The olfactory epithelium (OE) undergoes life-long renewal and regeneration. This process is supported by the globose basal cells (GBC) during the homeostatic state, as well as horizontal basal cells (HBC) during severe damage. Inflamm-aging refers to the low-grade, chronic and progressive state of heightened pro-inflammation associated with aging. However, the impact of inflamm-aging on OE homeostasis, regeneration, and the inflammatory microenvironment is not fully understood. In this study using mouse models, we elucidate the role of interleukin-17a (IL-17a) in OE regeneration and olfactory function. Our findings implicate that inflamm-aging in aged OE promotes the recruitment and activation of immune cells, accompanied by crosstalk between HBC and T cells. Elevated expression of IL-17a in aged OE triggers inflammatory signals and impairs olfactory function. Administration of IL-17a inhibitor Y-320 or neutralizing antibody promotes sensory neuronal regeneration and reverses age-related respiratory metaplasia in OE. Co-culturing mouse OE organoids with Th17 cells impairs neuronal generation and enhances the transformation towards respiratory cells, while neutralizing antibody against IL-17a alleviates neuronal loss and respiratory transformation. Additionally, conditional knockout of IL-17a in T cells facilitates OE regeneration by promoting HBC recruitment and differentiation into GBC. Collectively, our study identifies a function of IL-17a in OE regeneration and age-related deficits in olfactory function, providing evidence for further investigation of IL-17a as a possible therapeutic target against presbyosmia.

The coronavirus disease 2019 (COVID-19) has swept the world, posing a serious threat to people's lives and health. Several cases of COVID-19 infection in renal transplant recipients (RTRs) have been reported, but the treatment and prognosis have not been fully elucidated. We followed-up with RTRs infected with SARS-CoV2 in our center and classified them as five clinical types—asymptomatic, mild, moderate, severe, and critical. The immunosuppressive agents were not adjusted in asymptomatic carriers and mild patients, the former was mainly treated by isolation, and the latter was treated by low-dose intravenous immunoglobulin (IVIG) to enhance immunity. For moderate or severe patients, the immunosuppressive agents were largely reduced or even interrupted, low-dose IVIG was adopted, and low-dose methylprednisolone (MP) was used to inhibit inflammation and rejection. Immunosuppressants were discontinued early in critical patients; IVIG, high-dose MP, and antibiotics were used. Meanwhile, all patients received at least one antiviral drugs. After aggressive treatment, three patients developed acute kidney injury, and two showed reversal, while the remaining one lost the allograft kidney; one patient died, while other patients were discharged. For different clinical types of RTRs infected with COVID-19, personalized therapies were essential, Meanwhile, patients with COVID-19 infection may have different outcomes due to their different clinical manifestations.

Background: Retropharyngeal abscesses are rarely reported in adults and occur mostly in patients with immunocompromise or as a foreign body complication. Admittedly, the treatment of retropharyngeal abscesses frequently involves surgical drainage to achieve the best results. However, when retropharyngeal abscesses occurred in a highly suspected patient with COVID-19, the managements and treatments should be caution in order to prevent the spread of the virus. Case presentation: On Feb. 13, a 40-year-old male with retropharyngeal abscesses turned to our department complaining dyspnea and dysphagia. In addition, his chest CT scan shows a suspected COVID-19 infection, thus making out Multiple Disciplinary Team (MDT) determine to perform percutaneous drainage and catheterization through left anterior cervical approach under the guidance of B-ultrasound. Finally, the patient recovered and was discharged from the hospital on Feb. 27 after 14 days of isolation. There was no recurrence after half a year follow-up. Conclusions: By presenting this case, we aim at raising awareness of different surgical drainage methods and summarizing our experience in the management of retropharyngeal abscesses during the outbreak of COVID-19.

Background: Hearing loss is the most common sensory nervous system defect in humans. Approximately half of hearing loss cases have a genetic etiology. At present, more than 300 genes and 1000 mutations have been identified that cause hereditary hearing loss (HHL). However, there are still a large number of unknown genes related to hearing loss. Objective: The purpose of this study was to analyze the clinical audiological characteristics of a family with hereditary nonsyndromic hearing loss (NSHL) and identify the mutation of deafness‐related genes. Material and Methods: A Chinese Han–dominant deafness family including six members was enrolled in our study. In addition to collecting detailed clinical data on the audiology of this family, we employed whole‐exome sequencing (WES) and Sanger sequencing to identify the key gene causing deafness. Results: The pedigree chart of the HHL family suggested that the disease might be a dominant genetic disease. The WES and Sanger sequencing indicated that a novel mutation (c.842C > G) occurred in the ACTG1 gene on the fifth exon, which caused the change of the coding protein (p.S281C). This variant cosegregated perfectly with the hearing loss phenotype: All affected members carried the heterozygous c.842C > G mutation, whereas the only unaffected family member showed wild‐type ACTG1. Multiple sequence alignment revealed that the p.Ser281 residue was highly conserved across vertebrate species. Bioinformatic analyses showed high conservation of p.Ser281 across species and predicted damaging effects on protein structure and function. Conclusions and Significance: On the basis of our research, we identified a novel pathogenic variant in the ACTG1 gene responsible for NSHL, which expands the mutational spectrum of ACTG1‐related hearing loss. Further in vitro and in vivo studies may be performed to elucidate the underlying mechanism by which ACTG1 contributes to hearing function, potentially providing intervention targets for gene therapy of HHL.