Cytokine profiles in the detection of severe lung involvement in hospitalized patients with COVID-19: The IL-8/IL-32 axis

Bergantini, Laura; d’Alessandro, Miriana; Cameli, Paolo; Otranto, Ambra; Luzzi, Simona; Bianchi, Francesco Paolo; Bargagli, Elena

doi:10.1016/j.cyto.2022.155804

Cited by 27 publications

(28 citation statements)

References 38 publications

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“…Significant differences at p < 0.05 are indicated by asterisk (*) as compared to NI and by connecting lines for comparisons between Discharge versus Death. (25) or increased levels in COVID-19 patients (30). Our findings indicated elevated levels of IL-1b only systemically in COVID-19 patients and no significance was found either in airway or when groups with distinct outcomes were compared.…”

Section: Discussioncontrasting

confidence: 65%

Timeline Kinetics of Systemic and Airway Immune Mediator Storm for Comprehensive Analysis of Disease Outcome in Critically Ill COVID-19 Patients

et al. 2022

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In the present study, the levels of serum and airway soluble chemokines, pro-inflammatory/regulatory cytokines, and growth factors were quantified in critically ill COVID-19 patients (total n=286) at distinct time points (D0, D2-6, D7, D8-13 and D>14-36) upon Intensive Care Unit (ICU) admission. Augmented levels of soluble mediators were observed in serum from COVID-19 patients who progress to death. An opposite profile was observed in tracheal aspirate samples, indicating that systemic and airway microenvironment diverge in their inflammatory milieu. While a bimodal distribution was observed in the serum samples, a unimodal peak around D7 was found for most soluble mediators in tracheal aspirate samples. Systems biology tools further demonstrated that COVID-19 display distinct eccentric soluble mediator networks as compared to controls, with opposite profiles in serum and tracheal aspirates. Regardless the systemic-compartmentalized microenvironment, networks from patients progressing to death were linked to a pro-inflammatory/growth factor-rich, highly integrated center. Conversely, patients evolving to discharge exhibited networks of weak central architecture, with lower number of neighborhood connections and clusters of pro-inflammatory and regulatory cytokines. All in all, this investigation with robust sample size landed a comprehensive snapshot of the systemic and local divergencies composed of distinct immune responses driven by SARS-CoV-2 early on severe COVID-19.

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Section: Discussioncontrasting

confidence: 65%

Timeline Kinetics of Systemic and Airway Immune Mediator Storm for Comprehensive Analysis of Disease Outcome in Critically Ill COVID-19 Patients

et al. 2022

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“…Most of the studies identified "cytokine storm" as the pathogenetic mechanism leading to fibrosis, based on the release of proinflammatory cytokines. In fact, aberrant inflammation associated with dysregulated repair mechanisms and fibrogenesis can lead to fibrogenesis (Bergantini et al, 2021b;Bergantini et al, 2022). Changes in the cellular and molecular environment in lung tissue secondary to viral infection, as found in COVID-19, were the key factors behind fibrosis development.…”

Section: Cytokine Pathways and Development Of Fibrosismentioning

confidence: 99%

Common Molecular Pathways Between Post-COVID19 Syndrome and Lung Fibrosis: A Scoping Review

et al. 2022

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The pathogenetic mechanism of post-Covid-19 pulmonary fibrosis is currently a topic of intense research interest, but still largely unexplored. The aim of this work was to carry out a systematic exploratory search of the literature (Scoping review) to identify and systematize the main pathogenetic mechanisms that are believed to be involved in this phenomenon, in order to highlight the same molecular aspect of the lung. These aims could be essential in the future for therapeutic management. We identified all primary studies involving in post COVID19 syndrome with pulmonary fibrosis as a primary endpoint by performing data searches in various systematic review databases. Two reviewers independently reviewed all abstracts (398) and full text data. The quality of study has been assess through SANRA protocol. A total of 32 studies involving were included, included the possible involvement of inflammatory cytokines, concerned the renin-angiotensin system, the potential role of galectin-3, epithelial injuries in fibrosis, alveolar type 2 involvement, Neutrophil extracellular traps (NETs) and the others implied other specific aspects (relationship with clinical and mechanical factors, epithelial transition mesenchymal, TGF-β signaling pathway, midkine, caspase and macrophages, genetics). In most cases, these were narrative reviews or letters to the editor, except for 10 articles, which presented original data, albeit sometimes in experimental models. From the development of these researches, progress in the knowledge of the phenomenon and hopefully in its prevention and therapy may originate.

