美國科學(xué)家研究發(fā)現(xiàn)，一些非處方藥,，如阿司匹林,、羥苯基乙酰胺等抑制某些酶的藥物會影響疫苗的效果。
隨著流感季節(jié)的到來和N1H1的威脅,，疫苗的需求空前高漲。盡管那些疫苗是有效的,，但美國密蘇里州大學(xué)研究人員發(fā)現(xiàn),，一些非處方藥，如阿司匹林,、羥苯基乙酰胺等抑制某些酶的藥物會影響疫苗的效果,。
“如果你因為心血管病服用阿司匹林或者治療疼痛、發(fā)熱服用對乙酰氨基酚,，那么你注射疫苗后就不會產(chǎn)生良好的抗體反應(yīng),。”研究人員查爾斯·布朗說。“這些藥物會阻止身體組織中的酶COX-1,。我們發(fā)現(xiàn),，如果COX-1被阻止，那么你身體產(chǎn)生的抗體的數(shù)量會減少,，而你卻需要大量的抗體來保護(hù),。”
COX酶在免疫系統(tǒng)的調(diào)節(jié)上發(fā)揮重要作用,。這些酶的作用機(jī)制還不清楚，對其有抑制作用的藥物會有不良的副作用,。最近研究發(fā)現(xiàn),，抑制COX酶COX-2的藥物會影響疫苗的效果。布朗的研究證明,，抑制存在于全身身體組織（如大腦或腎）中的COX-1酶也會影響疫苗的效果,。
研究人員目前正在研究有關(guān)炎癥的調(diào)解，以及炎癥如何引起疾病和如何去防治疾病的發(fā)生,。許多疾病都是炎癥性疾病,，如關(guān)節(jié)炎、心血管病和糖尿病,。與過去人們認(rèn)為的不同,，炎癥一般情況下是幫助我們機(jī)體免遭感染，是一種有益的機(jī)體反應(yīng),。許多治療炎癥的非激素類藥物會降低抗體反應(yīng),，而這些反應(yīng)是抗擊感染所必需的。
“到目前我們已經(jīng)在動物身上做了試驗,，并發(fā)現(xiàn)這些非激素類藥物確實對疫苗有抑制作用,，下一步我們將要在人類身上進(jìn)行研究。”布朗說,，如果結(jié)果能證明COX-1抑制劑能影響疫苗的效果,，那么在注射疫苗前后兩周就不要服用阿司匹林、羥苯基乙酰胺,、布洛芬等藥物了,。（生物谷Bioon.com）
生物谷推薦原始出處：
The Journal of Immunology, 2009, 183, 5644 -5653
Cyclooxygenase-1 Orchestrates Germinal Center Formation and Antibody Class-Switch via Regulation of IL-171
Victoria A. Blaho,* Matthew W. Buczynski, Edward A. Dennis, and Charles R. Brown2*
*Department of Veterinary Pathobiology and Department of Molecular Microbiology and Immunology, University of Missouri, Columbia, MO 65211; and Department of Pharmacology and Department of Chemistry and Biochemistry, University of California, San Diego, La Jolla, CA 92093
The cyclooxygenase (COX) enzymes are known modulators of innate immune cell function; however, their contributions to adaptive immunity are relatively unknown. We investigated the roles of COX-1 and COX-2 in the humoral immune response to infection with the Lyme disease pathogen Borrelia burgdorferi. We report that in vitro, murine B cells constitutively expressed COX-1 and up-regulated expression of both COX-1 and COX-2 as well as their products PGE2, PGF2, and thromboxane B2 and their receptors following stimulation with B. burgdorferi or anti-CD40. In vitro inhibition of COX-1 and/or COX-2 in murine B cells resulted in decreased eicosanoid production and altered Ab production. Importantly, infection of mice lacking COX-1, but not COX-2, activity resulted in a defect in Ig class-switching and a lack of Borrelia-specific IgG production. This defect correlated with decreased germinal center formation and IL-6 and IL-17 production, and it could be partially recovered by restoration of IL-6, but fully recovered by IL-17. Furthermore, sera from COX-1 inhibitor-treated mice were dramatically less effective in killing B. burgdorferi, but borreliacidal activity was restored in COX-1 inhibitor-treated mice administered IL-17. We conclude that IL-17 plays a role in Ab production and Ig class-switching in response to infection and that COX-1 is a critical, previously unrecognized regulator of this response.
