Interleukin-17 enhances the removal of respiratory syncytial virus in mice by promoting neutrophil migration and reducing interferon-gamma expression

Zhang, G; Zhou, Kai; Lu, Zeqing

doi:10.4238/gmr.15017002

Cited by 8 publications

(9 citation statements)

References 14 publications

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“…However, the majority of Tc17 cells displayed no cytolytic activity, while the protection conferred by these cells coincided with an influx of neutrophils into the lung [53]. Consistent with this observation, following the infection of HSV in mice, IL-17 appears to be responsible for reduced viral load partly by strengthening inflammatory responses that promote neutrophil migration into the lung [54]. Following vaccinia virus infection, adoptively transferred Tc17 cells can acquire strong cytotoxic potential in vivo , as shown by their increased FasL expression levels that correlate with effective viral clearance [55].…”

Section: Il-17 Hinders Viral Infections and Limits Viral Infection-rementioning

confidence: 88%

The protective and pathogenic roles of IL-17 in viral infections: friend or foe?

et al. 2019

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Viral infections cause substantial human morbidity and mortality, and are a significant health burden worldwide. Following a viral infection, the host may initiate complex antiviral immune responses to antagonize viral invasion and replication. However, proinflammatory antiviral immune responses pose a great threat to the host if not properly held in check. Interleukin (IL)-17 is a pleiotropic cytokine participating in a variety of physiological and pathophysiological conditions, including tissue integrity maintenance, cancer progression, autoimmune disease development and, more intriguingly, infectious diseases. Abundant evidence suggests that while IL-17 plays a crucial role in enhancing effective antiviral immune responses, it may also promote and exacerbate virus-induced illnesses. Accumulated experimental and clinical evidence has broadened our understanding of the seemingly paradoxical role of IL-17 in viral infections and suggests that IL-17-targeted immunotherapy may be a promising therapeutic option. Herein, we summarize current knowledge regarding the protective and pathogenic roles of IL-17 in viral infections, with emphasis on underlying mechanisms. The various and critical roles of IL-17 in viral infections necessitate the development of therapeutic strategies that are uniquely tailored to both the infectious agent and the infection environment.

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Section: Il-17 Hinders Viral Infections and Limits Viral Infection-rementioning

confidence: 88%

The protective and pathogenic roles of IL-17 in viral infections: friend or foe?

et al. 2019

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“…Conversely, in murine CMV infection, neutrophils form a critical part of the antiviral response and are shown to play a direct role in controlling viral replication and limiting morbidity ( 17 ), a role also seen in RSV ( 72 ), HSV ( 15 ), and HIV infection ( 73 ). Interestingly, neutrophils support viral replication in West Nile virus infection and are actively recruited during infection, acting as a reservoir for replication, and only become involved in viral clearance at a later stage ( 74 ).…”

Section: Discussionmentioning

confidence: 99%

Human Cytomegalovirus Delays Neutrophil Apoptosis and Stimulates the Release of a Prosurvival Secretome

et al. 2017

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Human cytomegalovirus (HCMV) is a major cause of viral disease in the young and the immune-suppressed. At sites of infection, HCMV recruits the neutrophil, a cell with a key role in orchestrating the initial immune response. Herein, we report a profound survival response in human neutrophils exposed to the clinical HCMV isolate Merlin, but not evident with the attenuated strain AD169, through suppression of apoptosis. The initial survival event, which is independent of viral gene expression and involves activation of the ERK/MAPK and NF-κB pathways, is augmented by HCMV-stimulated release of a secretory cytokine profile that further prolongs neutrophil lifespan. As aberrant neutrophil survival contributes to tissue damage, we predict that this may be relevant to the immune pathology of HCMV, and the presence of this effect in clinical HCMV strains and its absence in attenuated strains implies a beneficial effect to the virus in pathogenesis and/or dissemination. In addition, we show that HCMV-exposed neutrophils release factors that enhance monocyte recruitment and drive monocyte differentiation to a HCMV-permissive phenotype in an IL-6-dependent manner, thus providing an ideal vehicle for viral dissemination. This study increases understanding of HCMV–neutrophil interactions, highlighting the potential role of neutrophil recruitment as a virulence mechanism to promote HCMV pathology in the host and influence the dissemination of HCMV infection. Targeting these mechanisms may lead to new antiviral strategies aimed at limiting host damage and inhibiting viral spread.

