Cytokine profile in Egyptian children and adolescents with COVID‐19 pneumonia: A multicenter study

Shafiek, Hala K; Lateef, Hanan Mohamed Abd El; Boraey, Naglaa F; Nashat, Mohamed; Abd-Elrehim, Ghada A. B.; Abouzeid, Heba; Hafez, Sahbaa F. M.; Shehata, Hassan; Elhewala, Ahmed; Abdel-Aziz, Alsayed; Zeid, Ahmed; Soliman, Mervat M.; Sallam, Mohammad M.; Nawara, Abdallah; Elgohary, Elsayed A.; Badr, Abd-Allah; Selim, Dalia; razek, suzan abd; Raouf, Batoul M. Abdel; Elmikaty, Hani A; Ibrahim, Lamya; Shahin, Gehan H.; Nabil, Rehab M.; Ibrahim, Mohamed; Salem, Hanan; Moustafa, Ahmed A.; Elshehawy, Naglaa A.; Abdel‐Aziz, Marwa M.; Eltrawy, Heba H; Osman, Sherif; Fouad, Rania A; Afify, Mona; Mohamed, Mohamed Y; Yousif, Yousif M.; Yousef, A. A.; Arafa, M.

doi:10.1002/ppul.25679

Cited by 19 publications

(19 citation statements)

References 42 publications

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“…The findings of inflammatory marker elevation in plasma corroborate results from other studies reporting a strong increment of pro-inflammatory cytokines in adults as well as in the few paediatric studies that exists to date (17,(26)(27)(28)(29). However, a striking feature of the present study is the lack of differences regarding cytokines that have been implicated as markers of disease severity, most notably IL-6 and IL-10 (30,31).…”

Section: Discussionsupporting

confidence: 91%

Inflammatory Markers, Pulmonary Function, and Clinical Symptoms in Acute COVID-19 Among Non-Hospitalized Adolescents and Young Adults

et al. 2022

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SummaryMild, subacute COVID-19 in young people show inflammatory enhancement, but normal pulmonary function. Inflammatory markers are associated with age and male sex, whereas clinical symptoms are associated with age and female sex, but not with objective disease markers.BackgroundCoronavirus Disease 2019 (COVID-19) is widespread among adolescents and young adults across the globe. The present study aimed to compare inflammatory markers, pulmonary function and clinical symptoms across non-hospitalized, 12 – 25 years old COVID-19 cases and non-COVID-19 controls, and to investigate associations between inflammatory markers, clinical symptoms, pulmonary function and background variables in the COVID-19 group.MethodsThe present paper presents baseline data from an ongoing longitudinal observational cohort study (Long-Term Effects of COVID-19 in Adolescents, LoTECA, ClinicalTrials ID: NCT04686734). A total of 31 plasma cytokines and complement activation products were assayed by multiplex and ELISA methodologies. Pulmonary function and clinical symptoms were investigated by spirometry and questionnaires, respectively.ResultsA total of 405 COVID-19 cases and 111 non-COVID-19 controls were included. The COVID-19 group had significantly higher plasma levels of IL-1β, IL-4, IL-7, IL-8, IL-12, TNF, IP-10, eotaxin, GM-CSF, bFGF, complement TCC and C3bc, and significantly lower levels of IL-13 and MIP-1α, as compared to controls. Spirometry did not detect any significant differences across the groups. IL-4, IL-7, TNF and eotaxin were negatively associated with female sex; eotaxin and IL-4 were positively associated with age. Clinical symptoms were positively associated with female sex and age, but not with objective disease markers.ConclusionsAmong non-hospitalized adolescents and young adults with COVID-19 there was significant alterations of plasma inflammatory markers in the subacute stage of the infection. Still, pulmonary function was normal. Clinical symptoms were independent of inflammatory and pulmonary function markers, but positively associated with age and female sex.

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Section: Discussionsupporting

confidence: 91%

Inflammatory Markers, Pulmonary Function, and Clinical Symptoms in Acute COVID-19 Among Non-Hospitalized Adolescents and Young Adults

et al. 2022

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“…21 A multicenter study demonstrated that for children with severe COVID-19, IL-1β, IL-6, and chemokine interferon-inducible protein-10 were dramatically increased, which could independently predict severe pneumonia in children with COVID-19. 22 In consistence with the above results, IL-6, IL-1β, and TNF-α were significantly upregulated in LPStreated WI-38 cells, but knockdown of EPSTI1 obviously suppressed inflammatory responses, indicating that IL-6, IL-1β, and TNF-α contributed to the inflammatory responses while inhibiting EPSTI1 alleviated LPS-caused inflammation.…”

Section: Discussionsupporting

confidence: 66%

Knockdown of EPSTI1 alleviates lipopolysaccharide-induced inflammatory injury through regulation of NF-κB signaling in a cellular pneumonia model

