美国科学家研究发现，一些非处方药，如阿司匹林、羟苯基乙酰胺等抑制某些酶的药物会影响疫苗的效果。
随着流感季节的到来和N1H1的威胁，疫苗的需求空前高涨。尽管那些疫苗是有效的，但美国密苏里州大学研究人员发现，一些非处方药，如阿司匹林、羟苯基乙酰胺等抑制某些酶的药物会影响疫苗的效果。
“如果你因为心血管病服用阿司匹林或者治疗疼痛、发热服用对乙酰氨基酚，那么你注射疫苗后就不会产生良好的抗体反应。”研究人员查尔斯·布朗说。“这些药物会阻止身体组织中的酶COX-1。我们发现，如果COX-1被阻止，那么你身体产生的抗体的数量会减少，而你却需要大量的抗体来保护。”
COX酶在免疫系统的调节上发挥重要作用。这些酶的作用机制还不清楚，对其有抑制作用的药物会有不良的副作用。最近研究发现，抑制COX酶COX-2的药物会影响疫苗的效果。布朗的研究证明，抑制存在于全身身体组织（如大脑或肾）中的COX-1酶也会影响疫苗的效果。
研究人员目前正在研究有关炎症的调解，以及炎症如何引起疾病和如何去防治疾病的发生。许多疾病都是炎症性疾病，如关节炎、心血管病和糖尿病。与过去人们认为的不同，炎症一般情况下是帮助我们机体免遭感染，是一种有益的机体反应。许多治疗炎症的非激素类药物会降低抗体反应，而这些反应是抗击感染所必需的。
“到目前我们已经在动物身上做了试验，并发现这些非激素类药物确实对疫苗有抑制作用，下一步我们将要在人类身上进行研究。”布朗说，如果结果能证明COX-1抑制剂能影响疫苗的效果，那么在注射疫苗前后两周就不要服用阿司匹林、羟苯基乙酰胺、布洛芬等药物了。（生物谷Bioon.com）
生物谷推荐原始出处：
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.
