Intestinal Candida albicans overgrowth in IgA deficiency.

Autor: Moreno-Sabater A; Sorbonne Université, Institut national de la santé et de la recherche médicale (INSERM), Centre d'Immunologie et des Maladies Infectieuses, Assistance Publique-Hôpitaux de Paris (AP-HP), Hôpital Saint Antoine, Paris, France., Sterlin D; Sorbonne Université, INSERM, Centre d'Immunologie et des Maladies Infectieuses, AP-HP, Hôpital Pitié-Salpêtrière, Paris, France., Imamovic L; Sorbonne Université, INSERM, Centre d'Immunologie et des Maladies Infectieuses, Paris, France., Bon F; UMR PAM Université de Bourgogne Franche-Comté (UBFC), AgroSup Dijon, Équipe Vin, Aliment, Microbiologie, Stress, Groupe Interactions Candida-muqueuses, Dijon, France., Normand AC; Service de Parasitologie-Mycologie, AP-HP, Groupement Hospitalier Pitié-Salpêtrière, Paris, France., Gonnin C; Département d'Immunologie, AP-HP, Groupement Hospitalier Pitié-Salpêtrière, Paris, France., Gazzano M; Département d'Immunologie, AP-HP, Groupement Hospitalier Pitié-Salpêtrière, Paris, France., Bensalah M; Département d'Immunologie, AP-HP, Groupement Hospitalier Pitié-Salpêtrière, Paris, France., Dorgham K; Sorbonne Université, INSERM, Centre d'Immunologie et des Maladies Infectieuses, Paris, France., Ben Salah E; Département d'Immunologie, AP-HP, Groupement Hospitalier Pitié-Salpêtrière, Paris, France., Acherar A; Sorbonne Université, INSERM, Institut Pierre Louis d'Épidémiologie et de Santé Publique, AP-HP, Hôpital Pitié-Salpêtrière, Paris, France., Parizot C; Département d'Immunologie, AP-HP, Groupement Hospitalier Pitié-Salpêtrière, Paris, France., Rigourd V; Lactarium régional d'Ile de France. AP-HP, Hôpital Necker-Enfants Malades, Paris, France., Begue H; UMR PAM Université de Bourgogne Franche-Comté (UBFC), AgroSup Dijon, Équipe Vin, Aliment, Microbiologie, Stress, Groupe Interactions Candida-muqueuses, Dijon, France., Dalle F; UMR PAM Université de Bourgogne Franche-Comté (UBFC), AgroSup Dijon, Équipe Vin, Aliment, Microbiologie, Stress, Groupe Interactions Candida-muqueuses, Dijon, France; Department of Parasitology/Mycology, Dijon Bourgogne University Hospital, Dijon, France., Bachmeyer C; Service de Médecine Interne, AP-HP, Hôpital Tenon, Paris, France., Hennequin C; Sorbonne Université, INSERM, Centre de Recherche Saint-Antoine, AP-HP, Hôpital Saint Antoine, Paris, France., Yssel H; Sorbonne Université, INSERM, Centre d'Immunologie et des Maladies Infectieuses, Paris, France., Malphettes M; Université Paris Cité, Department of Clinical Immunology, Hôpital Saint-Louis, Paris, AP-HP, France., Fieschi C; Université Paris Cité, Department of Clinical Immunology, Hôpital Saint-Louis, Paris, AP-HP, France., Fadlallah J; Université Paris Cité, Department of Clinical Immunology, Hôpital Saint-Louis, Paris, AP-HP, France., Gorochov G; Sorbonne Université, INSERM, Centre d'Immunologie et des Maladies Infectieuses, AP-HP, Hôpital Pitié-Salpêtrière, Paris, France. Electronic address: guy.gorochov@sorbonne-universite.fr.
Jazyk: angličtina
Zdroj: The Journal of allergy and clinical immunology [J Allergy Clin Immunol] 2023 Sep; Vol. 152 (3), pp. 748-759.e3. Date of Electronic Publication: 2023 May 09.
DOI: 10.1016/j.jaci.2023.03.033
Abstrakt: Background: Secretory IgA interacts with commensal bacteria, but its impact on human mycobiota ecology has not been widely explored. In particular, whether human IgA-deficiency is associated with gut fungal dysbiosis remains unknown.
Objectives: Our goal was to study the impact of IgA on gut mycobiota ecology.
Methods: The Fungi-Flow method was used to characterize fecal, systemic, and maternal IgA, IgM, and IgG responses against 14 representative fungal strains (yeast/spores or hyphae forms) in healthy donors (HDs) (n = 34, 31, and 20, respectively) and to also compare gut mycobiota opsonization by secretory antibodies in HDs (n = 28) and patients with selective IgA deficiency (SIgAd) (n = 12). Stool mycobiota composition was determined by internal transcribed spacer gene sequencing in HDs (n = 23) and patients with SIgAd (n = 17). Circulating CD4 + T-cell cytokine secretion profiles were determined by intracellular staining. The impact of secretory IgA, purified from breast milk (n = 9), on Candidaalbicans growth and intestinal Caco-2 cell invasion was tested in vitro.
Results: Homeostatic IgA binds commensal fungi with a body fluid-selective pattern of recognition. In patients with SIgAd, fungal gut ecology is preserved by compensatory IgM binding to commensal fungi. Gut Calbicans overgrowth nevertheless occurs in this condition but only in clinically symptomatic patients with decreased T H 17/T H 22 T-cell responses. Indeed, secretory IgA can reduce in vitro budding and invasion of intestinal cells by Calbicans and therefore exert control on this pathobiont.
Conclusion: IgA has a selective impact on Calbicans ecology to preserve fungal-host mutualism.
(Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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