Interleukin-6 (IL-6) expression of lung tissue in COVID-19 patient severity through core biopsy post mortem

Nugroho, Gilang Muhammad Setyo; Marhana, Isnin Anang; Kusumastuti, Etty Hary; Semedi, Bambang Pujo; Maimunah, Ummi; Lefi, Achmad; Suyanto, Edi; Rosyid, Alfian Nur; Wahyu, Dwi; Wiratama, Priangga Adi; Anggoro, Adhitri; Yandi, I Komang Rusgi; Djuanda, Stephanie Natasha; Lilihata, Jilieanastasia Godrace; Supriadi, _; Rinjani, Lalu Galih Pratama; Nugraha, Ricardo Adrian

doi:10.1016/j.amsu.2022.104648

Cited by 5 publications

(7 citation statements)

References 24 publications

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“…19 A study proved that increased expression of IL-6 in lung tissue indicates the severity of COVID-19 sufferers. 22 Interleukin-17 plays a role in the pathogenesis of ARDS by increasing the infiltration of neutrophils into the lung. Increased signaling of IL-17A and Th17 or regulatory T cells (Treg) is known to be positively correlated with disease severity in MERS infection, where the cause is a type of virus that belongs to the same family as MERS.…”

Section: Discussionmentioning

confidence: 99%

Differences in interleukin-6 and interleukin-17 expression in covid-19 post-mortem lung tissue biopsy compared with noncovid- 19

Kusumastuti¹,

Wiratama²,

Ariani³

et al. 2023

Pharmacogn J.

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Background: COVID-19 has spread rapidly around the world. It is necessary to study lung tissue of postmortem COVID19 patients to determine the molecular alteration particularly the role of IL-6 and IL-17 in causing fatality. Objective: This study aims to determine the differences in the expressions of IL-6 and IL-17 in lung tissue of post-mortem COVID-19 patients compared to non-COVID-19 patients. This study also aimed to analyze the correlation between the expressions of IL-6 and IL-17 in lung tissue of post-mortem COVID-19 patients. Methods: This research is an observational analytic study with crosssectional approach. The samples were 15 paraffin blocks of post-mortem lung tissue biopsy of COVID-19 patients, and 15 paraffin blocks of inflammatory lung tissue biopsy or surgery of non-COVID-19 patients. IL-6 and IL-17 expressions were evaluated by immunohistochemical procedure. Result: There was a significant difference in the expression of IL-6 in the COVID-19 group and the non-COVID-19 group with a p-value = 0.001 (p < 0.05). There was a significant difference in the expression of IL-17 in the COVID-19 group and the non-COVID-19 group with p-value = 0.001 (p < 0.05). There was a significant correlation between the expressions of IL-6 and IL-17 in the COVID-19 group, with the Spearman coefficient value (rs) of 0.548 with p = 0.034 (p < 0.05). Conclusion: There are differences in the expression of IL-6 and IL-17 between COVID-19 and non-COVID-19 lung tissue. There is a significant correlation between the expressions of IL-6 and IL-17 in post-mortem lung tissue of COVID-19 patients.

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Section: Discussionmentioning

confidence: 99%

Differences in interleukin-6 and interleukin-17 expression in covid-19 post-mortem lung tissue biopsy compared with noncovid- 19

Kusumastuti¹,

Wiratama²,

Ariani³

et al. 2023

Pharmacogn J.

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Section: Biological Mechanisms For In Situ Pulmonary Immunothrombosismentioning

confidence: 99%

“…COVID-19-associated coagulopathy with microvascular thrombosis is secondary to inflammation and endotheliopathy that are “orchestrated” by IL-6, a pleiotropic proinflammatory cytokine [ 79 ]. The severity of SARS-CoV-2 infection is associated with increased blood levels but also with IL-6 expression on lung tissue [ 79 , 80 ]. IL-6 has a proinflammatory role in vascular endothelial cells, and it favors hypercoagulation by interfering with the normal anticoagulant and profibrinolytic properties of ECs [ 81 ].…”

