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Ménière disease (MD) is an idiopathic inner ear disorder, and endolymphatic hydrops (EH) being considered to be its pathological basis. Currently, there is no gold standard for diagnosing MD. Previous study has reported visualized EH using MRI by intratympanic gadolinium-based contrast media (GBCM) administration (IT-Gd) in patients with MD, and this technique was gradually established for MD diagnosis. However, few studies reported their diagnostic sensitivity and specificity in clinical application. This prospective study aimed at investigating the clinical characteristics and magnetic resonance imaging (MRI) results of patients with MD, and analyzing the relationship between clinical results and MRI findings in MD patients. Our study shows that the diagnostic sensitivity and specificity of MRI were 79.2% and 80.7% respectively. Moreover, there was no significant correlation between hearing levels and cochlear grading scores, nor vestibular grading scores. The duration of disease was not significantly associated with cochlear or vestibular grading scores. These findings suggest that IT-Gd MRI offers reliable radiological diagnostic criteria for MD.

The CCR3 gene plays a critical role in allergic airway inflammation, such as allergic rhinitis (AR), and there is an inflammatory signal link between the nasal cavity and the CCR3 gene in bone marrow. However, the effects of the CCR3 gene in bone marrow cells on AR are not clear. The present study investigated the roles and underlying mechanisms of the bone marrow CCR3 gene in AR mice. Conditional knockout of the bone marrow CCR3 gene (CKO) in mice was generated using the Cre-LoxP recombination system, and offspring genotypes were identified using polymerase chain reaction (PCR). An ovalbumin-induced AR model was established in CKO and wild-type mice to measure eosinophilic inflammation and the Th2 immune response. The following mechanisms were explored using a specific PI3K/AKT pathway inhibitor (Ly294002). We successfully constructed and bred homozygous CKO mice and confirmed a significant increase in CCR3 expression and PI3K/AKT pathway activity in AR mice. Deficiency of the bone marrow CCR3 gene caused a remarkable reduction of CCR3 expression and the PI3K/AKT signaling pathway activity, inhibited histopathological lesions and eosinophil infiltration of the nasal cavity, and reduced the production of Th2 cytokines in serum, which led to the remission of allergic symptoms in AR mice. Ly294002 treatment also decreased these inflammatory indexes in a concentration-dependent manner and blocked inflammatory signals from CCR3, but it did not affect the high expression of CCR3 in AR mice. Collectively, our results suggest that conditional knockout of the bone marrow CCR3 gene can reduce eosinophilic inflammation and the Th2 immune response, which may be due to inhibition of the PI3K/AKT pathway.

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Sudden sensorineural hearing loss (SSNHL) is a multifactorial emergency disease. Until now, the etiology of SSNHL is still unknown. Previous studies regarding the etiology of SSNHL are clinical studies depending on clinical data collection and analysis. Due to the insufficient sample size or various selective bias in clinical studies, the results of these studies may be inaccurate. This prospective case–control study aimed at exploring the possible etiology and risk factors of SSNHL. We enrolled 255 SSNHL patients and 255 sex-, age- and residence-matched non-SSNHL subjects in the control group. Our study shows that there was no significant difference in the prevalence of comorbidities including hypertension and diabetes, as well as the incidence of smoking and drinking habits between the case and control groups (P > 0.05). In addition, the peripheral blood white blood cell count, neutrophil count, platelet-to-lymphocyte ratio (PLR) and fibrinogen level of the case group were significantly higher than those in the control group (P < 0.05). These findings suggest smoking, drinking, hypertension and diabetes may not be related to the onset of SSNHL. However, hypercoagulable state and inner ear vascular microthrombosis related to an elevated fibrinogen level might be the risk factors of the disease. In addition, inflammation play an important role of SSNHL onset.Trial Registration: Chinese Clinical Trial Registry. Registration number: ChiCTR2100048991.

The present study aimed to investigate the effects of C-C chemokine receptor type 3 (CCR3) gene knockout on allergic rhinitis (AR) in mice, as well as the underlying molecular mechanisms. Ovalbumin was administrated to CCR3+/+ and CCR3−/− BALB/c mice to establish an AR model. The mice were divided into four groups: i) Normal control (CG), ii) AR model (AR), iii) CCR3 knockout CG (CCR3−/−CG) and iv) AR model with CCR3 knockout (CCR3−/−AR). Histological sections of nasal mucosae were examined by hematoxylin and eosin staining, which revealed that CCR3 knockout suppressed the invasion of inflammatory cells and relieved the damage of nasal mucosae. Peripheral blood smear and nasal-washing smears were evaluated by Wright's staining. Eosinophil (EOS) numbers in nasal mucosae, peripheral blood, and nasal washings of the various groups were ranked in the order: AR>CCR3−/−AR>CG>CCR3−/−. mRNA expression levels of CCR3, EOS peroxidase (EPO), EOS cationic protein (ECP), and major basic protein (MBP) in the peripheral serum and nasal washings were detected by reverse transcription-polymerase chain reaction. Interferon-γ (IFN-γ), interleukin (IL)-4, IL-10, and immunoglobulin E (IgE) protein levels in the peripheral serum and nasal washings were investigated by ELISA. CCR3 mRNA expression was not detected in the CCR3−/− and CCR3−/−AR groups, whereas expression levels in the AR group were markedly higher compared with expression in the CG group. Compared with the CG-associated groups (i.e., the CG and CCR3−/−CG groups), the levels of EPO, ECP, MBP, IL-4, and IgE were significantly increased in the AR-associated groups (that is, R and CCR3−/−AR). In addition, the CCR3−/−AR group mice produced significantly lower levels of EPO, ECP, MBP, IL-4 and IgE compared with the AR group, whereas the expression levels of IFN-γ and IL-10 were increased. CCR3 gene knockout may alleviate EOS invasion and the inflammatory response in AR model mice by reducing the expression levels of EPO, ECP, MBP, IL-4, and IgE, and increasing the expression of IL-10 and IFN-γ.

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