ArticleJournal of immunology (Baltimore, Md. : 1950)2011
Prophylactic and therapeutic targeting of the neurokinin-1 receptor limits neuroinflammation in a murine model of pneumococcal meningitis.
Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 42 citations in OpenAlex.
- Substance P Augments Chemokine Production by Staphylococcus aureus Infected Murine Osteoclasts.Inflammation · 2025Article
- Substance P Exacerbates the Inflammatory and Pro-osteoclastogenic Responses of Murine Osteoclasts and Osteoblasts to Staphylococcus aureus.Inflammation · 2023Article
- Substance P-Friend or Foe.Journal of clinical medicine · 2022Article
- Mammalian Neuropeptides as Modulators of Microbial Infections: Their Dual Role in Defense versus Virulence and Pathogenesis.International journal of molecular sciences · 2021Review
- Biomarkers and Their Possible Functions in the Intestinal Microenvironment of Chagasic Megacolon: An Overview of the (Neuro)inflammatory Process.Journal of immunology research · 2021Review
- Retinoic acid inducible gene-I mediated detection of bacterial nucleic acids in human microglial cells.Journal of neuroinflammation · 2020Article
- Cellular and behavioral effects of lipopolysaccharide treatment are dependent upon neurokinin-1 receptor activation.Journal of neuroinflammation · 2018Article
- The Interleukin-10 Family of Cytokines and Their Role in the CNS.Frontiers in cellular neuroscience · 2018Review
- Neuro-Immune Mechanisms of Anti-Cryptococcal Protection.Journal of fungi (Basel, Switzerland) · 2017Review
- Human microglia and astrocytes constitutively express the neurokinin-1 receptor and functionally respond to substance P.Journal of neuroinflammation · 2017Article
- Role of Substance P Neuropeptide in Inflammation, Wound Healing, and Tissue Homeostasis.Journal of immunology (Baltimore, Md. : 1950) · 2017Review
- Aprepitant limits in vivo neuroinflammatory responses in a rhesus model of Lyme neuroborreliosis.Journal of neuroinflammation · 2017Article
- Transmission pathways and mediators as the basis for clinical pharmacology of pain.Expert review of clinical pharmacology · 2016Article
- Translational potential of astrocytes in brain disorders.Progress in neurobiology · 2016Review
- Investigating the role of MRGPRC11 and capsaicin-sensitive afferent nerves in the anti-influenza effects exerted by SLIGRL-amide in murine airways.Respiratory research · 2016Article
- The Therapeutic Potential of Targeting Substance P/NK-1R Interactions in Inflammatory CNS Disorders.Frontiers in cellular neuroscience · 2016Review
- Antagonist of the neurokinin-1 receptor curbs neuroinflammation in ex vivo and in vitro models of Lyme neuroborreliosis.Journal of neuroinflammation · 2015Article
- Analysis of nucleotide-binding oligomerization domain proteins in a murine model of pneumococcal meningitis.BMC infectious diseases · 2014Article
- Substance P exacerbates dopaminergic neurodegeneration through neurokinin-1 receptor-independent activation of microglial NADPH oxidase.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Neuroimmune pathways in alcohol consumption: evidence from behavioral and genetic studies in rodents and humans.International review of neurobiology · 2014Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
There is increasing evidence that the tachykinin substance P (SP) can augment inflammatory immune responses within the CNS. We have recently demonstrated that resident CNS cells express high-affinity receptors for this neuropeptide (neurokinin-1 receptors [NK-1R]), and we have shown that SP can significantly augment glial inflammatory responses to clinically relevant Gram-negative bacteria. Furthermore, we provided evidence that endogenous SP/NK-1R interactions are an essential component in the initiation and/or progression of CNS inflammation following in vivo exposure to these pathogens. In this study, we demonstrate that SP similarly enhances inflammatory glial responses to the major Gram-positive causative agent of bacterial meningitis, Streptococcus pneumoniae, and show that endogenous SP/NK-1R interactions play a critical role in the development of CNS inflammation in an in vivo model of pneumococcal meningitis. Importantly, we provide the first demonstration, to our knowledge, that pharmacological targeting of the NK-1R not only prevents the development of damaging inflammation when administered prophylactically, but can also limit or reverse neuroinflammation associated with an established streptococcal CNS infection when delivered therapeutically. We show that an NK-1R antagonist attenuates increases in CNS inflammatory cytokine levels and decreases in immunosuppressive cytokine production associated with an ongoing S. pneumoniae infection. Furthermore, we demonstrate that such a therapeutic intervention reverses infection-associated gliosis and demyelination in the absence of changes in CNS bacterial burden. Together, these results suggest that targeting SP/NK-1R interactions is a strategy worthy of further study for the treatment of microbially induced neuroinflammation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.