Elevated interleukin (IL)-6 as a predictor of disease severity among Covid-19 patients: a prospective cohort study

Nikkhoo, Bahram; Mohammadi, Matin; Hasani, Sabah; Sigari, Naseh; Borhani, Aryan; Ramezani, Chia; Charajoo, Arian; Badri, Shaho; Rostami, Farzin; Etemadi, Mashala; Rahmani, Khaled

doi:10.1186/s12879-023-08294-w

Cited by 20 publications

(5 citation statements)

References 33 publications

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“…6c). These genes were selected as their expression levels have been positively correlated with COVID-19 disease severity and/or they have been proposed as potential targets for prognosis or treatment; SerpinE1 [117], Cxcl10 [118], Nfkb1 [119], IL6 [120], and Hspa1b (a Hsp70 family member) [121, 122].…”

Section: Resultsmentioning

confidence: 99%

Tracking inflammation resolution signatures in lungs after SARS-CoV-2 omicron BA.1 infection of K18-hACE2 mice

Carolin,

Yan,

Bishop

et al. 2024

Preprint

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The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes Coronavirus Disease 2019 (COVID-19), which can result in severe disease often characterised by a 'cytokine storm' and the associated acute respiratory distress syndrome. However, many infections with SARS-CoV-2 are mild or asymptomatic throughout the course of infection. Although blood biomarkers of severe disease are well studied, less well understood are the inflammatory signatures in lung tissues associated with mild disease or silent infections, wherein infection and inflammation are rapidly resolved leading to sequelae-free recovery. Herein we described RNA-Seq and histological analyses of lungs over time in an omicron BA.1/K18-hACE2 mouse infection model, which displays these latter features. Although robust infection was evident at 2 days post infection (dpi), viral RNA was largely cleared by 10 dpi. Acute inflammatory signatures showed a slightly different pattern of cytokine signatures compared with severe infection models, but where much diminished 30 dpi and absent by 66 dpi. Cellular deconvolution identified significantly increased abundance scores for a number of anti-inflammatory pro-resolution cell types at 5/10 dpi. These included type II innate lymphoid cells, T regulatory cells, and interstitial macrophages. Genes whose expression trended downwards over 2 - 66 dpi included biomarkers of severe disease and were associated with 'cytokine storm' pathways. Genes whose expression trended upward during this period were associated with recovery of ciliated cells, AT2 to AT1 transition, reticular fibroblasts and innate lymphoid cells, indicating a return to homeostasis. Very few differentially expressed host genes were identified at 66 dpi, suggesting near complete recovery. The parallels between mild or subclinical infections in humans and those observed in this BA.1/K18-hACE2 mouse model are discussed.

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Section: Resultsmentioning

confidence: 99%

Tracking inflammation resolution signatures in lungs after SARS-CoV-2 omicron BA.1 infection of K18-hACE2 mice

Carolin,

Yan,

Bishop

et al. 2024

Preprint

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“…It showed that patients with increased IL-6 levels stayed in the hospital longer and had a higher risk of intensive care unit admission and death compared to patients with lower IL-6 levels. Researchers have suggested that elevated IL-6 levels are associated with worse outcomes in patients with COVID-19, consistent with its role as a potent proinflammatory cytokine and trigger of the cytokine storm in COVID-19 [7].…”

Section: Figure 1 Predictive Value Of Selected Biomarkers For the Sev...mentioning

confidence: 89%

Prognostic properties of biomarkers in COVID-19 infection and concomitant chronic coronary syndromes

Tomyn,

Fedorov

2024

ЕМ

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Background. The novel coronavirus disease 2019 (COVID-19), caused by a severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has become an unprecedented challenge for the health care system and has taken a leading position among infectious diseases due to the rapid spread and development of complications from various body systems. The problem of cardiac comorbidity in COVID-19 has several aspects: the impact of concomitant cardiovascular diseases on the incidence of a new viral infection, its severity and risk of mortality, as well as possible side effects of a number of drugs traditionally used to treat certain types of cardiovascular diseases. SARS-CoV-2 is not only a pneumonia pathogen, but also causes serious systemic consequences. Patients with cardiovascular diseases and risk factors for cardiovascular complications, such as hypertension and coronary heart disease, are more exposed to fatal consequences of COVID-19. In addition, a significant proportion of patients develop COVID-associated myocardial injury, which significantly increases the risk of in-hospital mortality. The purpose of the study was to investigate the prognostic role of individual biomarkers in patients with COVID-19-associated pneumonia on the background of chronic coronary syndromes. Materials and methods. This study was defined as an open-label, non-randomized, controlled, comparative one in parallel groups. 124 patients with COVID-19-associated pneumonia were selected upon admission, including 92 participants with a history of chronic coronary syndromes. Results. The study showed that elevated levels of biomarkers such as proinflammatory cytokine interleukin-6, iron-storage protein ferritin, serum angiotensin-converting enzyme-2, ketone body beta-hydroxybutyric acid, and fibrin breakdown product D-dimer may be associated with a more severe course of pneumonia caused by COVID-19 infection. Thus, these biomarkers had good prognostic value in predicting severe disease and death in patients with chronic coronary syndromes during hospitalization. Conclusions. The study confirms that an increase in the level of proinflammatory biomarkers is a predictor for the development of a severe coronavirus infection.