Kari

Zhihua

Aili

et al. 2022

Allergol Immunopathol

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Background: Although early diagnosis, antibiotic therapies, corticosteroid application, and health care services are conventional managements for pneumonia, antibiotic resistance and adverse reactions remain as limitations for pneumonia treatment. Objectives: The study attempted to evaluate the potential role of EPSTI1 against pneumonia and reveal its underlying mechanism. Methods: Lipopolysaccharide (LPS) (5, 10, and 20 μg/mL) was applied in WI-38 cells to establish the in vitro pneumonia model. Knockdown of epithelial-stromal interaction 1 (EPSTI1) was performed by transfection with EPSTI1 siRNA (siEPSTI1) into LPS-treated cells. Cell Counting Kit-8 assays were implemented to measure cell viability, and apoptotic cells were detected using flow cytometry. Interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α) were quantified using enzyme-linked immunosorbent assay (ELISA). Immunoblotting and quantitative real-time polymerase chain reaction (qRT-PCR) were conducted to quantify EPSTI1 expression, and proteins related to nuclear factor κ-light-chain-enhancer of activated B cell (NF-κB) signaling, including p-p65, p65, p-IκBα, and IκBα. Results: EPSTI1 was highly expressed in LPS-treated WI-38 cells. Cell apoptosis was promoted, and cell viability was inhibited after being exposed to LPS. Besides, IL-1β, IL-6, and TNF-α were dramatically upregulated. Knockdown of EPSTI1 restored cell viability, inhibited cell apoptosis, and attenuated expressions of proinflammatory factors. Additionally, knockdown of EPSTI1 visibly decreased the increased ratios of p-p65/p65 and p-IκBα/IκBα induced by LPS. Knockdown of EPSTI1 alleviated inflammatory injury through the inactivation of the NF-κB pathway. Conclusions: These results provided promising management in preventing pneumonia in patients.

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“…This agreed with findings of previous studies. 18,19,20 In contrary, a study by Burgos-Blasco et al, 2020, did not find a difference between COVID-19 patients and control subjects. 21 In the current study, by analyzing the mean IL-17 serum levels among the moderate and severe cases, we observed that although the mean serum titers of IL-17 were higher in the severe group compared to the moderate group, but the difference did not reach statistical significance.…”

Section: Discussionmentioning

confidence: 86%

IL-17A )rs2275913; G197A) gene polymorphism as predictor for disease severity and its correlation with IL-17 serum levels in COVID-19 patients

Rushdy

Elsayed

Ahmed

et al. 2022

EJI

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Severity of symptoms in COVID-19 has been shown to result from a cytokine storm. Interleukin (IL)-17 is one of these various cytokines, which results in a proinflammatory response, systemic inflammatory symptoms, inflammatory cell infiltration of lung tissue and thus leads to the massive lung pathology and multiorgan failure. Gene polymorphisms in the regulatory regions of cytokine-encoding genes affect the amounts of cytokines produced and possess a fundamental role in infectious diseases. This study aimed to investigate the role of IL-17A (rs2275913; G197A) gene polymorphism as predictor of disease severity and its correlation with IL-17 serum levels in COVID-19 patients. A group of 70 COVID-19 patients and 17 age and sex-matched control subjects were enrolled in the present work. Patients were classified into two groups moderate, severe and acute respiratory distress (ARDS) cases, defined according to the criteria established by the world health organization. Quantitative real time-polymerase chain reaction was done to detect IL-17A (rs2275913; G197A). Serum IL-17 levels were assessed by an enzyme-linked immunosorbent assay in both patients and controls. The distribution of different IL-17A G/A genotypes among COVID-19 patients were 44.3% for GG genotype, 44.3% for AG genotype and 11.4% for AA genotype. Genotypes among the control group were 43.8% for GG genotype, 50% for AG genotype and 6.3% for AA genotype. G allele distribution was 66.4%, 68.8% in patient and control group, respectively, and A allele was 33.6% and 31.3%, respectively. There was no association between the different genotypes, disease severity or IL-17 serum levels in the patient group. In conclusion, despite the possible role of IL-17 in the pathogenesis of inflammation, there was no association between IL-17 polymorphism and disease severity or IL-17 serum levels among Egyptian COVID-19 patients.

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Cytokine profile in Egyptian children and adolescents with COVID‐19 pneumonia: A multicenter study

Cited by 19 publications

References 42 publications

Inflammatory Markers, Pulmonary Function, and Clinical Symptoms in Acute COVID-19 Among Non-Hospitalized Adolescents and Young Adults

Inflammatory Markers, Pulmonary Function, and Clinical Symptoms in Acute COVID-19 Among Non-Hospitalized Adolescents and Young Adults

Knockdown of EPSTI1 alleviates lipopolysaccharide-induced inflammatory injury through regulation of NF-κB signaling in a cellular pneumonia model

IL-17A )rs2275913; G197A) gene polymorphism as predictor for disease severity and its correlation with IL-17 serum levels in COVID-19 patients

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