# Nerve Injury-Induced Immune Responses in the Taste Bud Target Field

## TL;DR

This study explores how nerve injury affects immune responses and taste bud regeneration, finding that immune cell changes are linked to recovery in mice.

## Contribution

The study reveals that immune cell changes after nerve injury depend on Il1r signaling and may support taste bud regeneration.

## Key findings

- CD45+, CD68+, and CD206+ M2-like macrophages increase near taste buds after injury in wild-type but not Il1r KO mice.
- Taste bud degeneration occurs similarly in both strains, indicating immune suppression is not the main cause of functional deficits.
- Pro-regenerative M2-like macrophages may aid taste bud regeneration and recovery in injured mice.

## Abstract

Damage to the chorda tympani (CT) nerve through trauma or experimental nerve axotomy results in the degeneration of anterior taste buds and taste loss. Our previous work demonstrated that interleukin-1 receptor 1 (Il1r) signaling is required for taste bud regeneration and the recovery of taste function. However, the effects of experimental axotomy on immune responses in the absence of Il1r signaling remain unclear. Here we performed unilateral CT sectioning in Il1r KO or wild-type mice to observe changes in innate immune cell populations in the anterior taste field. We found that CD45+ immune cells, CD68+ and CD206+ M2-like macrophages are significantly increased near anterior taste buds at days two and five post-injury in wild-type but not Il1r KO mice. However, taste buds degenerated at similar time points in both strains, suggesting that a suppressed immune responses in the absence of Il1r signaling is not the primary reason for later functional deficits. The presence of pro-regenerative M2-like macrophages may play a role in later taste bud regeneration and functional recovery in the injured peripheral taste system.