Search

Traditionally, the cochlea has been considered as an immunological privileged site, as the blood-labyrinth barrier provides isolation from the systemic immune system. However, the presence of immune cells in the cochlea has been recently reported, suggesting that immune-mediated processes can play a crucial role within the auditory system. In this context, both protective and detrimental T-cell functions have been linked to normal hearing and hearing loss, respectively, thereby emphasizing the dual role of T cells in cochlear health. Current knowledge also suggests that a balanced presence and activity of T cells is crucial for tissue homeostasis in the cochlea, avoiding pathologies such as age-related hearing loss and autoimmune inner ear diseases. Although cochlea-resident T cells are scarce under physiological conditions, the number of T cells appear to rise in response to acoustic trauma revealing the active recruitment of peripheral immune cells through cochlear blood vessels. In order to evaluate the induction of a peripheral inflammatory response upon noise trauma, we exposed mice to excessive noise (115 dB) for two hours. Hearing levels were determined 72 h and 1 week after noise-exposure, which revealed a substantial increase in hearing thresholds in all mice. To evaluate if the auditory stimulation would trigger a peripheral immune response we isolated splenocytes and analyzed cytokine production in different immune subsets by high parametric flow cytometry. The analyses revealed increased activation of both CD4+ and CD8+ T cells, illustrated by significant increases in the expression of INF-γ, TNF and CD44. These data suggest a peripheral component in the elevated inflammatory response following acoustic trauma. Future research will be performed to explore the link between noise-induced hearing loss, peripheral inflammation and more specifically antigen-specificity of the observed increase in activated CD4+ and CD8+ T-cell populations. [ABSTRACT FROM AUTHOR]

The spiral ligament in the cochlea has been suggested to play a significant role in the pathophysiology of sensorineural hearing loss (SNHL). Positioned between the stria vascula-ris and the bony otic capsule, this structure contains spiral ligament fibrocytes (SLFs), categorized into five main types based on their structural characteristics, immunostaining patterns and location within the spiral ligament. Together with the stria vascularis, the SLFs maintain a positive endo-cochlear potential (EP) in the scala media via K+ recycling, which is an essential component in the transduction mechanism of the auditory pathway. It has also been suggested that the SLFs contribute to the cochlear immune response, gluta-mate homeostasis and cochlear blood flow regulation. Spiral ligament damage disrupts K+ recycling, reducing the EP and subsequently causing SNHL. Despite their pivotal roles, a lot remains unknown about the SLFs. Therefore, this systematic review about SLFs in cell culture could give an overview of the current state of the art, providing a basis for future studies trying to investigate those cells in vitro. A literature search was performed using PubMed, Web of Science and Scopus taking into account the PRISMA guidelines. Twenty-five studies were included in this review that report on SLFs in cell culture. The differences in species, sex, age, method of culturing and used antibodies for immunohis-tochemistry are discussed. The majority of these studies cultured spiral ligament fragments onto type I collagen-coated petri dishes; a protocol described by Gratton et al. in 1996, while some recent studies are focussing more on growing these cells in a 3D environment. A better understanding of the currently published methods will help us to optimize fibrocyte culture techniques, thereby allowing to investigate a variety of possibilities that can significantly increase our knowledge about SLFs. Among others, these possibilities include to discover their functional characteristics, such as growth patterns, protein expression profiles and ion channel physiology, to expose the cells to hy-poxia or other toxic conditions and to assess the resulting effects, to genetically modify SLFs, to explore drug repurposing possibilities, to evaluate potential therapies for SNHL and to investigate their capability as a source for transplantable cells. [ABSTRACT FROM AUTHOR]