Neutrophils infiltrate into the spiral ligament but not the stria vascularis in the cochlea during lipopolysaccharide-induced inflammation

Bae, Seong Hoon; Yoo, Jee Eun; Choe, Young Ho; Kwak, Sang Hyun; Choi, Jae Young; Jung, Jinsei; Hyun, Young Youl

doi:10.7150/thno.49121

Cited by 22 publications

(20 citation statements)

References 59 publications

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“…In line with recent reports, we observed an increase in neutrophils 3 days after noise exposure (Bae et al, 2021;Rai et al, 2020).…”

Section: Lw Cells Downregulate Genes Related To Potassium Transport Following Noise Exposuresupporting

confidence: 93%

A cell-type-specific atlas of the inner ear transcriptional response to acoustic trauma

Milon

Shulman

et al. 2021

Cell Reports

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“…In line with recent reports, we observed an increase in neutrophils 3 days after noise exposure (Bae et al, 2021;Rai et al, 2020).…”

Section: Lw Cells Downregulate Genes Related To Potassium Transport Following Noise Exposuresupporting

confidence: 93%

A cell-type-specific atlas of the inner ear transcriptional response to acoustic trauma

Milon

Shulman

et al. 2021

Cell Reports

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“…However, several recent studies have demonstrated increased neutrophil numbers in the cochlea at 1 dpn ( Rai et al, 2020 ; Zhang et al, 2021 ). Unlike their known roles in lipopolysaccharide-induced or infectious inflammation, the involvement of neutrophil infiltration in acoustic overstimulation-induced cochlear inflammation is still unclear ( Bae et al, 2021b ).…”

Section: Introductionmentioning

confidence: 99%

The Time Course of Monocytes Infiltration After Acoustic Overstimulation

Shin

Jung

Park

et al. 2022

Front. Cell. Neurosci.

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Cochlea macrophages regulate cochlea inflammation and may harbors the potentials to protect hearing function from injury, including acoustic overstimulation. Cochlea macrophage numbers increase at 3–7 days after acoustic stimulation. However, the exact timing of macrophage infiltration and maturation from inflammatory monocytes is unclear. Furthermore, neutrophils may also be involved in this process. Therefore, in this study, we investigated time-dependent immune cell infiltration, macrophage transformation, and neutrophil involvement following acoustic stimulation. Flow cytometry and immunofluorescence were conducted in C-X3-C motif chemokine receptor 1 (CX3CR1)+/GFP mice after acoustic overstimulation (at baseline and at 1, 2, 3, and 5 days after exposure to 120 dB for 1 h) to identify inflammatory monocytes in the cochlea. RNA-sequencing and quantitative polymerase chain reaction were performed to identify differentially expressed genes. Inflammatory monocytes infiltrated into the lower portion of the lateral wall within 2 days after acoustic overstimulation (dpn), followed by transformation into macrophages at 3–5 dpn via CX3CR1 upregulation and Ly6C downregulation. In addition, inflammatory monocytes were aggregated inside the collecting venule only at 1 dpn. Neutrophils were not a major type of phagocyte during this response. The gene encoding C-C motif chemokine ligand 2 gene was significantly upregulated as early as 3 h after acoustic overstimulation. Given these results, treatment to control immune response after a noise-induced hearing loss should be applied as soon as possible.

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“…However, post infection, levels of IL-1β and IL-6 were significantly elevated in Coch +/+ mice compared to Coch −/− mice, suggesting that cochlin is necessary for local upregulation and increased secretion [ 6 ]. Another study [ 25 ] observed a massive neutrophil migration in the spiral ligament two days after LPS inoculation in the middle ear. In contrast, noise exposure did not induce migration of neutrophils in the lateral wall.…”

Section: Discussionmentioning

confidence: 99%

“…In contrast, noise exposure did not induce migration of neutrophils in the lateral wall. Noise exposure and bacterial infection with LPS have different inflammatory pathways because LPS is recognized as a pathogen-associated molecular pattern, but debris from the degenerated cells after noise exposure is recognized as a damage-associated molecular pattern (DAMP) [ 25 ].…”

Section: Discussionmentioning

confidence: 99%

Cochlin Deficiency Protects Aged Mice from Noise-Induced Hearing Loss

Verdoodt

Peeleman

Szewczyk

et al. 2021

IJMS

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Several studies have shown that type IV fibrocytes, located in the spiral ligament, degenerate first after noise exposure. Interestingly, this is the region where Coch expression is most abundant. As it is suggested that cochlin plays a role in our innate immune system, our goal is to investigate hearing thresholds and inner ear inflammation after noise exposure in Coch knockout (Coch−/−) mice compared to Coch wildtype (Coch+/+) mice. Animals were randomly allocated to a noise exposure group and a control group. Vestibular and auditory testing was performed at 48 h and one week after noise exposure. Whole mount staining and cryosectioning of the cochlea was performed in order to investigate hair cells, spiral ganglion neurons, inner ear inflammation, Coch expression and fibrocyte degeneration. Hearing assessment revealed that Coch+/+ mice had significantly larger threshold shifts than Coch−/− mice after noise exposure. We were unable to identify any differences in hair cells, neurons, fibrocytes and influx of macrophages in the inner ear between both groups. Interestingly, Coch expression was significantly lower in the group exposed to noise. Our results indicate that the absence of Coch has a protective influence on hearing thresholds after noise exposure, but this is not related to reduced inner ear inflammation in the knockout.

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Neutrophils infiltrate into the spiral ligament but not the stria vascularis in the cochlea during lipopolysaccharide-induced inflammation

Cited by 22 publications

References 59 publications

A cell-type-specific atlas of the inner ear transcriptional response to acoustic trauma

A cell-type-specific atlas of the inner ear transcriptional response to acoustic trauma

The Time Course of Monocytes Infiltration After Acoustic Overstimulation

Cochlin Deficiency Protects Aged Mice from Noise-Induced Hearing Loss

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