Neutrophil Extracellular Traps, Local IL-8 Expression, and Cytotoxic T-Lymphocyte Response in the Lungs of Patients With Fatal COVID-19.


Journal

Chest
ISSN: 1931-3543
Titre abrégé: Chest
Pays: United States
ID NLM: 0231335

Informations de publication

Date de publication:
11 2022
Historique:
received: 04 12 2021
revised: 04 06 2022
accepted: 07 06 2022
pubmed: 18 6 2022
medline: 10 11 2022
entrez: 17 6 2022
Statut: ppublish

Résumé

Excessive inflammation is pathogenic in the pneumonitis associated with severe COVID-19. Neutrophils are among the most abundantly present leukocytes in the inflammatory infiltrates and may form neutrophil extracellular traps (NETs) under the local influence of cytokines. NETs constitute a defense mechanism against bacteria, but have also been shown to mediate tissue damage in a number of diseases. Could NETs and their tissue-damaging properties inherent to neutrophil-associated functions play a role in the respiratory failure seen in patients with severe COVID-19, and how does this relate to the SARS-CoV-2 viral loads, IL-8 (CXCL8) chemokine expression, and cytotoxic T-lymphocyte infiltrates? Sixteen lung biopsy samples obtained immediately after death were analyzed methodically as exploratory and validation cohorts. NETs were analyzed quantitatively by multiplexed immunofluorescence and were correlated with local levels of IL-8 messenger RNA (mRNA) and the density of CD8+ T-cell infiltration. SARS-CoV-2 presence in tissue was quantified by reverse-transcriptase polymerase chain reaction and immunohistochemistry analysis. NETs were found in the lung interstitium and surrounding the bronchiolar epithelium with interindividual and spatial heterogeneity. NET density did not correlate with SARS-CoV-2 tissue viral load. NETs were associated with local IL-8 mRNA levels. NETs were also detected in pulmonary thrombi and in only one of eight liver tissues. NET focal presence correlated negatively with CD8+ T-cell infiltration in the lungs. Abundant neutrophils undergoing NETosis are found in the lungs of patients with fatal COVID-19, but no correlation was found with viral loads. The strong association between NETs and IL-8 points to this chemokine as a potentially causative factor. The function of cytotoxic T-lymphocytes in the immune responses against SARS-CoV-2 may be interfered with by the presence of NETs.

Sections du résumé

BACKGROUND
Excessive inflammation is pathogenic in the pneumonitis associated with severe COVID-19. Neutrophils are among the most abundantly present leukocytes in the inflammatory infiltrates and may form neutrophil extracellular traps (NETs) under the local influence of cytokines. NETs constitute a defense mechanism against bacteria, but have also been shown to mediate tissue damage in a number of diseases.
RESEARCH QUESTION
Could NETs and their tissue-damaging properties inherent to neutrophil-associated functions play a role in the respiratory failure seen in patients with severe COVID-19, and how does this relate to the SARS-CoV-2 viral loads, IL-8 (CXCL8) chemokine expression, and cytotoxic T-lymphocyte infiltrates?
STUDY DESIGN AND METHODS
Sixteen lung biopsy samples obtained immediately after death were analyzed methodically as exploratory and validation cohorts. NETs were analyzed quantitatively by multiplexed immunofluorescence and were correlated with local levels of IL-8 messenger RNA (mRNA) and the density of CD8+ T-cell infiltration. SARS-CoV-2 presence in tissue was quantified by reverse-transcriptase polymerase chain reaction and immunohistochemistry analysis.
RESULTS
NETs were found in the lung interstitium and surrounding the bronchiolar epithelium with interindividual and spatial heterogeneity. NET density did not correlate with SARS-CoV-2 tissue viral load. NETs were associated with local IL-8 mRNA levels. NETs were also detected in pulmonary thrombi and in only one of eight liver tissues. NET focal presence correlated negatively with CD8+ T-cell infiltration in the lungs.
INTERPRETATION
Abundant neutrophils undergoing NETosis are found in the lungs of patients with fatal COVID-19, but no correlation was found with viral loads. The strong association between NETs and IL-8 points to this chemokine as a potentially causative factor. The function of cytotoxic T-lymphocytes in the immune responses against SARS-CoV-2 may be interfered with by the presence of NETs.

Identifiants

pubmed: 35714708
pii: S0012-3692(22)01088-1
doi: 10.1016/j.chest.2022.06.007
pmc: PMC9197577
pii:
doi:

Substances chimiques

Interleukin-8 0
RNA, Messenger 0

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1006-1016

Subventions

Organisme : Wellcome Trust
Pays : United Kingdom
Organisme : NIAID NIH HHS
ID : U19 AI082630
Pays : United States

Informations de copyright

Copyright © 2022 The Author(s). Published by Elsevier Inc. All rights reserved.

