Neutrophils in the Pathogenesis of Rheumatic Diseases: Fueling the Fire

Liu, Yudong; Kaplan, Mariana J.

doi:10.1007/s12016-020-08816-3

Cited by 28 publications

(20 citation statements)

References 163 publications

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“…A particular phenotype of ME/CFS has been termed post-infectious fatigue syndrome, and it has been linked to acute viral infections such as Epstein–Barr virus (EBV) and human parvovirus (HPV)-B19 [ 74 , 75 ]. While the etiology of long COVID is likely multifaceted and the research is still ongoing, it has been similarly linked to inflammatory state and dysregulated immune response [ 76 , 77 ], further underlying the resemblance between long COVID and ME/CFS [ 78 ].…”

Section: Discussionmentioning

confidence: 99%

Long COVID and Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)—A Systemic Review and Comparison of Clinical Presentation and Symptomatology

2021

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Background and Objectives: Long COVID defines a series of chronic symptoms that patients may experience after resolution of acute COVID-19. Early reports from studies with patients with long COVID suggests a constellation of symptoms with similarities to another chronic medical illness—myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). A review study comparing and contrasting ME/CFS with reported symptoms of long COVID may yield mutualistic insight into the characterization and management of both conditions. Materials and Methods: A systemic literature search was conducted in MEDLINE and PsycInfo through to 31 January 2021 for studies related to long COVID symptomatology. The literature search was conducted in accordance with PRISMA methodology. Results: Twenty-one studies were included in the qualitative analysis. Long COVID symptoms reported by the included studies were compared to a list of ME/CFS symptoms compiled from multiple case definitions. Twenty-five out of 29 known ME/CFS symptoms were reported by at least one selected long COVID study. Conclusions: Early studies into long COVID symptomatology suggest many overlaps with clinical presentation of ME/CFS. The need for monitoring and treatment for patients post-COVID is evident. Advancements and standardization of long COVID research methodologies would improve the quality of future research, and may allow further investigations into the similarities and differences between long COVID and ME/CFS.

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Section: Discussionmentioning

confidence: 99%

Long COVID and Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)—A Systemic Review and Comparison of Clinical Presentation and Symptomatology

2021

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“…The global vaccination program against SARS-CoV-2 is actively ongoing, and the incidence of COVID-19 will soon decrease reasonably worldwide. Nevertheless, among the millions of COVID-19 survivors, many will require long-term assistance due to increased post-COVID-19 clinical sequelae defined as PPCS [ 37 , 38 ]. Despite the several manifestations associated with PPCS, there is a lack of potentially valuable molecular biomarkers for the monitoring of PPCS onset and evolution.…”

Section: Discussionmentioning

confidence: 99%

Evidence for Biological Age Acceleration and Telomere Shortening in COVID-19 Survivors

Mongelli

Barbi

zamperla

et al. 2021

IJMS

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The SARS-CoV-2 infection determines the COVID-19 syndrome characterized, in the worst cases, by severe respiratory distress, pulmonary and cardiac fibrosis, inflammatory cytokine release, and immunosuppression. This condition has led to the death of about 2.15% of the total infected world population so far. Among survivors, the presence of the so-called persistent post-COVID-19 syndrome (PPCS) is a common finding. In COVID-19 survivors, PPCS presents one or more symptoms: fatigue, dyspnea, memory loss, sleep disorders, and difficulty concentrating. In this study, a cohort of 117 COVID-19 survivors (post-COVID-19) and 144 non-infected volunteers (COVID-19-free) was analyzed using pyrosequencing of defined CpG islands previously identified as suitable for biological age determination. The results show a consistent biological age increase in the post-COVID-19 population, determining a DeltaAge acceleration of 10.45 ± 7.29 years (+5.25 years above the range of normality) compared with 3.68 ± 8.17 years for the COVID-19-free population (p < 0.0001). A significant telomere shortening parallels this finding in the post-COVID-19 cohort compared with COVID-19-free subjects (p < 0.0001). Additionally, ACE2 expression was decreased in post-COVID-19 patients, compared with the COVID-19-free population, while DPP-4 did not change. In light of these observations, we hypothesize that some epigenetic alterations are associated with the post-COVID-19 condition, particularly in younger patients (< 60 years).

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“…Survivors, and those with milder presentations, may suffer from loss of normal tissue function due to persistent inflammation and/or fibrosis. ( 2 , 3 ). The pathogenesis of COVID-19 and the causes of its variable severity are poorly understood, thus a better mechanistic understanding of the disease will help identify at-risk patients and allow for the development and refinement of much-needed treatments.…”

Section: Introductionmentioning

confidence: 99%

SARS-CoV-2 drives JAK1/2-dependent local complement hyperactivation

et al. 2021

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Patients with coronavirus disease 2019 (COVID-19) present a wide range of acute clinical manifestations affecting the lungs, liver, kidneys and gut. Angiotensin converting enzyme (ACE) 2, the best-characterized entry receptor for the disease-causing virus SARS-CoV-2, is highly expressed in the aforementioned tissues. However, the pathways that underlie the disease are still poorly understood. Here, we unexpectedly found that the complement system was one of the intracellular pathways most highly induced by SARS-CoV-2 infection in lung epithelial cells. Infection of respiratory epithelial cells with SARS-CoV-2 generated activated complement component C3a and could be blocked by a cell-permeable inhibitor of complement factor B (CFBi), indicating the presence of an inducible cell-intrinsic C3 convertase in respiratory epithelial cells. Within cells of the bronchoalveolar lavage of patients, distinct signatures of complement activation in myeloid, lymphoid and epithelial cells tracked with disease severity. Genes induced by SARS-CoV-2 and the drugs that could normalize these genes both implicated the interferon-JAK1/2-STAT1 signaling system and NF-κB as the main drivers of their expression. Ruxolitinib, a JAK1/2 inhibitor, normalized interferon signature genes and all complement gene transcripts induced by SARS-CoV-2 in lung epithelial cell lines, but did not affect NF-κB-regulated genes. Ruxolitinib, alone or in combination with the antiviral remdesivir, inhibited C3a protein produced by infected cells. Together, we postulate that combination therapy with JAK inhibitors and drugs that normalize NF-κB-signaling could potentially have clinical application for severe COVID-19.

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Neutrophils in the Pathogenesis of Rheumatic Diseases: Fueling the Fire

Cited by 28 publications

References 163 publications

Long COVID and Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)—A Systemic Review and Comparison of Clinical Presentation and Symptomatology

Long COVID and Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)—A Systemic Review and Comparison of Clinical Presentation and Symptomatology

Evidence for Biological Age Acceleration and Telomere Shortening in COVID-19 Survivors

SARS-CoV-2 drives JAK1/2-dependent local complement hyperactivation

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