Scholarlink

Introduction <p>The transition from regulated to dysregulated parainflammation is a new concept that needs to be elucidated to clarify the pathogenesis of dry eye disease (DED). This review summarizes the recent evidence about mechanisms that could lead to dysregulated parainflammation, proposing a new hypothesis to correlate this process with the progression to chronic inflammation.</p> Methods <p>A group of European experts on DED participated in a roundtable to discuss the role of parainflammation in the most common ocular diseases with regard to DED. Starting from the roundtable contents, a narrative review was conducted through a PubMed search based on the main topics discussed, namely: parainflammation, dysfunctional parainflammation, tear film lipid and mucin alterations, and tear cortisol.</p> Results <p>Parainflammation is involved in different ocular pathologies and is characterized by the involvement of the immune system and complement factors. In DED, continuous and persistent insults are responsible for the qualitative and quantitative alteration of the lipid and mucin components of the tear film. In addition, other contributing factors have recently been described, such as the reduction of cortisol synthesis by corneal epithelial cells. This altered condition leads to excessive macrophage activity, releasing cytokines and adhesion molecules, losing tissue homeostasis, and possibly progressing to chronic inflammation.</p> Conclusions <p>Literature evidence supports the crucial role of parainflammation and its usefulness in improving the diagnosis and treatment of DED. At the same time, further investigations are necessary to better define the transition from functional to dysfunctional parainflammation, including the role of ocular surface components other than the tear film.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Parainflammation in the Ocular System: Considerations on the Underlying Mechanisms and Treatment of Dry Eye Disease

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年3月29日

查看全文
  • Stefano Barabino,
  • Pasquale Aragona,
  • Christophe Baudouin,
  • Kostas Boboridis,
  • José Salgado-Borges,
  • Jose M. Benitez-del-Castillo,
  • Elisabeth M. Messmer,
  • Adriana Stanila,
  • Jutta Horwath-Winter,
  • Edward Wylegala,
  • Maurizio Rolando

摘要

Introduction

The transition from regulated to dysregulated parainflammation is a new concept that needs to be elucidated to clarify the pathogenesis of dry eye disease (DED). This review summarizes the recent evidence about mechanisms that could lead to dysregulated parainflammation, proposing a new hypothesis to correlate this process with the progression to chronic inflammation.

Methods

A group of European experts on DED participated in a roundtable to discuss the role of parainflammation in the most common ocular diseases with regard to DED. Starting from the roundtable contents, a narrative review was conducted through a PubMed search based on the main topics discussed, namely: parainflammation, dysfunctional parainflammation, tear film lipid and mucin alterations, and tear cortisol.

Results

Parainflammation is involved in different ocular pathologies and is characterized by the involvement of the immune system and complement factors. In DED, continuous and persistent insults are responsible for the qualitative and quantitative alteration of the lipid and mucin components of the tear film. In addition, other contributing factors have recently been described, such as the reduction of cortisol synthesis by corneal epithelial cells. This altered condition leads to excessive macrophage activity, releasing cytokines and adhesion molecules, losing tissue homeostasis, and possibly progressing to chronic inflammation.

Conclusions

Literature evidence supports the crucial role of parainflammation and its usefulness in improving the diagnosis and treatment of DED. At the same time, further investigations are necessary to better define the transition from functional to dysfunctional parainflammation, including the role of ocular surface components other than the tear film.