# Inflaming and Immune-Resolving: The Ambivalent Role of Eosinophils in Osteoarthritis

## TL;DR

Eosinophils, known for their role in allergies, also play a dual role in osteoarthritis by both causing and resolving joint inflammation.

## Contribution

The paper highlights the novel dual role of eosinophils in osteoarthritis as both inflammatory and immune-resolving agents.

## Key findings

- Eosinophils contribute to synovial inflammation in osteoarthritis.
- They also promote tissue repair by secreting anti-inflammatory cytokines and SPMs.
- Eosinophils may serve as therapeutic targets to shift joint inflammation toward resolution.

## Abstract

Osteoarthritis (OA), the most prevalent form of arthropathy, is characterized by progressive degradation of cartilage, synovial inflammation, and other pathological changes that gradually affect the entire joint. Once regarded as a purely degenerative disease with minimal immune involvement, recent evidence reveals that chronic low-grade inflammation, insidiously fueled by the destructive crosstalk between cartilage and synovium, plays a key role in OA pathophysiology. Among the immune cells involved, eosinophils have emerged as unexpected yet significant contributors, exhibiting both pro-inflammatory and immunoregulatory properties. Traditionally associated with allergic responses and antiparasitic defense, eosinophils can also secrete anti-inflammatory cytokines along with specialized pro-resolving lipid mediators (SPMs) that promote macrophage polarization toward reparative M2 phenotypes. Eosinophils may sustain inflammation or, conversely, act as “silent modulators” that subtly shape the immune microenvironment and support tissue homeostasis. This immunological plasticity positions them at the intersection of joint damage and repair. This article explores emerging evidence on eosinophil activity in OA, emphasizing their dual nature and potential as therapeutic targets to shift the joint milieu from a pro-inflammatory state toward resolution. Understanding eosinophil-mediated pathways may pave the way for novel strategies to reduce synovial inflammation, preserve cartilage integrity, and improve clinical outcomes.