Inflammation and kidney involvement in human viral diseases caused by SARS-CoV-2, HIV, HCV and HBV

Mata, Gustavo Ferreira da; Fernandes, Danilo Euclides; Luciano, Eduardo de Paiva; Sales, Gabriel Teixeira Montezuma; Riguetti, Michelle Tiveron Passos; Kirsztajn, Gianna Mastroianni

doi:10.1590/1678-9199-jvatitd-2020-0154

Cited by 5 publications

(4 citation statements)

References 77 publications

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“…Severe COVID-19 patients that developed AKI had increased levels of proinflammatory cytokines (e.g., IFN-g, IL-1b, IL-8 and TNF-a) compared with non-severe patients (181). Inflammasomes are likely an underlying contributor to hyperactivated inflammatory response and vascular thrombosis that consequently lead to AKI in COVID-19 patients (182). Moreover, the cytokine storm may cause renal impairment by triggering intrarenal inflammation (183).…”

Section: Inflammasome Activation and Other Pathologiesmentioning

confidence: 99%

Inflammasomes: a rising star on the horizon of COVID-19 pathophysiology

Wang

Chang

et al. 2023

Front. Immunol.

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a contagious respiratory virus that is the cause of the coronavirus disease 2019 (COVID-19) pandemic which has posed a serious threat to public health. COVID-19 is characterized by a wide spectrum of clinical manifestations, ranging from asymptomatic infection to mild cold-like symptoms, severe pneumonia or even death. Inflammasomes are supramolecular signaling platforms that assemble in response to danger or microbial signals. Upon activation, inflammasomes mediate innate immune defense by favoring the release of proinflammatory cytokines and triggering pyroptotic cell death. Nevertheless, abnormalities in inflammasome functioning can result in a variety of human diseases such as autoimmune disorders and cancer. A growing body of evidence has showed that SARS-CoV-2 infection can induce inflammasome assembly. Dysregulated inflammasome activation and consequent cytokine burst have been associated with COVID-19 severity, alluding to the implication of inflammasomes in COVID-19 pathophysiology. Accordingly, an improved understanding of inflammasome-mediated inflammatory cascades in COVID-19 is essential to uncover the immunological mechanisms of COVID-19 pathology and identify effective therapeutic approaches for this devastating disease. In this review, we summarize the most recent findings on the interplay between SARS-CoV-2 and inflammasomes and the contribution of activated inflammasomes to COVID-19 progression. We dissect the mechanisms involving the inflammasome machinery in COVID-19 immunopathogenesis. In addition, we provide an overview of inflammasome-targeted therapies or antagonists that have potential clinical utility in COVID-19 treatment.

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Section: Inflammasome Activation and Other Pathologiesmentioning

confidence: 99%

Inflammasomes: a rising star on the horizon of COVID-19 pathophysiology

Wang

Chang

et al. 2023

Front. Immunol.

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“…Despite the role of elevated IL-8 levels in other disease-associated AKIs, little is known about their association with COVID-19-associated AKI. Critical SARS-CoV-2-associated AKI patients depict an increase in inflammatory cytokine levels (IL-1β, IL-8, IFN-γ, TNF-α), favoring renal dysfunction through intrarenal inflammation, elevated vascular permeability, volume depletion, microvasculature thromboembolic events, and persistent local inflammation [ 29 ]. Therefore, multiple chemokines were selected within 24 h of recruitment, such as IL-8, to predict persistent AKI.…”

Section: Discussionmentioning

confidence: 99%

Serum chemokine IL-8 acts as a biomarker for identifying COVID-19-associated persistent severe acute kidney injury

He,

Liu,

2024

Renal Failure

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Objectives Persistent severe acute kidney injury (PS-AKI) is associated with poor clinical outcomes. Our study attempted to evaluate the diagnostic value of chemokines for early-stage PS-AKI prediction. Methods According to the KDIGO criteria, 115 COVID-19 patients diagnosed with stage 2/3 AKI were recruited from the intensive care unit between December 2022 and February 2023. Primary clinical outcomes included detecting PS-AKI in the first week (≥ KDIGO stage 2 ≥ 72 h). Cytometric Bead Array was used to detect patient plasma levels (interleukin-8 (IL-8), C-C chemokine ligand 5 (CCL5), chemokine (C-X-C Motif) ligand 9 (CXCL9), and interferon-inducible protein 10 (IP-10)) of chemokines within 24 h of enrollment. Results Of the 115 COVID-19 patients with stage 2/3 AKI, 27 were diagnosed with PS-AKI. Among the four measured chemokines, only the IL-8 level was significantly elevated in the PS-AKI group than in the Non-PS-AKI group. IL-8 was more effective as a biomarker while predicting PS-AKI with an area under the curve of 0.769 (0.675-0.863). This was superior to other biomarkers related to AKI, including serum creatinine. Moreover, plasma IL-8 levels of >32.2 pg/ml on admission could predict PS-AKI risk (sensitivity = 92.6%, specificity = 51.1%). Additionally, the IL-8 level was associated with total protein and IL-6 levels. Conclusion Plasma IL-8 is a promising marker for the early identification of PS-AKI among COVID-19 patients. These findings should be validated in further studies with a larger sample size.

