AI Article Synopsis
- Hepatitis B virus (HBV) is a major global health issue linked to severe liver diseases, and vaccination is crucial in lowering its incidence.
- Approximately 5-10% of vaccinated individuals fail to develop adequate protective antibodies, which may be related to inflammatory responses mediated by the NF‑κB signaling pathway.
- In a study comparing 32 non-responders to 36 responders, it was found that certain gene expression levels were significantly higher in non-responders, suggesting that inflammatory pathways could influence vaccine efficacy and warrant further research on hepatitis B vaccine immunity mechanisms.
Article Abstract
Hepatitis B virus (HBV) infection is a global health problem leading to cirrhosis, hepatocellular carcinoma, and liver failure. The Hepatitis B vaccine plays a significant role in reducing the incidence of HBV worldwide. Approximately 5-10% of vaccinated people do not produce protective antibody levels. Nuclear factor kappa B (NF‑κB) mediates inflammatory responses through pro-inflammatory cytokines. However, the role of the NF‑κB signaling pathway and its association with pro-inflammatory cytokines in hepatitis B vaccine response is unclear. We aimed to assess changes in the , and expression levels in the non-responder and responder. A total of 32 non-responders and 36 responders were included in the study. The expression level of determined genes was analyzed by RT-PCR. Our results showed that , and mRNA levels significantly increased in the non-responders compared to the responders (p < .01). Furthermore, there was a significant correlation between , and in the non-responder and responders. In conclusion, inflammatory signaling pathways may play an important role in response to HBV vaccine. Therefore, NF‑κB signaling and associated pro-inflammatory cytokine mRNA levels could predict hepatitis B vaccine response. However, the underlying molecular mechanisms of hepatitis B vaccine immunity need further investigation.
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| http://dx.doi.org/10.1080/15321819.2022.2164507 | DOI Listing |
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