Mechanisms Of Cytokine Balance Disturbance And Immune Response In Children With Bronchial Asthma After Covid-19

Abstract

The interplay between COVID-19 infection and pre-existing bronchial asthma in children necessitates a thorough understanding of the resulting immune dysregulation. This study investigated the immunological alterations in children with bronchial asthma following COVID-19 infection, comparing them to a control group of asthmatic children without a history of COVID-19. Objective: To evaluate the mechanism of the immune response and cytokine balance features in children with bronchial asthma after COVID-19.

Materials and methods. The study involved 125 children aged 7-15 years, divided into two groups: Group 1 (n=60) comprised children with bronchial asthma and confirmed COVID-19; Group 2 (n=65) consisted of asthmatic children without COVID-19. Both groups exhibited varying asthma severities. Immunological analysis revealed significant differences between the groups.

Results and discussion: Children in Group 1 (COVID-19 positive) demonstrated a marked reduction (p<0.01) in CD3+ lymphocytes (46.57 ± 0.67%), representing total T lymphocytes, compared to the control group (Group 2). This decrease highlights a compromised cellular immune response, potentially impacting the body's ability to effectively fight off future infections. Further analysis showed significant deviations from normal ranges in CD4+ (helper T cells) and CD8+ (cytotoxic T cells) lymphocyte populations in the COVID-19 group, suggesting an imbalance in T-cell mediated immunity. Intriguingly, CD20+ lymphocytes (B cells) were significantly elevated (p<0.001) in the COVID-19 group (40.7 ± 1.01%), indicating a possible over-activation of the humoral immune response, possibly contributing to the overall inflammatory state. This might be linked to increased antibody production, potentially including autoantibodies, which could worsen asthma symptoms. The observed decrease in T-lymphocytes might be explained by several factors. Viral infection can directly deplete T-cells, or indirectly through cytokine storm, where an overproduction of pro-inflammatory cytokines like IL-6 and TNF-α leads to immune cell exhaustion and apoptosis. The elevation in CD20+ lymphocytes could also be a consequence of the cytokine storm, as B-cell activation is influenced by these cytokines. Additionally, the prolonged inflammatory environment in asthma could further exacerbate the impact of COVID-19, creating a synergistic effect on immune dysregulation. Conclusion. These findings underscore the importance of individualized immunotherapy approaches tailored to the specific immunological profiles of children with bronchial asthma post-COVID-19. Further research should focus on the long-term effects of COVID-19 on the immune system of asthmatic children and the development of targeted interventions to mitigate these effects. Studies exploring the efficacy of various immunomodulatory therapies, such as biologics targeting specific cytokines or pathways, are warranted. Longitudinal studies monitoring immune function and respiratory health outcomes would be crucial in assessing the long-term impact of COVID-19 on this vulnerable population.