Serological and cellular inflammatory signatures in end‐stage kidney disease and latent tuberculosis

Abstract Objectives Tuberculosis comorbidity with chronic diseases including diabetes, HIV and chronic kidney disease is of rising concern. In particular, latent tuberculosis infection (LTBI) comorbidity with end‐stage kidney disease (ESKD) is associated with up to 52.5‐fold increased risk of TB rea...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Milla R McLean, Kathleen M Wragg, Ester Lopez, Sandra A Kiazyk, Terry Blake Ball, Joe Bueti, Stephen J Kent, Jennifer A Juno, Amy W Chung
Formato:	article
Lenguaje:	EN
Publicado:	Wiley 2021
Materias:	end‐stage kidney disease glycosylation inflammation monocytes tuberculosis unconventional T cells Immunologic diseases. Allergy RC581-607
Acceso en línea:	https://doaj.org/article/76cfc55d07b34fe8b4af19c8ed672243
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:76cfc55d07b34fe8b4af19c8ed672243
record_format	dspace
spelling	oai:doaj.org-article:76cfc55d07b34fe8b4af19c8ed6722432021-11-25T13:32:30ZSerological and cellular inflammatory signatures in end‐stage kidney disease and latent tuberculosis2050-006810.1002/cti2.1355https://doaj.org/article/76cfc55d07b34fe8b4af19c8ed6722432021-01-01T00:00:00Zhttps://doi.org/10.1002/cti2.1355https://doaj.org/toc/2050-0068Abstract Objectives Tuberculosis comorbidity with chronic diseases including diabetes, HIV and chronic kidney disease is of rising concern. In particular, latent tuberculosis infection (LTBI) comorbidity with end‐stage kidney disease (ESKD) is associated with up to 52.5‐fold increased risk of TB reactivation to active tuberculosis infection (ATBI). The immunological mechanisms driving this significant rise in TB reactivation are poorly understood. To contribute to this understanding, we performed a comprehensive assessment of soluble and cellular immune features amongst a unique cohort of patients comorbid with ESKD and LTBI. Methods We assessed the plasma and cellular immune profiles from patients with and without ESKD and/or LTBI (N = 40). We characterised antibody glycosylation, serum complement and cytokine levels. We also assessed classical and non‐classical monocytes and T cells with flow cytometry. Using a systems‐based approach, we identified key immunological features that discriminate between the different disease states. Results Individuals with ESKD exhibited a highly inflammatory plasma profile and an activated cellular state compared with those without ESKD, including higher levels of inflammatory antibody Fc glycosylation structures and activated CX3CR1+ monocytes that correlate with increased inflammatory plasma cytokines. Similar elevated inflammatory signatures were also observed in ESKD+/LTBI+ compared with ESKD−/LTBI+, suggesting that ESKD induces an overwhelming inflammatory immune state. In contrast, no significant inflammatory differences were observed when comparing LTBI+ and LTBI− individuals. Conclusion Our study highlights the highly inflammatory state induced by ESKD. We hypothesise that this inflammatory state could contribute to the increased risk of TB reactivation in ESKD patients.Milla R McLeanKathleen M WraggEster LopezSandra A KiazykTerry Blake BallJoe BuetiStephen J KentJennifer A JunoAmy W ChungWileyarticleend‐stage kidney diseaseglycosylationinflammationmonocytestuberculosisunconventional T cellsImmunologic diseases. AllergyRC581-607ENClinical & Translational Immunology, Vol 10, Iss 11, Pp n/a-n/a (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	end‐stage kidney disease glycosylation inflammation monocytes tuberculosis unconventional T cells Immunologic diseases. Allergy RC581-607
spellingShingle	end‐stage kidney disease glycosylation inflammation monocytes tuberculosis unconventional T cells Immunologic diseases. Allergy RC581-607 Milla R McLean Kathleen M Wragg Ester Lopez Sandra A Kiazyk Terry Blake Ball Joe Bueti Stephen J Kent Jennifer A Juno Amy W Chung Serological and cellular inflammatory signatures in end‐stage kidney disease and latent tuberculosis
