01

Abstract Inflammatory bowel diseases are associated with a loss of epithelial barrier integrity that can lead to an imbalance in gut homeostasis and severe inflammation. Studies mice have shown CD1d, lipid antigen-presenting molecule, natural killer T (NKT) cells play important roles forming maintaining the intestines. However, it is currently unknown what specific lipids presented NKT during or inflammation gut. We hypothesize inflammation, CD1d ligands replaced pathogenic alter activation...

10.4049/jimmunol.204.supp.217.18 article EN The Journal of Immunology 2020-05-01
Coming Soon ...