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“…IL-17, a recently discovered inflammatory cytokine, can induce the expression of other inflammatory cytokines [including IL-6 and tumor necrosis factor-α (TNF-α)] and chemotactic factors (18,19). In this way, IL-17 promotes neutrophil migration to sites of inflammation and mediates inflammatory responses to enhance the antitumor effects of the body (20). IL-8 is a chemotactic inflammatory factor that plays an important role in maintaining cancer cell self-renewal and resistance to chemotherapy drugs through its regulation of cancer stem cells (21)(22)(23).…”

Section: Introductionmentioning

confidence: 99%

Involvement of soluble B7‑H3 in combination with the serum inflammatory cytokines interleukin‑17, ‑8 and ‑6 in the diagnosis of hepatocellular carcinoma

Wang

et al. 2017

Oncol Lett

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Abstract. Previous studies have demonstrated that B7-H3, and the inflammatory cytokines interleukin (IL)-17, IL-8 and IL-6, are involved in the development of a variety of tumors. The objectives of the present study were: i) To investigate the association between soluble B7-H3 (sB7-H3) and cytokine levels of IL-17, IL-8 and IL-6 in the serum of patients with hepatocellular carcinoma (HCC); and ii) to determine their potential value for use in HCC diagnosis. Serum sB7-H3, IL-17, IL-8 and IL-6 levels in the HCC patients and healthy control subjects were measured using ELISA. The accuracy of each of these biomarkers in HCC diagnosis was compared using a receiver operating characteristic curve and the area under the curve (AUC). A logistic regression model was used to investigate the accuracy of diagnosing HCC when evaluated using combined determinations of sB7-H3, IL-17, IL-8 and IL-6 levels. The data demonstrated that serum levels of sB7-H3, IL-17, IL-8 and IL-6 were significantly increased in HCC patients compared with those in the healthy control group. Serum sB7-H3 levels were positively associated with serum IL-17, whereas serum IL-8 levels were negatively correlated with serum IL-17 levels. The AUC values for sB7-H3, IL-17, IL-8 and IL-6 were 83.2, 65.7, 95.3 and 97.0%, respectively, and indicated that all four biomarkers exhibited a statistically significant capacity for diagnosing HCC. Using the logistic regression model, the AUC value, sensitivity and specificity, as determined for the combination of the four biomarkers, were 99.2, 96.67 and 97.14%, respectively. This was significantly greater than that achieved when any single biomarker was used alone in the logistic regression model to assess their accuracy in HCC diagnosis. The optimum cutoff value of the predicted probability obtained by the combination of sB7-H3, IL-17, IL-8 and IL-6 in the regression model was 0.5745. To conclude, the present study revealed that there exists a positive association between serum sB7-H3 and IL-17 levels in HCC patients. Determinations involving the combination of serum sB7-H3, IL-17, IL-8 and IL-6 levels demonstrate great potential for use in HCC diagnosis.

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Interleukin-17 enhances the removal of respiratory syncytial virus in mice by promoting neutrophil migration and reducing interferon-gamma expression

Cited by 8 publications

References 14 publications

The protective and pathogenic roles of IL-17 in viral infections: friend or foe?

The protective and pathogenic roles of IL-17 in viral infections: friend or foe?

Human Cytomegalovirus Delays Neutrophil Apoptosis and Stimulates the Release of a Prosurvival Secretome

Involvement of soluble B7‑H3 in combination with the serum inflammatory cytokines interleukin‑17, ‑8 and ‑6 in the diagnosis of hepatocellular carcinoma

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