Pathogenesis of the eosinophilic pleural effusions

Our plain-English summary of Pathogenesis of the eosinophilic pleural effusions, by I. Kalomenidis, R.W. Light (Current Opinion in Pulmonary Medicine, 2004).

The study

• Authors: I. Kalomenidis, R.W. Light
• Journal: Current Opinion in Pulmonary Medicine
• Published: 2004;10(4):289-93
• Type of article: Review
• Cited by: 34 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Purpose Of Review: Eosinophilic pleural effusions (EPE) are defined as those that contain at least 10% eosinophils. EPEs account for 5 to 16% of exudative pleural effusions. However, their pathogenesis is poorly understood. The purpose of this review is to discuss the mechanisms that lead to eosinophilic pleural inflammation.

Recent Findings: Eosinophilic pleural effusions are caused by the presence of air or blood or both in the pleural space, infectious or other inflammatory diseases, malignancy, pulmonary emboli, asbestos exposure, and drug reactions. Differences in the clinical features suggest that a variety of mechanisms operate to induce eosinophilic pleural inflammation and pleural fluid accumulation. Human and animal studies indicate that interleukin (IL)-5 is an important common contributor of different pathogenetic pathways. The possible role of other cytokines, chemokines, and adhesion molecules in the development of EPE is under investigation.

Summary: Understanding the pathogenesis of EPE will permit the development of novel therapies for the persistent, symptomatic, posttraumatic and idiopathic EPE. Anti-IL-5 treatment is an interesting option that requires further research.

In plain English

This was a review article about how eosinophilic pleural effusions develop. These are fluid collections around the lung in which at least 10% of the nucleated cells are eosinophils, a type of white blood cell. Citing earlier work, the authors stated that such effusions make up 5 to 16% of exudative pleural effusions. They listed asbestos among the possible causes, along with air or blood in the chest cavity, infections, other inflammatory diseases, cancer, pulmonary emboli and drug reactions. The review did not discuss asbestos-related effusions any further. Drawing on human studies, including their own, the authors reported that levels of a signaling molecule called interleukin-5 (IL-5) were raised in these effusions and correlated with eosinophil numbers. In mice given air injected into the chest, eosinophil buildup depended on IL-5 but not IL-13. They described the role of other molecules, such as eotaxin, as debated. The authors concluded that different causes may act through different mechanisms, and that anti-IL-5 treatment requires further research. They noted that the human evidence was limited and indirect.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Review of published human and animal studies on the mechanisms of eosinophilic pleural effusions
• Who was studied: No study population of its own. The review covered human studies of eosinophilic pleural effusions and animal models of pleural eosinophilia, including the authors' own mouse pneumothorax experiments.
• Exposure: Asbestos is named only as one of several possible causes of eosinophilic pleural effusion. No fiber type, job or dose is discussed. The mechanisms reviewed concern air or blood in the pleural space, drugs, parasites, cancer and inflammation.
• Main results:
  • The authors defined an eosinophilic pleural effusion as one in which at least 10% of the nucleated cells are eosinophils.
  • Citing their earlier review, the authors stated that eosinophilic pleural effusions account for 5 to 16% of exudative pleural effusions.
  • Pneumothorax and hemothorax (air or blood in the chest cavity) were described as the most common causes.
  • In human studies by the authors and others, IL-5 levels were elevated in eosinophilic effusions from various causes and correlated with the number of pleural fluid or lavage eosinophils.
  • In the authors' earlier study, levels of VCAM-1 (an adhesion molecule) were higher in eosinophilic than in non-eosinophilic effusions and correlated with pleural fluid eosinophil numbers.
  • In the authors' mouse pneumothorax model, pleural eosinophils gradually increased and peaked 48 hours after air was injected. This eosinophilia depended on IL-5 but not IL-13.
  • The authors described the contribution of eotaxin as debatable: three studies found no difference between eosinophilic and non-eosinophilic effusions, while one found higher levels.
  • Based on the IgE findings they reviewed, the authors suggested that IgE does not commonly take part in causing these effusions.
• The authors' conclusion: The authors concluded that the variety of causes may mean a variety of mechanisms. They wrote that understanding these mechanisms may allow new therapies for persistent posttraumatic and idiopathic effusions, and that anti-IL-5 treatment is an option requiring further research.
• Limitations the authors state:
  • The authors stated that only a limited number of human studies exist, and that these give only indirect information.
  • The authors said their theory that mechanical injury of the pleura triggers eosinophil accumulation remains speculative.
  • The authors noted that the allergic animal model is probably relevant only to the small minority of human effusions caused by hypersensitivity reactions.

Topics

The National Library of Medicine indexes this study under subjects our site covers: Pleural plaques and thickening.

Medical terms in this study, explained in our Lexicon: Eosinophilic, Pleural Effusion, Inflammation, Asbestos Exposure, Cytokine, Idiopathic.

Related studies

• Eosinophilic pleural effusions — I. Kalomenidis, R.W. Light (2003)
• Effectiveness of Nivolumab on Sarcomatoid Malignant Pleural Mesothelioma With Eosinophilia and Eosinophilic Pleural Effusion — M. Yamazoe, H. Ozasa, et al. (2019)
• Occupational Exposures and Smoking in Eosinophilic Granulomatosis With Polyangiitis: A Case-Control Study — F. Maritati, F. Peyronel, et al. (2021)
• Eosinophil colony-stimulating factor induced by administration of interleukin-2 into the pleural cavity of patients with malignant pleurisy — Y. Nakamura, T. Ozaki, et al. (1990)
• Diagnostic utility of pleural fluid eosinophilia — M. Adelman, S.M. Albelda, et al. (1984)
• Interleukin-5-producing malignant pleural mesothelioma with eosinophilic pleural effusion — E. Takeuchi, N. Takahashi, et al. (2020)

Browse more research in Current Opinion in Pulmonary Medicine, or return to medical research.