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“…IL-6, a pro-inflammatory cytokine, plays a crucial role in the immune response and inflammation. Previous suggestions have implicated its involvement in the severity of COVID-19, with elevated IL-6 levels being associated with a more severe disease course [ 18 , 19 ]. Understanding the genetic factors that influence the severity of COVID-19 disease has clinical implications.…”

Section: Discussionmentioning

confidence: 99%

The Interleukin-6 gene variants may protect against SARS-CoV-2 infection and the severity of COVID-19: a case-control study in a Moroccan population

Noureddine,

Baba,

Aqillouch

et al. 2024

BMC Med Genomics

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The symptoms of SARS-CoV-2 infection vary widely, ranging from asymptomatic cases to severe forms marked by acute respiratory distress syndrome, multi-organ damage, and fatalities. Studies indicate a correlation between specific genes and susceptibility to SARS-CoV-2 infection and disease severity, particularly involving variants in genes linked to inflammation and immune responses. The objective of this study is to investigate the association between rs1800795 (− 174 G > C) and rs1800797 (− 597 A > G) variants in the interleukin-6 (IL-6) promoter region and susceptibility to SARS-CoV-2 infection. Additionally, we aim to explore their correlation with COVID-19 severity in a Moroccan population. In this case-control study, we enrolled 270 unvaccinated COVID-19 patients, consisting of 132 with severe COVID-19 and 138 with asymptomatic-moderate COVID-19. Additionally, we included 339 SARS-CoV-2-negative group. Genotyping of rs1800795 and rs1800797 polymorphisms of the IL-6 gene was performed using predesigned TaqMan SNP genotyping. The median age of SARS-CoV-2-negative controls was 50 years, while severe COVID-19 cases exhibited a median age of 61 years. Additionally, individuals with asymptomatic to moderate COVID-19 had a median age of 36 years. We observed a significant age difference between severe and mild COVID-19 patients (p < 0.0001), and an association was noted between gender and the severity of COVID-19 (p = 0.011). The allele and genotype frequencies of the IL-6 − 597G > A and − 174G > C variants did not show significant associations with susceptibility to SARS-CoV-2 infection (p > 0.05). However, further analysis revealed that the linkage disequilibrium between rs1800797 and rs1800795 indicated that individuals with the GC* haplotype (OR = 0.04, 95% CI 0.01–0.30, p = 0.001) and AG* haplotype (OR = 0.11, 95% CI 0.03–0.46, p = 0.002) were significantly associated with protection against SARS-CoV-2 infection. Moreover, in the overdominant model, the IL-6 − 174 G/C genotype was found to be protective against the development of severe disease compared to those with the G/G-C/C genotypes (p = 0.03; OR = 0.41, 95% CI 0.18–0.96). However, correlations between complete blood count markers, hematological markers, D-dimer, C-reactive protein, and ferritin levels according to − 597 A > G and − 174G > C genotypes showed no significant differences (all p > 0.05). Our findings provide valuable insights into the pathogenesis of COVID-19, suggesting that genetic variations at the IL-6 gene may contribute to the susceptibility to severe SARS-CoV-2 infection within the Moroccan population.

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Elevated interleukin (IL)-6 as a predictor of disease severity among Covid-19 patients: a prospective cohort study

Cited by 20 publications

References 33 publications

Tracking inflammation resolution signatures in lungs after SARS-CoV-2 omicron BA.1 infection of K18-hACE2 mice

Tracking inflammation resolution signatures in lungs after SARS-CoV-2 omicron BA.1 infection of K18-hACE2 mice

Prognostic properties of biomarkers in COVID-19 infection and concomitant chronic coronary syndromes

The Interleukin-6 gene variants may protect against SARS-CoV-2 infection and the severity of COVID-19: a case-control study in a Moroccan population

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