Chronic Disseminated Candidiasis During Hematological Malignancies: An Immune Reconstitution Inflammatory Syndrome With Expansion of Pathogen-Specific T Helper Type 1 Cells.


Journal

The Journal of infectious diseases
ISSN: 1537-6613
Titre abrégé: J Infect Dis
Pays: United States
ID NLM: 0413675

Informations de publication

Date de publication:
11 05 2020
Historique:
received: 17 12 2019
accepted: 23 12 2019
pubmed: 28 12 2019
medline: 1 4 2021
entrez: 28 12 2019
Statut: ppublish

Résumé

Chronic disseminated candidiasis (CDC) is a rare disease that mostly occurs after chemotherapy-induced prolonged neutropenia in patients with hematological malignancies. It is believed to ensue from Candida colonization, breach of the intestinal epithelial barrier, and venous translocation to organs. Fungal blood or liver biopsy cultures are generally negative, suggesting the absence of an ongoing invasive fungal disease. To unravel the contribution of the immune system to CDC pathogenesis, we undertook a prospective multicentric exploratory study in 44 CDC patients at diagnosis and 44 matched controls. Analysis of Candida-specific T-cell responses using enzyme-linked immunospot assays revealed higher numbers of interferon (IFN)γ-producing T cells reactive to mp65 or candidin in 27 CDC cases compared with 33 controls. Increased plasma levels of soluble CD25, interleukin (IL)-6, IL-1β, tumor necrosis factor-α, and IL-10 and lower levels of IL-2 were observed in CDC patients versus controls. Neutrophilia and higher levels of CD4 and CD8 T-cell activation were found in CDC patients as well as increased proportions of CXCR3-expressing TCRγδ +Vδ2+ cells. The expansion of Candida-specific IFNγ-producing T cells together with features of T-cell activation and systemic inflammation identified here support the view that CDC belongs to the broad spectrum of fungal-associated immune reconstitution inflammatory syndromes.

Sections du résumé

BACKGROUND
Chronic disseminated candidiasis (CDC) is a rare disease that mostly occurs after chemotherapy-induced prolonged neutropenia in patients with hematological malignancies. It is believed to ensue from Candida colonization, breach of the intestinal epithelial barrier, and venous translocation to organs. Fungal blood or liver biopsy cultures are generally negative, suggesting the absence of an ongoing invasive fungal disease.
METHODS
To unravel the contribution of the immune system to CDC pathogenesis, we undertook a prospective multicentric exploratory study in 44 CDC patients at diagnosis and 44 matched controls.
RESULTS
Analysis of Candida-specific T-cell responses using enzyme-linked immunospot assays revealed higher numbers of interferon (IFN)γ-producing T cells reactive to mp65 or candidin in 27 CDC cases compared with 33 controls. Increased plasma levels of soluble CD25, interleukin (IL)-6, IL-1β, tumor necrosis factor-α, and IL-10 and lower levels of IL-2 were observed in CDC patients versus controls. Neutrophilia and higher levels of CD4 and CD8 T-cell activation were found in CDC patients as well as increased proportions of CXCR3-expressing TCRγδ +Vδ2+ cells.
CONCLUSIONS
The expansion of Candida-specific IFNγ-producing T cells together with features of T-cell activation and systemic inflammation identified here support the view that CDC belongs to the broad spectrum of fungal-associated immune reconstitution inflammatory syndromes.

Identifiants

pubmed: 31879764
pii: 5687810
doi: 10.1093/infdis/jiz688
doi:

Substances chimiques

Interferon-gamma 82115-62-6

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1907-1916

Informations de copyright

© The Author(s) 2019. Published by Oxford University Press for the Infectious Diseases Society of America. All rights reserved. For permissions, e-mail: journals.permissions@oup.com.

Auteurs

Sophie Candon (S)

Université Paris-Descartes, Faculté de Médecine, INSERM U1151-CNRS UMR 8253, Assistance Publique-Hôpitaux de Paris (APHP), Hôpital Necker-Enfants Malades, APHP, Immunologie Biologique, Paris, France.
Université de Rouen Normandie, INSERM U1234, CHU de Rouen Normandie, Rouen, France.

Blandine Rammaert (B)

Université Paris Descartes, Faculté de Médecine, APHP, Hôpital Necker-Enfants Malades, Service de Maladies Infectieuses et Tropicales, Centre d'Infectiologie Necker-Pasteur, IHU Imagine, Paris, France.
Université de Poitiers, Faculté de Médecine et Pharmacie, Poitiers, France.
CHU de Poitiers, Service de Maladies Infectieuses et Tropicales, Poitiers, France.

Anne Perrine Foray (AP)

Université Paris-Descartes, Faculté de Médecine, INSERM U1151-CNRS UMR 8253, Assistance Publique-Hôpitaux de Paris (APHP), Hôpital Necker-Enfants Malades, APHP, Immunologie Biologique, Paris, France.

Baptiste Moreira (B)

Université Paris-Descartes, Faculté de Médecine, INSERM U1151-CNRS UMR 8253, Assistance Publique-Hôpitaux de Paris (APHP), Hôpital Necker-Enfants Malades, APHP, Immunologie Biologique, Paris, France.

Maria Pilar Gallego Hernanz (MP)

CHU de Poitiers, Service d'Hématologie, Poitiers, France.

Lucienne Chatenoud (L)

Université Paris-Descartes, Faculté de Médecine, INSERM U1151-CNRS UMR 8253, Assistance Publique-Hôpitaux de Paris (APHP), Hôpital Necker-Enfants Malades, APHP, Immunologie Biologique, Paris, France.

Olivier Lortholary (O)

Université Paris Descartes, Faculté de Médecine, APHP, Hôpital Necker-Enfants Malades, Service de Maladies Infectieuses et Tropicales, Centre d'Infectiologie Necker-Pasteur, IHU Imagine, Paris, France.
Institut Pasteur, Unité de Mycologie Moléculaire, Paris, France.

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Classifications MeSH