Center for Allergy and Asthma Research at SUNY Downstate, State University of New York (SUNY) Downstate Medical Center, 450 Clarkson Ave., Brooklyn, NY 11203, USA.
J Antimicrob Chemother. 2013 Oct;68(10):2363-8. doi: 10.1093/jac/dkt179. Epub 2013 Jun 7.
Chlamydia pneumoniae, an obligate intracellular bacterium, has been associated with asthma and the induction of immunoglobulin E (IgE) responses. Whereas tetracyclines have anti-chlamydial activity, their effect on human IgE responses to C. pneumoniae has not been studied.
Peripheral blood mononuclear cells (PBMCs) from serum IgE+ allergic asthmatic subjects (n = 11) and healthy controls (n = 12) were infected with C. pneumoniae and cultured for 12 days with or without doxycycline (0.01-1.0 mg/L). IgE, interferon (IFN)-γ and interleukin (IL)-4 levels in supernatants were determined on days 1-12 post-infection, and C. pneumoniae DNA copy numbers in PBMC culture were measured on day 2 (quantitative PCR).
C. pneumoniae-infected PBMCs from allergic asthmatic individuals had increased levels of IgE in supernatants compared with uninfected PBMCs (520% on day 10 post-infection, P = 0.008). IgE levels in PBMC cultures from controls were undetectable (<0.3 ng/mL). Increases in C. pneumoniae-induced IgE in asthmatics correlated with those of C. pneumoniae-induced IL-4 (r = 0.98; P < 0.001), but not with IFN-γ. The addition of doxycycline (1.0 mg/L) to the culture strongly suppressed the production of IgE (>70%, P = 0.04) and IL-4 (75%, P = 0.018), but not IFN-γ. The suppressive effect on IL-4 production remained significant even at concentrations of doxycycline that were subinhibitory (0.01 mg/L) for C. pneumoniae. In both asthmatic participants and controls, no significant effect of doxycycline on DNA copy numbers of C. pneumoniae was observed.
Doxycycline suppressed the C. pneumoniae-induced production of IgE and IL-4, but not IFN-γ, in PBMCs from IgE+ allergic asthmatic subjects. These findings resulted from the immunomodulatory anti-allergic properties of tetracyclines.
肺炎衣原体是一种专性细胞内细菌,与哮喘和免疫球蛋白 E(IgE)反应的诱导有关。虽然四环素具有抗衣原体活性,但它们对人类对肺炎衣原体的 IgE 反应的影响尚未得到研究。
从血清 IgE+过敏性哮喘患者(n=11)和健康对照者(n=12)的外周血单核细胞(PBMC)中分离出肺炎衣原体,并在有或没有强力霉素(0.01-1.0 mg/L)的情况下培养 12 天。在感染后第 1-12 天测定上清液中的 IgE、干扰素(IFN)-γ和白细胞介素(IL)-4 水平,并在第 2 天(定量 PCR)测定 PBMC 培养物中的肺炎衣原体 DNA 拷贝数。
与未感染的 PBMC 相比,来自过敏性哮喘患者的肺炎衣原体感染的 PBMC 上清液中 IgE 水平升高(感染后第 10 天升高 520%,P=0.008)。对照者 PBMC 培养物中的 IgE 水平无法检测到(<0.3 ng/mL)。哮喘患者肺炎衣原体诱导的 IgE 增加与肺炎衣原体诱导的 IL-4 增加相关(r=0.98;P<0.001),但与 IFN-γ无关。在培养物中加入强力霉素(1.0 mg/L)可强烈抑制 IgE(>70%,P=0.04)和 IL-4(75%,P=0.018)的产生,但不能抑制 IFN-γ。即使在强力霉素对肺炎衣原体的亚抑菌浓度(0.01 mg/L)下,对 IL-4 产生的抑制作用仍然显著。在哮喘患者和对照者中,强力霉素对肺炎衣原体 DNA 拷贝数均无显著影响。
强力霉素抑制了 IgE+过敏性哮喘患者 PBMC 中肺炎衣原体诱导的 IgE 和 IL-4 的产生,但不抑制 IFN-γ。这些发现是由于四环素的免疫调节抗过敏特性。