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. 2024 Nov 16:17:8921-8934.
doi: 10.2147/JIR.S486301. eCollection 2024.

Chronic Inflammation and Age-Related Hearing: Based on Mendelian Randomization

Yan Wang #  1   2   3   4 , He Zhao #  2   3   4 , Kun Zhao #  1   2   3   4 , Huhuifen He #  1   2   3   4 , Xinyu Li  5 , Jingjing Qiu  2   3   4 , Limei Cui  2   3   4 , Liang Chen  2   3   4 , Wenjing Shang  6   7 , Yan Sun  2   3   4
Affiliations

Chronic Inflammation and Age-Related Hearing: Based on Mendelian Randomization

Yan Wang et al. J Inflamm Res. .

Abstract

Introduction: Age-related hearing loss (ARHL) is a degenerative condition that involves both peripheral and central auditory system pathologies. There is a close relationship between chronic inflammation and ARHL, but there is currently a lack of in-depth exploration of this relationship, particularly regarding causality.

Methods: Using age-appropriate mice for basic experiments to examine changes in central auditory nervous system inflammation, a cohort study was conducted to select relevant clinical data and observe inflammation changes in the elderly population with ARHL. Mendelian randomization was employed to investigate the causal relationship between chronic inflammation and ARHL.

Results: Clinical results indicate that CRP levels in the ARHL group are significantly higher than those in the normal group. Chronic inflammation also occurs in the auditory centers. Mendelian randomization studies provide causal evidence that genetic chronic inflammation factors do not increase the risk of ARHL.

Discussion: This article provides reliable causal evidence of the relationship between chronic inflammation and ARHL, confirming the accumulation of inflammatory factors in the auditory center, which provides a basis for the prevention and treatment of ARHL and has a good prevention prospect. However, due to the differences of research objects, this study has limitations and needs further research.

Keywords: CRP; Mendelian randomization; TNF-α; age-related hearing loss; chronic inflammation.

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Conflict of interest statement

The authors report no conflicts of interest in this work.

Figures

Figure 1
Figure 1
Two-sample MR Design to investigate the causal relationship between inflammatory markers and ARHL.
Figure 2
Figure 2
ABR audiometry. Hearing thresholds were measured in mice aged 4 weeks and 48 weeks with different interference conditions using an auditory brain-stem response test. **P<0.005 compared with normal control 4 weeks mice at SPL, sound pressure level.
Figure 3
Figure 3
The relative expression levels of cochlear inflammatory factors in 4W and 48W groups. C1q (A), complement C3 factor (B), IL-1β (C) and TNF-α (D).
Figure 4
Figure 4
Expression of markers in microglia and astrocytes. Comparison of IBA1 (A), CD16 (B), GFAP and C3 (C). (*P<0.05 and **P<0.005).
Figure 5
Figure 5
Clinical data verified the serum expression of CRP. (A) Comparison of CRP content between ARHL group and normal elderly group. (B) After excluding the data of female patients, comparison of CRP content between ARHL group and normal elderly group.
Figure 6
Figure 6
Causal effects from CRP to ARHL. (A) Forest plot and (B) Scatter plot of the potential effects of CRP to ARHL.
Figure 7
Figure 7
Causal effects from IL-1β, TNF-α, and C3 to ARHL. (A) Forest plot and (B) scatter plot of the potential effects of C3 to ARHL. (C) Scatter plot and (D) Forest plot of the potential effects of TNF-α to ARHL. (E) Forest plot of the potential effects of IL-1β to ARHL.
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