- Oral presentation
- Open Access
0034. Changes of TLR2, TLR4, MYD88 MRNA expressions on peripheral blood mononuclear cell in severe sepsis patients during treatment with thymosin α1
© Tang et al; licensee Springer. 2014
- Published: 26 September 2014
- Public Health
- Mortality Rate
- mRNA Expression
- High Mortality
- Randomize Control Trial
Severe sepsis is associated with a high mortality rate despite implementation of guidelinerecommendations. Thymosin alpha 1 (Ta1) has been used to treat severe sepsis as a promising beneficial immunomodulatory drug, but its mechanism remains unclear.
To examine the TLR2, TLR4 and MyD88 mRNA expressions on human peripheral blood mononuclear cells during treatment.
A prospective randomized control trial was designed. Fifty-four patients with severe sepsis were enrolled and randomized into thymosin group (26 cases, treated with thymosin alpha 1) and control group (28 cases). TLR2, TLR4 and MyD88 mRNA were tested by RT-PCR on the day of enrollment, day 3 and day 7 after treatment in both groups, 28 day mortality in these patients was analyzed.
There was no statistical significance between 28 day mortality rate in the control group and that of thymosin group(35.7% vs 23.1%, P=0.310). TLR2, TLR4 and MyD88 mRNA expressions in the thymosin group were respectively increased on enrollment day, day 3 and day 7, however, this increasing trend was not found in the control group. On day 3, TLR2 and TLR4 mRNA expressions in the thymosin group were higher than those in the control group (2.31±0.79 vs 1.83±0.51, 7.31±0.79 vs 6.55±0.92, P<0.05). On day 7, TLR2, TLR4 and MyD88 mRNA expressions in the thymosin group were higher than those in the control group (2.75±1.17 vs 1.63±0.36; 7.75±1.03 vs 6.39±0.72; 4.26±0.77 vs 3.77±0.68, P<0.05).
Thymosin alpha 1 may increase TLR2,TLR4 and MyD88 mRNA expressions in severe sepsis patients.
- Hotchkiss RS, Karl IE: The pathophysiology and treatment of sepsis[J]. N Engl J Med 2003,348(2):138–150. 10.1056/NEJMra021333PubMedView ArticleGoogle Scholar
- Garaci E: Thymosin alpha1: a historical overview[J]. Ann N Y Acad Sci 2007, 1112: 14–20. 10.1196/annals.1415.039PubMedView ArticleGoogle Scholar
- Romani L, Bistoni F, Gaziano R, et al.: Thymosin alpha 1 activates dendritic cells for antifungal Th1 resistance through toll-like receptor signaling[J]. Blood 2004,103(11):4232–4239. 10.1182/blood-2003-11-4036PubMedView ArticleGoogle Scholar
- Peck-Palmer OM, Unsinger J, Chang KC, et al.: Deletion of MyD88 markedly attenuates sepsis-induced T and B lymphocyte apoptosis but worsens survival[J]. J Leukoc Biol 2008,83(4):1009–1018. 10.1189/jlb.0807528PubMedView ArticleGoogle Scholar
- De Luca A, Montagnoli C, Zelante T, et al.: Functional yet balanced reactivity to Candida albicans requires TRIF, MyD88, and IDO-dependent inhibition of Rorc[J]. J Immunol 2007,179(9):5999–6008. 10.4049/jimmunol.179.9.5999PubMedView ArticleGoogle Scholar
This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.