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“… 6 , 7 It is reported that changes in immune cells and different cytokines along with clinical and biochemical indexes can be served as predicting factors for clarifying disease severity and survival for patients with COVID-19. 8 The reduced numbers of lymphocytes and elevated levels of erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are the most frequent abnormalities associated with COVID-19 and contribute to acute lung injury. 5 …”

Section: Introductionmentioning

confidence: 99%

“…Until now, many cytokines and chemokines along with immune cells have been investigated to clarify their roles in COVID-19 pathogenesis and provide a targeted personalized approach for its management. 8 , 9 Severe COVID-19 patients show the increased levels of IL-1, IL-8, IL-6, and tumor necrosis factor-alpha (TNF-α), and a decreased expression of IFN-γ. 6 , 10 , 11…”

Section: Introductionmentioning

confidence: 99%

“…Although a few studies have reported the levels of IL-27 and IL-32 in COVID-19, 8 , 16 , 17 impacts of these cytokines on the disease severity and mechanisms involved in their roles in the disease development have not yet been identified. Therefore, this study was focused on determining whether the levels of IL-27 and IL-32 are associated with the severity and progression of COVID-19.…”

Section: Introductionmentioning

confidence: 99%

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Predicting roles of IL-27 and IL-32 in determining the severity and outcome of COVID-19

Zamani

Najafizadeh

Motedayyen

et al. 2022

Int J Immunopathol Pharmacol

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Objective Immune changes play fundamental roles in the pathogenesis and severity of coronavirus disease 2019 (COVID-19). Previous studies have revealed alterations in immune responses of patients with non-severe and severe COVID-19. Therefore, this study investigated whether interleukin-27 (IL-27) and interleukin-32 (IL-32) levels may be considered as predicting factors for determining the severity and outcome of COVID-19. Methods The blood samples were collected from 50 non-severe and severe patients infected with COVID-19 and 25 healthy subjects. The serum samples were isolated from the whole blood. The levels of IL-27 and IL-32 were measured by enzyme-linked immunosorbent assay and percentages of some immune cells were studied by cell counter. Results The levels of IL-27 and IL-32 were significantly higher in COVID-19 patients than healthy subjects ( p < 0.0001–0.01). IL-27 was significantly reduced in severe COVID-19 patients who needed to undergo ICU therapy ( p < 0.05). Disease severity was significantly associated with IL-27 level in patients with COVID-19 ( p < 0.05), unlike IL-32 level. There was a significant association between IL-27 and IL-32 in participants ( p < 0.0001, odds ratio (OR) = 0.9873; 95% confidence interval (CI) = 0.9998 to 1.000; p < 0.05, OR = 0.4462; 95% CI = 0.08,579 to 0.7802; p < 0.01, OR = 0.6640, 95% CI = 0.3007–0.8590). IL-27 level was significantly higher in the recovered subjects than dead cases ( p < 0.0001). IL-27 and IL-32 levels in patients who had fever were significantly higher than those who did not have ( p < 0.01–0.05), unlike patients who suffered from cough ( p < 0.001–0.01). The IL-27 level in patients with non-severe COVID-19 was directly correlated with CRP value ( p < 0.05, OR = 0.5,722,357, 95% CI = 0.06,807,176–0.8,435,928). IL-27 and IL-32 levels in non-severe patients were positively associated with NLR ( p < 0.01, OR = 0.7292; 95% CI = 0.2809 to 0.9163; p < 0.01, OR = 0.6537, 95% CI = 0.1425–0.8896). Patients with severe COVID-19 had a significant increase in NLR ( p < 0.0001–0.05). NLR was significantly correlated with the disease severity ( p < 0.0001–0.05). Survivors had a significant reduction in NLR compared with those who succumbed to COVID-19 ( p < 0.05). Conclusion Change in IL-27 level along with the frequencies of some immune cells may serve as a predictor of the severity and outcome of COVID-19.

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Cytokine profiles in the detection of severe lung involvement in hospitalized patients with COVID-19: The IL-8/IL-32 axis

Cited by 27 publications

References 38 publications

Timeline Kinetics of Systemic and Airway Immune Mediator Storm for Comprehensive Analysis of Disease Outcome in Critically Ill COVID-19 Patients

Timeline Kinetics of Systemic and Airway Immune Mediator Storm for Comprehensive Analysis of Disease Outcome in Critically Ill COVID-19 Patients

Common Molecular Pathways Between Post-COVID19 Syndrome and Lung Fibrosis: A Scoping Review

Predicting roles of IL-27 and IL-32 in determining the severity and outcome of COVID-19

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