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“…The pathway of "Hepatitis B" has been enriched in the KEGG pathway analysis. The impaired liver function, although poorly understood, is an important clinically significant outcome after COVID-19 infection (da Mata et al, 2021;Yu et al, 2021). COVID-19 can also trigger hepatitis B reactivation, but no direct pathophysiological overlap between both diseases has been reported to date (Aldhaleei et al, 2020;.…”

Section: Viral Infection Pathwaysmentioning

confidence: 99%

Shared miRNA landscapes of COVID-19 and neurodegeneration confirm neuroinflammation as an important overlapping feature

Trampuž

Vogrinc

Goričar

et al. 2023

Front. Mol. Neurosci.

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IntroductionDevelopment and worsening of most common neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease, and multiple sclerosis, have been associated with COVID-19 However, the mechanisms associated with neurological symptoms in COVID-19 patients and neurodegenerative sequelae are not clear. The interplay between gene expression and metabolite production in CNS is driven by miRNAs. These small non-coding molecules are dysregulated in most common neurodegenerative diseases and COVID-19.MethodsWe have performed a thorough literature screening and database mining to search for shared miRNA landscapes of SARS-CoV-2 infection and neurodegeneration. Differentially expressed miRNAs in COVID-19 patients were searched using PubMed, while differentially expressed miRNAs in patients with five most common neurodegenerative diseases (Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, amyotrophic lateral sclerosis, and multiple sclerosis) were searched using the Human microRNA Disease Database. Target genes of the overlapping miRNAs, identified with the miRTarBase, were used for the pathway enrichment analysis performed with Kyoto Encyclopedia of Genes and Genomes and Reactome.ResultsIn total, 98 common miRNAs were found. Additionally, two of them (hsa-miR-34a and hsa-miR-132) were highlighted as promising biomarkers of neurodegeneration, as they are dysregulated in all five most common neurodegenerative diseases and COVID-19. Additionally, hsa-miR-155 was upregulated in four COVID-19 studies and found to be dysregulated in neurodegeneration processes as well. Screening for miRNA targets identified 746 unique genes with strong evidence for interaction. Target enrichment analysis highlighted most significant KEGG and Reactome pathways being involved in signaling, cancer, transcription and infection. However, the more specific identified pathways confirmed neuroinflammation as being the most important shared feature.DiscussionOur pathway based approach has identified overlapping miRNAs in COVID-19 and neurodegenerative diseases that may have a valuable potential for neurodegeneration prediction in COVID-19 patients. Additionally, identified miRNAs can be further explored as potential drug targets or agents to modify signaling in shared pathways.Graphical AbstractShared miRNA molecules among the five investigated neurodegenerative diseases and COVID-19 were identified. The two overlapping miRNAs, hsa-miR-34a and has-miR-132, present potential biomarkers of neurodegenerative sequelae after COVID-19. Furthermore, 98 common miRNAs between all five neurodegenerative diseases together and COVID-19 were identified. A KEGG and Reactome pathway enrichment analyses was performed on the list of shared miRNA target genes and finally top 20 pathways were evaluated for their potential for identification of new drug targets. A common feature of identified overlapping miRNAs and pathways is neuroinflammation. AD, Alzheimer’s disease; ALS, amyotrophic lateral sclerosis; COVID-19, coronavirus disease 2019; HD, Huntington’s disease; KEGG, Kyoto Encyclopedia of Genes and Genomes; MS, multiple sclerosis; PD, Parkinson’s disease.

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Inflammation and kidney involvement in human viral diseases caused by SARS-CoV-2, HIV, HCV and HBV

Cited by 5 publications

References 77 publications

Inflammasomes: a rising star on the horizon of COVID-19 pathophysiology

Inflammasomes: a rising star on the horizon of COVID-19 pathophysiology

Serum chemokine IL-8 acts as a biomarker for identifying COVID-19-associated persistent severe acute kidney injury

Shared miRNA landscapes of COVID-19 and neurodegeneration confirm neuroinflammation as an important overlapping feature

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