description	Abstract Objectives Tuberculosis comorbidity with chronic diseases including diabetes, HIV and chronic kidney disease is of rising concern. In particular, latent tuberculosis infection (LTBI) comorbidity with end‐stage kidney disease (ESKD) is associated with up to 52.5‐fold increased risk of TB reactivation to active tuberculosis infection (ATBI). The immunological mechanisms driving this significant rise in TB reactivation are poorly understood. To contribute to this understanding, we performed a comprehensive assessment of soluble and cellular immune features amongst a unique cohort of patients comorbid with ESKD and LTBI. Methods We assessed the plasma and cellular immune profiles from patients with and without ESKD and/or LTBI (N = 40). We characterised antibody glycosylation, serum complement and cytokine levels. We also assessed classical and non‐classical monocytes and T cells with flow cytometry. Using a systems‐based approach, we identified key immunological features that discriminate between the different disease states. Results Individuals with ESKD exhibited a highly inflammatory plasma profile and an activated cellular state compared with those without ESKD, including higher levels of inflammatory antibody Fc glycosylation structures and activated CX3CR1+ monocytes that correlate with increased inflammatory plasma cytokines. Similar elevated inflammatory signatures were also observed in ESKD+/LTBI+ compared with ESKD−/LTBI+, suggesting that ESKD induces an overwhelming inflammatory immune state. In contrast, no significant inflammatory differences were observed when comparing LTBI+ and LTBI− individuals. Conclusion Our study highlights the highly inflammatory state induced by ESKD. We hypothesise that this inflammatory state could contribute to the increased risk of TB reactivation in ESKD patients.
format	article
author	Milla R McLean Kathleen M Wragg Ester Lopez Sandra A Kiazyk Terry Blake Ball Joe Bueti Stephen J Kent Jennifer A Juno Amy W Chung
author_facet	Milla R McLean Kathleen M Wragg Ester Lopez Sandra A Kiazyk Terry Blake Ball Joe Bueti Stephen J Kent Jennifer A Juno Amy W Chung
author_sort	Milla R McLean
title	Serological and cellular inflammatory signatures in end‐stage kidney disease and latent tuberculosis
title_short	Serological and cellular inflammatory signatures in end‐stage kidney disease and latent tuberculosis
title_full	Serological and cellular inflammatory signatures in end‐stage kidney disease and latent tuberculosis
title_fullStr	Serological and cellular inflammatory signatures in end‐stage kidney disease and latent tuberculosis
title_full_unstemmed	Serological and cellular inflammatory signatures in end‐stage kidney disease and latent tuberculosis
title_sort	serological and cellular inflammatory signatures in end‐stage kidney disease and latent tuberculosis
publisher	Wiley
publishDate	2021
url	https://doaj.org/article/76cfc55d07b34fe8b4af19c8ed672243
work_keys_str_mv	AT millarmclean serologicalandcellularinflammatorysignaturesinendstagekidneydiseaseandlatenttuberculosis AT kathleenmwragg serologicalandcellularinflammatorysignaturesinendstagekidneydiseaseandlatenttuberculosis AT esterlopez serologicalandcellularinflammatorysignaturesinendstagekidneydiseaseandlatenttuberculosis AT sandraakiazyk serologicalandcellularinflammatorysignaturesinendstagekidneydiseaseandlatenttuberculosis AT terryblakeball serologicalandcellularinflammatorysignaturesinendstagekidneydiseaseandlatenttuberculosis AT joebueti serologicalandcellularinflammatorysignaturesinendstagekidneydiseaseandlatenttuberculosis AT stephenjkent serologicalandcellularinflammatorysignaturesinendstagekidneydiseaseandlatenttuberculosis AT jenniferajuno serologicalandcellularinflammatorysignaturesinendstagekidneydiseaseandlatenttuberculosis AT amywchung serologicalandcellularinflammatorysignaturesinendstagekidneydiseaseandlatenttuberculosis
_version_	1718413444473946112

Serological and cellular inflammatory signatures in end‐stage kidney disease and latent tuberculosis

Ejemplares similares