SARS-CoV-2 Proteins Induce IFNG in Th1 Lymphocytes Generated from CD4+ Cells from Healthy, Unexposed Polish Donors

Sałkowska, Anna; Karwaciak, Iwona; Karaś, Kaja; Dastych, Jarosław; Ratajewski, Marcin

doi:10.3390/vaccines8040673

Cited by 16 publications

(19 citation statements)

References 44 publications

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“…Therefore, it can be concluded that Th1 cells increase inflammation in patients with COVID-19 by INF-γ production. Consistent with these results, it has been reported that the SARS-CoV-2 virus induces polyclonal Th1 cells, that the rate of these responses varies from patient to patient based on the immune system status and history of the underlying disease [45] . In another study, Elizaldi and colleagues indicated that Th1 cell responses dramatically increased after infection with the SARS-CoV-2 virus [46] .…”

Section: Discussionsupporting

confidence: 81%

Different T cell related immunological profiles in COVID-19 patients compared to healthy controls

Khesht

Karpisheh

Saeed

et al. 2021

International Immunopharmacology

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In various pathological conditions, cellular immunity plays an important role in immune responses. Among immune cells, T lymphocytes pdomote cellular and humoral responses as well as innate immunity. Therefore, careful investigation of these cells has a significant impact on accurate knowledge in COVID-19 disease pathogenesis. In current research, the frequency and function of various T lymphocytes involved in immune responses examined in SARS‐CoV-2 patients with various disease severity compared to normal subjects. In order to make an accurate comparison among patients with various disease severity, this study was performed on asymptomatic recovered cases (n=20), ICU hospitalized patients (n=30), non-ICU hospitalized patients (n=30), and normal subjects (n=20). To precisely evaluate T cells activity following purification, their cytokine secretion activity was examined. Similarly, immediately after purification of Treg cells, their inhibitory activity on T cells was investigated. The results showed that COVID-19 patients with severe disease (ICU hospitalized patients) not only had a remarkable increase in Th1 and Th17 but also a considerable decrease in Th2 and Treg cells. More importantly, as the IL-17 and IFN-γ secretion was sharply increased in severe disease, the secretion of IL-10 and IL-4 was decreased. Furthermore, the inhibitory activity of Treg cells was reduced in severe disease patients in comparison to other groups. In severe COVID-19 disease, current findings indicate when the inflammatory arm of cellular immunity is significantly increased, a considerable reduction in anti-inflammatory and regulatory arm occurred.

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Section: Discussionsupporting

confidence: 81%

Different T cell related immunological profiles in COVID-19 patients compared to healthy controls

Khesht

Karpisheh

Saeed

et al. 2021

International Immunopharmacology

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“…However, it should be noted that we have no direct evidence that this is the case and further research is required. Interestingly, the SARS-CoV-2 S protein also showed an activating effect on cytokine expression in Th1 cells [ 27 ]. However, in contrast to monocytes, which showed a higher response to the SARS-CoV-2 N protein ( Figure 2 A), Th1 cells did not show such a preference [ 27 ], which is somewhat contradictory to the results of a bioinformatics study by Dhall et al [ 41 ].…”

Section: Discussionmentioning

confidence: 99%

“…Interestingly, the SARS-CoV-2 S protein also showed an activating effect on cytokine expression in Th1 cells [ 27 ]. However, in contrast to monocytes, which showed a higher response to the SARS-CoV-2 N protein ( Figure 2 A), Th1 cells did not show such a preference [ 27 ], which is somewhat contradictory to the results of a bioinformatics study by Dhall et al [ 41 ]. This observation might be of importance in the context of developing vaccines based on SARS-CoV-2 proteins, as it suggests that SARS-CoV-2 N protein-based vaccines might be more likely to induce a Th2 immune response, leading to humoral immunity, than vaccines utilizing the SARS-CoV-2 S protein.…”

Section: Discussionmentioning

confidence: 99%

“…The resulting cDNA were used as temple in real-time RT-PCR, which was run using SYBR Green I Master Mix on a LightCycler 480 (Roche, Basel, Switzerland). The cycling conditions were as follows: 95 °C for 5 min, followed by 55 cycles of 95 °C for 10 s, 60 °C for 10 s, and 72 °C for 20 s. The primer sequences used in this study were as follows: IL6 , 5′-CCTGAACCTTCCAAAGATGG-3′ (forward) and 5′-GGTCAGGGGTGGTTATTGC-3′ (reverse), as previously described [ 26 ]; IL1B , 5′-GGACAGGATATGGAGCAACAAGTG-3′ (forward), and 5′- ACACGCAGGACAGGTACAGATTC-3′ (reverse); IL10 , 5′- TTGCTGGAGGACTTTAAGGG-3′ (forward), and 5′-GGGAAGAAATCGATGACAGC-3′ (reverse); TNF , 5′-CCAGGCAGTCAGATCATCTTCTCG-3′ (forward), and 5′-ATCTCTCAGCTCCACGCCATTG-’3 (reverse), as previously described [ 27 ]; RELA , 5′-TATCAGTCAGCGCATCCAGACC-3′ (forward), and 5′-CGCTGCTCTTCTATAGGAACTTGG-3′ (reverse); NFKB1 , 5′- CCTCCACAAGGCAGCAAATAGACG-3′ (forward), and 5′-AGCTGAGTTTGCGGAAGGATGTC-3′ (reverse) as previously described [ 28 ]; NFKBIA , 5′-TGAAGGCTACCAACTACAATGGC-3′ (forward), and 5′-TGACATCAGCACCCAAGGACAC-3′ (reverse). The expression of cognate mRNA was normalized by the geometric mean of the housekeeping genes HPRT1 , 5′-TGACACTGGCAAAACAATGCA-3′ (forward), and 5′-GGTCCTTTTCACCAGCAAGCT-3′ (reverse); HMBS , 5′-GGCAATGCGGCTGCAA-3′ (forward), and 5′-GGGTACCCACGCGAATCAC-3′ (reverse); and RPL13A , 5′-CCTGGAGGAGAAGAGGAAAGAGA-3′ (forward), and 5′-TTGAGGACCTCTGTGTATTTGTCAA-3′ (reverse), as previously described [ 29 ].…”

