4.8 Article

Chronic Inflammation Might Protect Hemodialysis Patients From Severe COVID-19

Journal

FRONTIERS IN IMMUNOLOGY
Volume 13, Issue -, Pages -

Publisher

FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2022.821818

Keywords

inflammation; COVID-19; hemodialysis patients; CD8(+) T cells; cytokines

Categories

Funding

  1. Austrian Science Funds (FWF) [W1241]
  2. Austrian National Bank OeNB [.17212]
  3. Chiesi - Austrian Federal Government within the COMET K1 Centre Program, Land Steiermark and Land Wien
  4. [MOLIN PhD program W1241]

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HD patients may be protected from severe COVID-19 due to their chronic inflammatory state, characterized by increased specific immune cells, while non-HD patients show the opposite results in severe COVID-19.
Hemodialysis patients (HD) are expected to have excess mortality in coronavirus disease 2019 (COVID-19). This was challenged by a recent study reporting HD patients to have comparable mortality and less ICU admissions when hospitalized with COVID-19. An altered immune system due to chronic inflammation might protect HD-patients from severe COVID-19. Therefore, we aimed to describe the peripheral blood immune phenotype in HD-patients and respective controls with COVID-19. MethodsSixty-four patients (31 HD, 33 non-HD) with PCR-confirmed COVID-19 and 16 control patients (10 HD, 6 non-HD) were prospectively included. According to symptoms, COVID-19 patients were categorized as asymptomatic/mild, moderate or severe COVID-19 phenotypes. Cytokine profiling and immune phenotyping was performed. ResultsTh1 and Th17 plasma cytokine levels were highly increased in HD patients without COVID-19 and were not significantly regulated during COVID-19. In non-HD COVID-19 patients these cytokines increased significantly with disease severity. While all patients with moderate or severe COVID-19 showed hallmarks of COVID-19 such as decreased CD3(+), CD4(+) and CD8(+) and CD4(+)CD25(hi)FoxP3(+) regulatory T cells, significantly increased CD38(+)CD8(+) effector memory and CD38(+)CD8(+) TEMRA T cells were detected in moderate/severe COVID-19 HD patients, which was not observed in non-HD patients with moderate or severe COVID-19. Furthermore, CD161(+)CD8(+) T cells decreased significantly in non-HD COVID-19 patients dependent on disease severity, but not in HD patients. Dynamics of B cells and subtypes were comparable in HD and non-HD COVID-19 patients. ConclusionsHD patients might be protected from severe COVID-19 due to their chronic inflammatory state with increased CD38(+)CD8(+) effector memory and TEMRA T cells as well as CD161(+)CD8(+) T cells.

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