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Home / Equine Research Bank / Viruses / Could Interleukin-33 (IL-33) Govern the Outcome of an Equine...
Viruses2021; 13(12); 2519; doi: 10.3390/v13122519

Could Interleukin-33 (IL-33) Govern the Outcome of an Equine Influenza Virus Infection? Learning from Other Species.

Abstract: Influenza A viruses (IAVs) are important respiratory pathogens of horses and humans. Infected individuals develop typical respiratory disorders associated with the death of airway epithelial cells (AECs) in infected areas. Virulence and risk of secondary bacterial infections vary among IAV strains. The IAV non-structural proteins, NS1, PB1-F2, and PA-X are important virulence factors controlling AEC death and host immune responses to viral and bacterial infection. Polymorphism in these proteins impacts their function. Evidence from human and mouse studies indicates that upon IAV infection, the manner of AEC death impacts disease severity. Indeed, while apoptosis is considered anti-inflammatory, necrosis is thought to cause pulmonary damage with the release of damage-associated molecular patterns (DAMPs), such as interleukin-33 (IL-33). IL-33 is a potent inflammatory mediator released by necrotic cells, playing a crucial role in anti-viral and anti-bacterial immunity. Here, we discuss studies in human and murine models which investigate how viral determinants and host immune responses control AEC death and subsequent lung IL-33 release, impacting IAV disease severity. Confirming such data in horses and improving our understanding of early immunologic responses initiated by AEC death during IAV infection will better inform the development of novel therapeutic or vaccine strategies designed to protect life-long lung health in horses and humans, following a One Health approach.
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Publication Date: 2021-12-15 PubMed ID: 34960788PubMed Central: PMC8704309DOI: 10.3390/v13122519Google Scholar: Lookup
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  • Journal Article
  • Research Support
  • Non-U.S. Gov't
  • Review

Summary

This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.

This research paper explores the role of Interleukin-33 (IL-33) in determining the severity of an equine influenza virus infection by comparing studies in human and murine models. The exploration aims to improve these therapeutic and vaccine strategies that aim to protect lung health in horses and humans.

Background and Objective

  • The study begins by examining the impact of Influenza A viruses (IAVs) – significant respiratory pathogens in both humans and horses.
  • It is observed that individuals infected with IAVs develop respiratory disorders related to the death of airway epithelial cells (AECs).
  • The virulence of IAVs varies across strains, influencing the risk of secondary bacterial infections.
  • The research aims to explore the role of Interleukin-33 (IL-33) – a crucial inflammatory mediator – in determining the severity of an equine influenza virus infection.

Variations in IAV Strains and their Impacts

  • The study considers non-structural proteins in IAVs, like NS1, PB1-F2, and PA-X, as vital elements in controlling AEC death and a host’s immune response to bacterial and viral infections.
  • The function of these proteins is influenced by their polymorphism – variations in their structural traits.

The Role of IL-33

  • IL-33 is released during cell necrosis – a form of cell death – and plays a significant role in immunity against viral and bacterial infections.
  • The death type depicted by AECs crucially impacts disease severity, with apoptosis acting as anti-inflammatory and necrosis causing lung damage via the release of IL-33.

Disease Severity and Control Factors

  • The article discusses human and murine model studies investigating how viral elements and host immune responses regulate AEC death and consecutive pulmonary IL-33 release.
  • The findings gathered here impact how severe an IAV infection is for the infected individual.

Significance and Application

  • Confirming such study results in horses can considerably forward the understanding of early immunologic responses triggered by AEC death.
  • These learnings would contribute to the evolution of therapeutic and vaccine strategies ensuring long-term lung health in horses and humans, adhering to a “One Health” approach.

Cite This Article

APA
Rozario C, Martínez-Sobrido L, McSorley HJ, Chauché C. (2021). Could Interleukin-33 (IL-33) Govern the Outcome of an Equine Influenza Virus Infection? Learning from Other Species. Viruses, 13(12), 2519. https://doi.org/10.3390/v13122519

Publication

Viruses
ISSN: 1999-4915
NlmUniqueID: 101509722
Country: Switzerland
Language: English
Volume: 13
Issue: 12
PII: 2519

Researcher Affiliations

Rozario, Christoforos
  • Centre for Inflammation Research, The Queen's Medical Research Institute, The University of Edinburgh, Edinburgh BioQuarter, Edinburgh EH16 4TJ, UK.
Martínez-Sobrido, Luis
  • Texas Biomedical Research Institute, San Antonio, TX 78227, USA.
McSorley, Henry J
  • Division of Cell Signalling and Immunology, School of Life Sciences, University of Dundee, Wellcome Trust Building, Dow Street, Dundee DD1 5EH, UK.
Chauché, Caroline
  • Centre for Inflammation Research, The Queen's Medical Research Institute, The University of Edinburgh, Edinburgh BioQuarter, Edinburgh EH16 4TJ, UK.

MeSH Terms

  • Animals
  • Apoptosis
  • Asthma
  • Cell Death
  • Epithelial Cells
  • Horses
  • Humans
  • Influenza A virus / immunology
  • Influenza, Human / virology
  • Interleukin-33 / immunology
  • Lung / immunology
  • Lung / virology
  • Mice
  • Orthomyxoviridae Infections / immunology
  • Orthomyxoviridae Infections / virology
  • Pneumonia, Bacterial / immunology
  • Virulence
  • Virulence Factors / metabolism

Grant Funding

  • R01 AI145332 / NIAID NIH HHS

Conflict of Interest Statement

The authors declare no conflict of interest.

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Citations

This article has been cited 1 times.
  1. Borgia F, Custurone P, Li Pomi F, Vaccaro M, Alessandrello C, Gangemi S. IL-33 and IL-37: A Possible Axis in Skin and Allergic Diseases.. Int J Mol Sci 2022 Dec 26;24(1).
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