Section: Methodsmentioning

confidence: 99%

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Nucleocapsid and Spike Proteins of the Coronavirus SARS-CoV-2 Induce IL6 in Monocytes and Macrophages—Potential Implications for Cytokine Storm Syndrome

et al. 2021

Self Cite

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The pandemic of the new coronavirus SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) has led to the deaths of more than 1.5 million people worldwide. SARS-CoV-2 causes COVID-19, which exhibits wide variation in the course of disease in different people, ranging from asymptomatic and mild courses to very severe courses that can result in respiratory failure and death. Despite the rapid progression of knowledge, we still do not know how individual cells of the immune system interact with the virus or its components, or how immune homeostasis becomes disrupted, leading to the rapid deterioration of a patient’s condition. In the present work, we show that SARS-CoV-2 proteins induce the expression and secretion of IL-6 by human monocytes and macrophages, the first line cells of antiviral immune responses. IL-6 may play a negative role in the course of COVID-19 by inhibiting Th1-dependent immunity and stimulating Th17 lymphocytes, thus leading to an increased probability of a cytokine storm.

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“…In SARS-CoV-2 infected patients, cytokine storm has been reported in which there are massive increases in inflammatory cytokines, such as, interleukins, TNF, colony stimulating factors (CSFs), and growth factors (GFs). Emerging evidence suggests the involvement of epigenetic modifications in these increases [ 249 , 250 ]. Variable response of individuals infected with SARS-CoV-2 could possibly be influenced by epigenetic regulators of cytokines, as has been reported in lupus patients [ 187 ].…”

Section: Epigenetic Regulation Of Inflammationmentioning

confidence: 99%

Epigenetic underpinnings of inflammation: Connecting the dots between pulmonary diseases, lung cancer and COVID-19

Ahmad

Manzoor

Siddiqui

et al. 2022

Seminars in Cancer Biology

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Inflammation is an essential component of several respiratory diseases, such as chronic obstructive pulmonary disease (COPD), asthma and acute respiratory distress syndrome (ARDS). It is central to lung cancer, the leading cancer in terms of associated mortality that has affected millions of individuals worldwide. Inflammation and pulmonary manifestations are also the major causes of COVID-19 related deaths. Acute hyperinflammation plays an important role in the COVID-19 disease progression and severity, and development of protective immunity against the virus is greatly sought. Further, the severity of COVID-19 is greatly enhanced in lung cancer patients, probably due to the genes such as ACE2, TMPRSS2, PAI-1 and furin that are commonly involved in cancer progression as well as SAR-CoV-2 infection. The importance of inflammation in pulmonary manifestations, cancer and COVID-19 calls for a closer look at the underlying processes, particularly the associated increase in IL-6 and other cytokines, the dysregulation of immune cells and the coagulation pathway. Towards this end, several reports have identified epigenetic regulation of inflammation at different levels. Expression of several key inflammation-related cytokines, chemokines and other genes is affected by methylation and acetylation while non-coding RNAs, including microRNAs as well as long non-coding RNAs, also affect the overall inflammatory responses. Select miRNAs can regulate inflammation in COVID-19 infection, lung cancer as well as other inflammatory lung diseases, and can serve as epigenetic links that can be therapeutically targeted. Furthermore, epigenetic changes also mediate the environmental factors-induced inflammation. Therefore, a better understanding of epigenetic regulation of inflammation can potentially help develop novel strategies to prevent, diagnose and treat chronic pulmonary diseases, lung cancer and COVID-19.

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SARS-CoV-2 Proteins Induce IFNG in Th1 Lymphocytes Generated from CD4+ Cells from Healthy, Unexposed Polish Donors

Cited by 16 publications

References 44 publications

Different T cell related immunological profiles in COVID-19 patients compared to healthy controls

Different T cell related immunological profiles in COVID-19 patients compared to healthy controls

Nucleocapsid and Spike Proteins of the Coronavirus SARS-CoV-2 Induce IL6 in Monocytes and Macrophages—Potential Implications for Cytokine Storm Syndrome

Epigenetic underpinnings of inflammation: Connecting the dots between pulmonary diseases, lung cancer and COVID-19

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