| Summary: | 碩士 === 中興大學 === 化學系所 === 94 === IL-4 is a pleiotropic cytokine which exerts its actions on various lineages of hematopoietic and nonhematopoients cells. This cytokine is one of the central regulators of immunity in health and disease states. IL-4 is a 15-kD polypeptide with widespread effects on many cell types and secreted by helper T cell. IL-4 participates in a lot of inflammatory responses. The IL-4δ2 is a naturally occurring splice variant of human IL-4 with exons 1, 3, and 4 in an open reading frame. It is known to antagonize many biological activities of IL-4. Mycobacterial infections are chiefly controlled by cellular immunity that is through to be the activation of infected macrophages by Th1-type cytokines particularly interferon (INF)-γ. Sepsis is a complicated syndrome in which pro-inflammatory and anti-inflammatory cytokines are expressed simultaneously. Many of the components of the innate immune response are cause cell and tissue damage and hence multiple organ failure. However, it is still unclear for the expression of IL-4 and IL-4δ2 in patients with severe sepsis and TB. Does IL-4 gene polymorphism increase the organic susceptibility to inflammability and IL-4 gene expression associate with sepsis or TB？This is we want to discussion.
Many factors determined capacity of cytokine production and release; the hereditary factor is a important ones of them. Genomic variations also may affect gene expression profiles, as well as the structure and production of proteins. In this study, we investigate the IL-4 gene expression polymorphism, and we also investigate the quantification of IL-4 and IL-4δ2 mRNA expression by reverse transcription-polymerase chain reaction (RT-PCR) techniques. We observed no significant differences in genotype distribution and allele frequency of the IL-4 gene. But IL-4 and IL-4 δ 2 mRNA expressions were significantly decreased in patients (p<0.05). The IL-4/IL-4δ2 ratio is no significantly lower than controls (p>0.05).
These results suggest that there is no association with IL-4 encoding gene polymorphisms in TB and sepsis. Although the expression of IL-4 and IL-4δ2 were decreased in sepsis, they can not be used to predict the outcome of sepsis. Differences in cytokine expression likely determine whether disease progresses, resolves, or becomes latent. Greater IL-4δ2 expression trends to good reason in TB. The ratio of IL-4/IL-4δ2 is as a possible marker of the phase of disease in TB. The relative roles of IL-4 and IL-4δ2 in the pathogenesis of sepsis and TB deserve further investigation.
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