Zanardo Vincenzo, Nicolussi Silvia, Cavallin Stefania, Trevisanuto Daniele, Barbato Angelo, Faggian Diego, Favaro Flaviano, Plebani Mario
Department of Pediatrics, Padua University School of Medicine, Padua, Italy.
Environ Health Perspect. 2005 Oct;113(10):1410-3. doi: 10.1289/ehp.7702.
Tobacco smoke is immunotoxic, but the effect of smoking on the immunologic function of the mammary gland of mothers who smoke cigarettes ("smoker mothers") has not been studied. Our objective was to test, in smoker mothers, the colostral and transitional milk concentrations of interleukin-(IL)1alpha. The immunomodulators beta-endorphin and leptin were also tested. Pregnant women who self-identified as smokers (greater than or equal to 5 cigarettes per day through pregnancy) or nonsmokers were recruited for study participation. The study population included 42 smoker and 40 nonsmoker nursing mothers, with otherwise uncomplicated gestation, delivery, and puerperium, who were breast-feeding ad libitum their healthy neonates. Colostrum was obtained on the third postpartum day at 0900 hr and transitional milk on the 10th postpartum day at 0900 hr. IL-1alpha concentrations were significantly reduced in the colostrum of smoker mothers compared with nonsmoker mothers (p < 0.01). Colostral beta-endorphin and leptin concentrations were comparable. No significant differences were found between smoker and nonsmoker lactating mothers in transitional milk concentrations of IL-1alpha, beta-endorphin, and leptin. Moreover, beta-endorphin and leptin concentrations were significantly reduced in transitional milk samples compared with colostrum of both smoker and nonsmoker mothers (p < 0.05); also, IL-1alpha transitional milk concentrations were reduced compared with colostrum, but without any significance. This analysis shows that maternal smoking alters the colostral milk levels of the proinflammatory cytokine IL-1alpha. The altered postnatal provision of alternative source of the proinflammatory cytokine IL-1alpha adds understanding to how breast-feeding could be nonprotective against infections among the neonates nursed by smoker mothers.
烟草烟雾具有免疫毒性，但吸烟对吸烟母亲（“吸烟母亲”）乳腺免疫功能的影响尚未得到研究。我们的目的是检测吸烟母亲初乳和过渡乳中白细胞介素 -（IL）1α 的浓度。还检测了免疫调节剂β-内啡肽和瘦素。招募了自认为是吸烟者（整个孕期每天吸烟大于或等于5支）或非吸烟者的孕妇参与研究。研究人群包括42名吸烟和40名不吸烟的哺乳母亲，她们的妊娠、分娩和产褥期均无并发症，正在随意母乳喂养其健康的新生儿。在产后第三天09:00采集初乳，在产后第十天09:00采集过渡乳。与不吸烟母亲相比，吸烟母亲初乳中的IL-1α浓度显著降低（p < 0.01）。初乳中β-内啡肽和瘦素的浓度相当。吸烟和不吸烟的哺乳母亲在过渡乳中IL-1α、β-内啡肽和瘦素的浓度没有显著差异。此外，与吸烟和不吸烟母亲的初乳相比，过渡乳样本中β-内啡肽和瘦素的浓度显著降低（p < 0.05）；同样，与初乳相比，过渡乳中IL-1α的浓度也降低了，但无显著差异。该分析表明，母亲吸烟会改变初乳中促炎细胞因子IL-1α的水平。促炎细胞因子IL-1α产后供应的改变，有助于理解母乳喂养对吸烟母亲所哺育新生儿感染为何可能没有保护作用。