Section: Biological Mechanisms For In Situ Pulmonary Immunothrombosismentioning

confidence: 99%

“…Cytokines, especially IL-1 and IL-6, and chemokines are involved in all phases of inflammation and thrombosis, using multiple biological pathways [ 18 , 29 , 43 , 44 , 45 , 50 , 51 , 58 , 59 , 60 , 61 , 62 , 66 , 69 , 72 , 73 , 74 , 75 , 76 , 77 , 78 , 79 , 80 , 81 , 82 , 83 , 93 , 94 , 101 , 103 , 129 , 132 , 136 , 137 , 138 ].…”

Section: Figurementioning

confidence: 99%

“…In vascular ECs, IL-6 favors hypercoagulation by interfering with their normal anticoagulant and profibrinolytic properties [ 79 , 81 ].…”

Section: Figurementioning

confidence: 99%

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Mechanisms of COVID-19 Associated Pulmonary Thrombosis: A Narrative Review

2023

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COVID-19, the infectious disease caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), is frequently associated with pulmonary thrombotic events, especially in hospitalized patients. Severe SARS-CoV-2 infection is characterized by a proinflammatory state and an associated disbalance in hemostasis. Immune pathology analysis supports the inflammatory nature of pulmonary arterial thrombi composed of white blood cells, especially neutrophils, CD3+ and CD20+ lymphocytes, fibrin, red blood cells, and platelets. Immune cells, cytokines, chemokines, and the complement system are key drivers of immunothrombosis, as they induce the damage of endothelial cells and initiate proinflammatory and procoagulant positive feedback loops. Neutrophil extracellular traps induced by COVID-19-associated “cytokine storm”, platelets, red blood cells, and coagulation pathways close the inflammation–endotheliopathy–thrombosis axis, contributing to SARS-CoV-2-associated pulmonary thrombotic events. The hypothesis of immunothrombosis is also supported by the minor role of venous thromboembolism with chest CT imaging data showing peripheral blood clots associated with inflammatory lesions and the high incidence of thrombotic events despite routine thromboprophylaxis. Understanding the complex mechanisms behind COVID-19-induced pulmonary thrombosis will lead to future combination therapies for hospitalized patients with severe disease that would target the crossroads of inflammatory and coagulation pathways.

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Vitamin D and SARS‐CoV‐2

Ødum

Kongsbak-Wismann

2023

Basic Clin Pharma Tox

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The single-stranded RNA virus, SARS-CoV-2, causing the COVID-19 pandemic, has severely impacted daily life globally. It has been suggested to supplement the general population with vitamin D to reduce the impact of COVID-19. Nevertheless, no clear consensus can be found as to whether vitamin D affects COVID-19 disease burden. Some studies found that vitamin D levels and/or vitamin D supplementation alleviated COVID-19 disease severity and mortality.Contrarily, other studies found no such effects of vitamin D. To understand this lack of consensus, it is relevant to investigate molecular studies of the vitamin D receptor (VDR), as such studies might explain apparent controversies. We have investigated recent studies of how transcriptional regulation by the VDR affects the immune response against SARS-CoV-2. One study found that cells from severe COVID-19 patients displayed a dysregulated vitamin D response. Contrarily, another study observed a normal immune response towards SARS-CoV-2 in a patient with a non-functional VDR. These observations indicate that hypovitaminosis D is not a prerequisite for an efficient immune response against SARS-CoV-2 and therefore not a driving factor for developing severe COVID-19. However, should a patient develop severe COVID-19, vitamin D seems to be beneficial potentially by dampening the cytokine storm.

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Interleukin-6 (IL-6) expression of lung tissue in COVID-19 patient severity through core biopsy post mortem

Cited by 5 publications

References 24 publications

Differences in interleukin-6 and interleukin-17 expression in covid-19 post-mortem lung tissue biopsy compared with noncovid- 19

Differences in interleukin-6 and interleukin-17 expression in covid-19 post-mortem lung tissue biopsy compared with noncovid- 19

Mechanisms of COVID-19 Associated Pulmonary Thrombosis: A Narrative Review

Vitamin D and SARS‐CoV‐2

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