ArticleInflammation2023
Substance P Exacerbates the Inflammatory and Pro-osteoclastogenic Responses of Murine Osteoclasts and Osteoblasts to Staphylococcus aureus.
Article in Inflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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.
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Who cites it
20 citing papers in PubMed, 21 citations in OpenAlex.
- Dual-Action Nucleic Acid Nanoparticles: Innate Immune Activation and Silver Nanocluster-Mediated Targeting of Intracellular Bacteria.ACS nano medicine · 2026Article
- The Innate and Adaptive Immune Functions of Osteoblast-Lineage Cells.Current osteoporosis reports · 2026Review
- Neural regulation of bone: from central neural circuits to peripheral innervation of the skeletal stem cell niche.Bone research · 2026Review
- Spatially Organized DNA-Templated Silver Nanoclusters as Potent Antimicrobial Agents for ESKAPE Infections.ACS applied materials & interfaces · 2026Article
- Article
- TRPV1-linked neuropeptide axes in periodontitis and peri-implantitis.Frontiers in endocrinology · 2026Review
- Neuro-immune-bone axis in post-traumatic bone regeneration: temporal regulation, dysregulation mechanisms, and therapeutic implications.Frontiers in immunology · 2026Review
- CGRP at the Neuroimmune Interface: Regulator of Host Defense, Tumor Immunity, and Tissue Homeostasis.Research (Washington, D.C.) · 2026Review
- Potential involvement of the KLF2-GPX4 axis in ferroptosis during S.aureus-induced osteomyelitis.Human genomics · 2025Article
- Drug Repurposing: An Emerging Strategy inJournal of microbiology and biotechnology · 2025Review
- Substance P Augments Chemokine Production by Staphylococcus aureus Infected Murine Osteoclasts.Inflammation · 2025Article
- Article
- RIG-I drives protective type I interferon production by glial cells in response toFrontiers in immunology · 2025Article
- Nanomaterial-mediated antibiotic delivery: a novel strategy for osteomyelitis therapy.Frontiers in bioengineering and biotechnology · 2025Review
- Immunostimulatory nucleic acid nanoparticles (NANPs) augment protective osteoblast and osteoclast type I interferon responses to Staphylococcus aureus.Nanomedicine : nanotechnology, biology, and medicine · 2024Article
- Capsaicin: Emerging Pharmacological and Therapeutic Insights.Current issues in molecular biology · 2024Review
- Antimicrobial Properties of Capsaicin: Available Data and Future Research Perspectives.Nutrients · 2023Review
- Staphylococcus aureus Infection Induces the Production of the Neutrophil Chemoattractants CXCL1, CXCL2, CXCL3, CXCL5, CCL3, and CCL7 by Murine Osteoblasts.Infection and immunity · 2023Article
- The osteoblast secretome inFrontiers in immunology · 2022Review
- Induction of protective interferon-β responses in murine osteoblasts followingFrontiers in microbiology · 2022Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Staphylococcus aureus infections of bone tissue are associated with inflammatory bone loss. Resident bone cells, including osteoblasts and osteoclasts, can perceive S. aureus and produce an array of inflammatory and pro-osteoclastogenic mediators, thereby contributing to such damage. The neuropeptide substance P (SP) has been shown to exacerbate microbially induced inflammation at sites such as the gut and the brain and has previously been shown to affect bone cell differentiation and activity. Here we demonstrate that the interaction of SP with its high affinity receptor, neurokinin-1 receptor (NK-1R), expressed on murine osteoblasts and osteoclasts, augments the inflammatory responses of these cells to S. aureus challenge. Additionally, SP alters the production of pro- and anti-osteoclastogenic factors by bacterially challenged bone cells and their proteolytic functions in a manner that would be anticipated to exacerbate inflammatory bone loss at sites of infection. Furthermore, we have demonstrated that the clinically approved NK-1R antagonist, aprepitant, attenuates local inflammatory and pro-osteoclastogenic mediator expression in an in vivo mouse model of post-traumatic staphylococcal osteomyelitis. Taken together, these results indicate that SP/NK-1R interactions could play a significant role in the initiation and/or progression of damaging inflammation in S. aureus bone infections and suggest that the repurposing of currently approved NK-1R antagonists might represent a promising new adjunct therapy for such conditions.
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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.