ArticleBMC infectious diseases2010
Spiral ligament fibrocyte-derived MCP-1/CCL2 contributes to inner ear inflammation secondary to nontypeable H. influenzae-induced otitis media.
Article in BMC infectious diseases, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 29 citations in OpenAlex.
- Immunological mechanisms in Meniere's disease.Frontiers in immunology · 2025Review
- Investigating the causal relationship between inflammation and multiple types of hearing loss: a multi-omics approach combining Mendelian randomization and molecular docking.Frontiers in neurology · 2024Article
- Immuno-surveillance and protection of the human cochlea.Frontiers in neurology · 2024Article
- Intratympanic Lipopolysaccharide Elevates Systemic Fluorescent Gentamicin Uptake in the Cochlea.The Laryngoscope · 2021Article
- Neutrophils infiltrate into the spiral ligament but not the stria vascularis in the cochlea during lipopolysaccharide-induced inflammation.Theranostics · 2021Article
- Ultrastructure and three-dimensional architecture of the anterior cruciate ligament in the knee joints of young and old monkeys.Medical molecular morphology · 2020Article
- Genomics of Otitis Media (OM): Molecular Genetics Approaches to Characterize Disease Pathophysiology.Frontiers in genetics · 2020Review
- Autoinflammatory characteristics and short-term effects of delivering high-dose steroids to the surface of the intact endolymphatic sac and incus in refractory Ménière's disease.Journal of otology · 2019Article
- Cellular content plays a crucial role in Non-typeable Haemophilus influenzae infection of preinflamed Junbo mouse middle ear.Cellular microbiology · 2019Article
- Article
- Panel 3: Genetics and Precision Medicine of Otitis Media.Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery · 2017Review
- Involvement of Ubiquitin-Editing Protein A20 in Modulating Inflammation in Rat Cochlea Associated with Silver Nanoparticle-Induced CD68 Upregulation and TLR4 Activation.Nanoscale research letters · 2016Article
- Biology and pathobiology of lipid droplets and their potential role in the protection of the organ of Corti.Hearing research · 2015Review
- Correlative mRNA and protein expression of middle and inner ear inflammatory cytokines during mouse acute otitis media.Hearing research · 2015Article
- IL-10/HMOX1 signaling modulates cochlear inflammation via negative regulation of MCP-1/CCL2 expression in cochlear fibrocytes.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Cytokine, chemokine, and Toll-like receptor expression in middle ear fluids of children with acute otitis media.The Laryngoscope · 2015Article
- NOD2/RICK-dependent β-defensin 2 regulation is protective for nontypeable Haemophilus influenzae-induced middle ear infection.PloS one · 2014Article
- Inner ear tissue remodeling and ion homeostasis gene alteration in murine chronic otitis media.Otology & neurotology : official publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology · 2013Article
- Article
- Suppression of vaccine immunity by inflammatory monocytes.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundOtitis media (OM), one of the most common pediatric infectious diseases, causes inner ear inflammation resulting in vertigo and sensorineural hearing loss. Previously, we showed that spiral ligament fibrocytes (SLFs) recognize OM pathogens and up-regulate chemokines. Here, we aim to determine a key molecule derived from SLFs, contributing to OM-induced inner ear inflammation.
methodsLive NTHI was injected into the murine middle ear through the tympanic membrane, and histological analysis was performed after harvesting the temporal bones. Migration assays were conducted using the conditioned medium of NTHI-exposed SLFs with and without inhibition of MCP-1/CCL2 and CCR2. qRT-PCR analysis was performed to demonstrate a compensatory up-regulation of alternative genes induced by the targeting of MCP-1/CCL2 or CCR2.
resultsTranstympanic inoculation of live NTHI developed serous and purulent labyrinthitis after clearance of OM. THP-1 cells actively migrated and invaded the extracellular matrix in response to the conditioned medium of NTHI-exposed SLFs. This migratory activity was markedly inhibited by the viral CC chemokine inhibitor and the deficiency of MCP-1/CCL2, indicating that MCP-1/CCL2 is a main attractant of THP-1 cells among the SLF-derived molecules. We further demonstrated that CCR2 deficiency inhibits migration of monocyte-like cells in response to NTHI-induced SLF-derived molecules. Immunolabeling showed an increase in MCP-1/CCL2 expression in the cochlear lateral wall of the NTHI-inoculated group. Contrary to the in vitro data, deficiency of MCP-1/CCL2 or CCR2 did not inhibit OM-induced inner ear inflammation in vivo. We demonstrated that targeting MCP-1/CCL2 enhances NTHI-induced up-regulation of MCP-2/CCL8 in SLFs and up-regulates the basal expression of CCR2 in the splenocytes. We also found that targeting CCR2 enhances NTHI-induced up-regulation of MCP-1/CCL2 in SLFs.
conclusionsTaken together, we suggest that NTHI-induced SLF-derived MCP-1/CCL2 is a key molecule contributing to inner ear inflammation through CCR2-mediated recruitment of monocytes. However, deficiency of MCP-1/CCL2 or CCR2 alone was limited to inhibit OM-induced inner ear inflammation due to compensation of alternative genes.
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