ArticleInfection and immunity2009
MyD88-deficient mice exhibit decreased parasite-induced immune responses but reduced disease severity in a murine model of neurocysticercosis.
Article in Infection and immunity, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Chronic administration of cryptolepine nanoparticle formulation alleviates seizures in a neurocysticercosis model.Current research in pharmacology and drug discovery · 2021Article
- Host immune responses during Taenia solium Neurocysticercosis infection and treatment.PLoS neglected tropical diseases · 2020Review
- Galectin-3 in M2 Macrophages Plays a Protective Role in Resolution of Neuropathology in Brain Parasitic Infection by Regulating Neutrophil Turnover.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Inhibition of store-operated calcium entry in microglia by helminth factors: implications for immune suppression in neurocysticercosis.Journal of neuroinflammation · 2014Article
- Experimental cerebral malaria pathogenesis--hemodynamics at the blood brain barrier.PLoS pathogens · 2014Article
- Immunology of Taenia solium taeniasis and human cysticercosis.Parasite immunology · 2014Review
- Helminth induced suppression of macrophage activation is correlated with inhibition of calcium channel activity.PloS one · 2014Article
- Increased accumulation of regulatory granulocytic myeloid cells in mannose receptor C type 1-deficient mice correlates with protection in a mouse model of neurocysticercosis.Infection and immunity · 2013Article
- Toll-like receptors in health and disease in the brain: mechanisms and therapeutic potential.Clinical science (London, England : 1979) · 2011Review
- Increased disease severity of parasite-infected TLR2-/- mice is correlated with decreased central nervous system inflammation and reduced numbers of cells with alternatively activated macrophage phenotypes in a murine model of neurocysticercosis.Infection and immunity · 2011Article
- STAT6⁻/⁻ mice exhibit decreased cells with alternatively activated macrophage phenotypes and enhanced disease severity in murine neurocysticercosis.Journal of neuroimmunology · 2011Article
- TLR2 mediates immunity to experimental cysticercosis.International journal of biological sciences · 2011Article
- Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The symptomatic phase of neurocysticercosis (NCC), a parasitic disease of the central nervous system (CNS) in humans, is characterized by inflammatory responses leading to neuropathology and, in some cases, death. In an animal model of NCC in which mice were intracranially inoculated with the parasite Mesocestoides corti, the infection in mice lacking the myeloid differentiation primary response gene 88 (MyD88(-/-)) resulted in decreased disease severity and improved survival compared with that in wild-type (WT) mice. The CNS of MyD88(-/-) mice was more quiescent, with decreased microgliosis and tissue damage. These mice exhibited substantially reduced primary and secondary microglial nodule formations and lacked severe astrogliotic reactions, which were seen in WT mice. Significantly reduced numbers of CD11b(+) myeloid cells, alphabeta T cells, gammadelta T cells, and B cells were present in the brains of MyD88(-/-) mice in comparison with those of WT mice. This decrease in cellular infiltration correlated with a decrease in blood-brain barrier permeability, as measured by reduced fibrinogen extravasation. Comparisons of cytokine expression indicated a significant decrease in the CNS levels of several inflammatory mediators, such as tumor necrosis factor alpha, gamma interferon, CCL2, and interleukin-6, during the course of infection in MyD88(-/-) mice. Collectively, these findings suggest that MyD88 plays a prominent role in the development of the hyperinflammatory response, which in turn contributes to neuropathology and disease severity in NCC.
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