# Neutrophils in Intracerebral Hemorrhage: Roles, Mechanisms, and Therapeutic Implications

## TL;DR

This paper explores how neutrophils contribute to brain inflammation after intracerebral hemorrhage and suggests ways to target them for treatment.

## Contribution

The paper provides a comprehensive review of neutrophil roles and mechanisms in ICH, highlighting their dual function and therapeutic potential.

## Key findings

- Neutrophils initially worsen brain damage by releasing harmful molecules and NETs.
- Later, neutrophils can switch to an immunosuppressive state, potentially aiding recovery.
- Targeting neutrophil pathways offers a promising therapeutic strategy for ICH.

## Abstract

Nontraumatic intracerebral hemorrhage (ICH), characterized by bleeding into the brain parenchyma, is a major cause of adult disability and mortality. The pathophysiology of ICH involves complex processes, including mass effect and subsequent inflammatory responses, which cause severe primary and secondary brain damage. As the first responders in neuroinflammatory reactions, neutrophils are rapidly recruited to the hemorrhage site. They interact with other immune cells, release cytotoxic molecules, and significantly exacerbate neuroinflammation. In the acute phase, neutrophils secrete cytokines, chemokines and neutrophil extracellular traps (NETs), which are particularly detrimental to brain tissue. However, in later stages, infiltrated neutrophils can adopt an immunosuppressive phenotype, exerting beneficial effects. Emerging evidence reveals that neutrophils play a multifaceted role in ICH progression, shifting between anti‐inflammatory or pro‐inflammatory phenotypes depending on brain tissue niche. Hence, tuning neutrophils into a beneficial phenotype represents a promising therapeutic strategy for ICH. We conducted a comprehensive literature search in PubMed and Web of Science databases for relevant studies published up to July 2025, using keywords including “intracerebral hemorrhage (ICH),” “neutrophil,” “inflammation,” “neuroinflammation,” “ neutrophil extracellular traps (NETs),” “treatment,” “therapy,“ and “therapeutics.” In this article, we explore the roles of neutrophils in ICH, encompassing their recruitment, activation mechanisms, interactions with other immune cells, and impact on neuroinflammation and neuronal injury. Furthermore, we discuss therapeutic strategies targeting neutrophil‐mediated pathways in ICH, highlighting potential avenues for future research and clinical intervention.