Changes in T-Cell Subsets and Serum IFN-γ, IL-17, and IgE Levels in Children with Respiratory Syncytial Virus Capillary Bronchitis and Their Clinical Significance

Abstract

Objective. To investigate the changes in T-cell subsets and serum IFN-γ, IL-17, and IgE levels in children with respiratory syncytial virus capillary bronchitis and their clinical significance. Methods. The clinical data of 50 children with respiratory syncytial virus capillary bronchitis admitted to our hospital between July 2020 and June 2021 were retrospectively reviewed, and they were included in the observation group, while 50 children with a healthy physical examination during the same period were chosen as the control group. The T-cell subsets (CD4, CD8, and CD4/CD8) and serum IL-4, IL-8, IFN-, IL-17, and IgE levels of children in the two groups were compared, and the clinical significance of the changes in the levels of the indices mentioned above was analyzed. Results. There was no statistically significant difference in T-cell subset levels (CD4 and CD8) between the two groups ( P > 0.05 ); the level of CD4/CD8, IL-4, IL-8, IL-17, and IgE in the observation group were substantially higher than those in the control group ( P < 0.05 ), while the serum IFN-γ levels in the observation group were significantly lower than those in the control group ( P < 0.05 ). Conclusion. Increased CD4/CD8 levels in children with respiratory syncytial virus capillary bronchitis cause an imbalance in the Th1/Th2 immune response, similar to changes in bronchial asthma, suggesting a link between the two diseases. Increased serum levels of IL-4, IL-8, IL-17, and IgE and decreased serum levels of IFN-γ have been seen in children with respiratory syncytial virus capillary bronchitis, suggesting the severity of the children’s disease may in part be reflected in the levels of the aforementioned serum indicators.

Intermittent hypoxic pretreatment exacerbates house dust mite‐induced asthma airway inflammation

“… 40 As a type 1 cytokine, IFN‐γ exerts an indirect inhibitory effect on Th2 cell differentiation, thereby suppressing IgE synthesis. 41 This could potentially explain the less pronounced increase in IgE levels observed in the IHP group. Th17 cells are known to secrete a variety of cytokines, including IL‐17A and IL‐6, which play crucial roles in neutrophil recruitment, activation, and migration.…”

“…IFN‐γ has been shown to activate eosinophils through the induction of CD69 expression 40 . As a type 1 cytokine, IFN‐γ exerts an indirect inhibitory effect on Th2 cell differentiation, thereby suppressing IgE synthesis 41 . This could potentially explain the less pronounced increase in IgE levels observed in the IHP group.…”

Salivary interleukin-17A and interferon-γ levels are elevated in children with food allergies in China

“…Th17/Th1 cells can secrete both IL-17A and IFN-g as potentially pathogenic Th17 cells (41,42). An increasing number of studies have revealed the clinical relevance of Th17/Th1 cells and IL-17A and IFN-g in patients with immune diseases such as autoimmune diseases (43,44) and many other intestinal immune diseases (12)(13)(14)(15). Given the results of the present study, whether the elevated levels of IFN-g and IL-17A in saliva are related to Th17/Th1 cells and whether Th17/Th1 cells contribute to FA require further study.…”

Retracted: Changes in T-Cell Subsets and Serum IFN-γ, IL-17, and IgE Levels in Children with Respiratory Syncytial Virus Capillary Bronchitis and Their Clinical Significance

“…This article has been retracted by Hindawi following an investigation undertaken by the publisher [ 1 ]. This investigation has uncovered evidence of one or more of the following indicators of systematic manipulation of the publication process: Discrepancies in scope Discrepancies in the description of the research reported Discrepancies between the availability of data and the research described Inappropriate citations Incoherent, meaningless and/or irrelevant content included in the article Peer-review manipulation …”

“…This article has been retracted by Hindawi following an investigation undertaken by the publisher [1]. This investigation has uncovered evidence of one or more of the following indicators of systematic manipulation of the publication process:…”