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Auteurs

Ignacio Melero (I)

Division of Immunology and Immunotherapy, Centre for Applied Medical Research (CIMA), University of Navarra, Pamplona, Spain; Navarra Institute for Health Research, Pamplona, Spain; Centro de Investigación Biomédica en Red de Cáncer, Madrid, Spain.

María Villalba-Esparza (M)

Navarra Institute for Health Research, Pamplona, Spain; Centro de Investigación Biomédica en Red de Cáncer, Madrid, Spain; Department of Pathology, Clínica Universidad de Navarra, Pamplona, Spain.

Borja Recalde-Zamacona (B)

Service of Pulmonary Medicine, Clínica Universidad de Navarra, Pamplona, Spain.

Daniel Jiménez-Sánchez (D)

Department of Pathology, Clínica Universidad de Navarra, Pamplona, Spain.

Álvaro Teijeira (Á)

Division of Immunology and Immunotherapy, Centre for Applied Medical Research (CIMA), University of Navarra, Pamplona, Spain; Navarra Institute for Health Research, Pamplona, Spain; Centro de Investigación Biomédica en Red de Cáncer, Madrid, Spain.

Alan Argueta (A)

Department of Pathology, Clínica Universidad de Navarra, Pamplona, Spain.

Laura García-Tobar (L)

Department of Pathology, Clínica Universidad de Navarra, Pamplona, Spain.

Laura Álvarez-Gigli (L)

Department of Pathology, Clínica Universidad de Navarra, Pamplona, Spain.

Cristina Sainz (C)

Department of Pathology, Clínica Universidad de Navarra, Pamplona, Spain.

David Garcia-Ros (D)

Department of Anatomy, Physiology and Pathology, University of Navarra, Pamplona, Spain.

Estefanía Toledo (E)

Department of Preventive Medicine and Public Health, IdiSNA, University of Navarra, Pamplona, Spain; Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y la Nutrición, Institute of Health Carlos III, Madrid, Spain.

Marta Abengozar-Muela (M)

Department of Pathology, Clínica Universidad de Navarra, Pamplona, Spain.

Mirian Fernández-Alonso (M)

Navarra Institute for Health Research, Pamplona, Spain; Department of Microbiology and Infectious Diseases, Clínica Universidad de Navarra, Pamplona, Spain.

Mariano Rodríguez-Mateos (M)

Department of Microbiology and Infectious Diseases, Clínica Universidad de Navarra, Pamplona, Spain.

Gabriel Reina (G)

Navarra Institute for Health Research, Pamplona, Spain; Department of Microbiology and Infectious Diseases, Clínica Universidad de Navarra, Pamplona, Spain.

Francisco Carmona-Torre (F)

Navarra Institute for Health Research, Pamplona, Spain; Department of Microbiology and Infectious Diseases, Clínica Universidad de Navarra, Pamplona, Spain.

Jorge Augusto Quiroga (JA)

Department of Internal Medicine, Clínica Universidad de Navarra, Pamplona, Spain.

Jose L Del Pozo (JL)

Navarra Institute for Health Research, Pamplona, Spain; Department of Microbiology and Infectious Diseases, Clínica Universidad de Navarra, Pamplona, Spain.

Amy Cross (A)

Nuffield Department of Surgical Sciences, John Radcliffe Hospital, University of Oxford, Oxford, England.

Álvaro López-Janeiro (Á)

Department of Pathology, Hospital Universitario La Paz, IdiPAZ, Madrid, Spain.

David Hardisson (D)

Department of Pathology, Hospital Universitario La Paz, IdiPAZ, Madrid, Spain.

José I Echeveste (JI)

Centro de Investigación Biomédica en Red de Cáncer, Madrid, Spain; Department of Pathology, Clínica Universidad de Navarra, Pamplona, Spain; Department of Anatomy, Physiology and Pathology, University of Navarra, Pamplona, Spain.

Maria D Lozano (MD)

Navarra Institute for Health Research, Pamplona, Spain; Centro de Investigación Biomédica en Red de Cáncer, Madrid, Spain; Department of Pathology, Clínica Universidad de Navarra, Pamplona, Spain; Department of Anatomy, Physiology and Pathology, University of Navarra, Pamplona, Spain.

Ling-Pei Ho (LP)

MRC Human Immunology Unit, University of Oxford, Oxford, England.

Paul Klenerman (P)

Nuffield Department of Clinical Medicine, Peter Medawar Building for Pathogen Research, Oxford, England.

Fadi Issa (F)

Nuffield Department of Surgical Sciences, John Radcliffe Hospital, University of Oxford, Oxford, England.

Manuel F Landecho (MF)

Department of Internal Medicine, Clínica Universidad de Navarra, Pamplona, Spain.

Carlos E de Andrea (CE)

Navarra Institute for Health Research, Pamplona, Spain; Centro de Investigación Biomédica en Red de Cáncer, Madrid, Spain; Department of Pathology, Clínica Universidad de Navarra, Pamplona, Spain; Department of Anatomy, Physiology and Pathology, University of Navarra, Pamplona, Spain. Electronic address: ceandrea@unav.es.

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