Interleukin‐17—A multifaceted cytokine in viral infections

Sahu, Utkarsha; Biswas, Debasis; Prajapati, Vijay Kumar; Singh, Anirudh; Samant, Mukesh; Khare, Prashant

doi:10.1002/jcp.30471

Cited by 39 publications

(29 citation statements)

References 196 publications

(333 reference statements)

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“…These mice also produced low pro-inflammatory cytokine IL-17α [72]. IL-17α can be protective by inducing secretion of G-CSF, or pathogenic if dysregulated, promoting the accumulation of neutrophils at the injection site [73,74]. In the case of CC057 mice, high levels of G-CSF prevailed, contributing to a protective effect that was likely key to the minimal clinical symptoms observed during the acute phase.…”

Section: Discussionmentioning

confidence: 99%

Serum Cytokines Predict Neurological Damage in Genetically Diverse Mouse Models

Gómez

Karmakar

Carroll

et al. 2022

Cells

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Viral infections contribute to neurological and immunological dysfunction driven by complex genetic networks. Theiler’s murine encephalomyelitis virus (TMEV) causes neurological dysfunction in mice and can model human outcomes to viral infections. Here, we used genetically distinct mice from five Collaborative Cross mouse strains and C57BL/6J to demonstrate how TMEV-induced immune responses in serum may predict neurological outcomes in acute infection. To test the hypothesis that serum cytokine levels can provide biomarkers for phenotypic outcomes of acute disease, we compared cytokine levels at pre-injection, 4 days post-injection (d.p.i.), and 14 d.p.i. Each strain produced unique baseline cytokine levels and had distinct immune responses to the injection procedure itself. Thus, we eliminated the baseline responses to the injection procedure itself and identified cytokines and chemokines induced specifically by TMEV infection. Then, we identified strain-specific longitudinal cytokine profiles in serum during acute disease. Using stepwise regression analysis, we identified serum immune markers predictive for TMEV-induced neurological phenotypes of the acute phase, e.g., IL-9 for limb paralysis; and TNF-α, IL-1β, and MIP-1β for limb weakness. These findings indicate how temporal differences in immune responses are influenced by host genetic background and demonstrate the potential of serum biomarkers to track the neurological effects of viral infection.

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Section: Discussionmentioning

confidence: 99%

Serum Cytokines Predict Neurological Damage in Genetically Diverse Mouse Models

Gómez

Karmakar

Carroll

et al. 2022

Cells

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“…Accordingly, targeting JAK with specific inhibitors could be a possible approach to restrict Th17 cells-induced hyperinflammation. Evidence instantiates that JAK2 inhibitors such as fedratinib could decrease IL-17 secretion in murine Th17 cells [ 120 ].…”

Section: The Role Of Il-17 Cytokine In Covid-19 Infectionmentioning

confidence: 99%

COVID-19 infection: an overview on cytokine storm and related interventions

Montazersaheb

Khatibi

Hejazi

et al. 2022

Virol J

338

203

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Coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) has posed a significant threat to global health. This virus affects the respiratory tract and usually leads to pneumonia in most patients and acute respiratory distress syndrome (ARDS) in 15% of cases. ARDS is one of the leading causes of death in patients with COVID-19 and is mainly triggered by elevated levels of pro-inflammatory cytokines, referred to as cytokine storm. Interleukins, such as interleukin-6 (1L-6), interleukin-1 (IL-1), interleukin-17 (IL-17), and tumor necrosis factor-alpha (TNF-α) play a very significant role in lung damage in ARDS patients through the impairments of the respiratory epithelium. Cytokine storm is defined as acute overproduction and uncontrolled release of pro-inflammatory markers, both locally and systemically. The eradication of COVID-19 is currently practically impossible, and there is no specific treatment for critically ill patients with COVID-19; however, suppressing the inflammatory response may be a possible strategy. In light of this, we review the efficacy of specific inhibitors of IL6, IL1, IL-17, and TNF-α for treating COVID-19-related infections to manage COVID-19 and improve the survival rate for patients suffering from severe conditions. Graphical Abstract

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“…High HBV DNA load, and high HBeAg and HBsAg levels may inhibit the immune cell function of patients, leading to the reduction of Flt-3L, IFN-g, IL-17A, and other cytokines with virus clearance effect (8,13,(22)(23)(24), and to the increase in the level of the most important cytokine for immunosuppression (IL-10) and other cytokines with immunosuppressive effect such as TGF-b1 (8,13,(25)(26)(27). In this study, compared with the incomplete virus response group, the complete virus response group had lower HBV DNA load, lower HBeAg and HBsAg levels, lower IL-10 level, and lower TGF-b level, which indicate that patients with complete virus response may have better immune clearance ability against virus.…”

Section: Discussionmentioning

confidence: 99%

Dynamic changes of cytokine profiles and virological markers during 48 weeks of entecavir treatment for HBeAg-positive chronic hepatitis B

Gao²,

Yang³

et al. 2022

Front. Immunol.

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ObjectiveThe aims of this study were to investigate the kinetic changes of serum, virological, and immunological markers during entecavir (ETV) antiviral therapy and to explore whether these indicators can predict the antiviral efficacy of ETV in hepatitis B e antigen (HBeAg)-positive chronic hepatitis B (CHB) patients.MethodsHBeAg-positive CHB patients were enrolled and treated with ETV 0.5 mg/day. Clinical biochemical, virological, and serological tests were performed at baseline and every 12 weeks during the 48-week treatment. Plasma levels of cytokines (Flt-3L, IFN-α2, IFN-γ, IL-10, IL-17A, IL-6, TGF-β1, TGF-β2, TGF-β3, and TNF-α) were measured at baseline and at 12 and 24 weeks after treatment. Analysis of the trends of these clinical indicators in ETV antiviral therapy was performed.ResultsA total of 105 HBeAg-positive CHB patients were enrolled, and 100 of them completed 48 weeks of ETV treatment and follow-up. After 48 weeks of treatment, hepatitis B s antigen (HBsAg) decline ≥ 1 log10 was found in seven patients, but no patient achieved HBsAg disappearance. serological HBeAg disappeared in 13 patients, and serological HBeAg transformed in 3 patients. The baseline HBsAg and HBeAg levels, HBV DNA load, IL-10, and TGF-β1 levels in the complete virological response group were lower than those in the incomplete virological response group, while the ALT level in the complete virological response group was higher than that in the incomplete virological response group. Both univariate analysis and multivariate analysis showed that baseline biochemical indexes, virological indexes, and cytokine levels had no correlation with the complete virological response at 48 weeks. In multivariate analysis, low baseline HBV DNA load, and HBeAg and IL-10 levels were significantly associated with ALT normalization after 48 weeks of ETV treatment (HBeAg OR = 1.003, 95% CI 1.001–1.006, p = 0.007; HBV DNA OR = 0.184, 95% CI 0.046–0.739, p = 0.017; IL-10 OR = 0.040, 95% CI 0.972–0.999, p = 0.040).ConclusionCytokine levels changed dynamically during ETV antiviral therapy. Low baseline HBV DNA load, and HBeAg and IL-10 levels were significantly associated with ALT normalization after 48 weeks of ETV treatment.

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Interleukin‐17—A multifaceted cytokine in viral infections

Cited by 39 publications

References 196 publications

Serum Cytokines Predict Neurological Damage in Genetically Diverse Mouse Models

Serum Cytokines Predict Neurological Damage in Genetically Diverse Mouse Models

COVID-19 infection: an overview on cytokine storm and related interventions

Dynamic changes of cytokine profiles and virological markers during 48 weeks of entecavir treatment for HBeAg-positive chronic hepatitis B

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