Department of Pulmonology and Allergology, Université Libre de Bruxelles (ULB), University Children's Hospital Queen Fabiola, Avenue J,J, Crocq 15, Brussels, 1020, Belgium.
J Inflamm (Lond). 2010 Jun 2;7:28. doi: 10.1186/1476-9255-7-28.
Gender influences clinical presentations and markers in inflammatory diseases. In many chronic conditions, frequency of complications is greater in females, suggesting that continuous inflammatory reaction may induce greater damage in targeted organs and functions.
To investigate gender dimorphism at a cellular level, we evaluated the production of cytokines implicated in inflammatory processes (IL -1, IL- 6, PGE-2 and TNF alpha), in healthy prepubescent children of both sex and Turner's syndrome (TS) patients (genotype XO). We used stimulation by LPS (0.2 and 1 ng/ml) and Pokeweed Mitogen (PWM) on overnight cultures from whole blood samples, collected in 57 subjects: 22 girls/26 boys (5-96 months), and 9 TS patients (6-15 years). The primary outcome was to evaluate if gender influences the production of cytokines, with potential relation to X chromosome monosomy. Secondary endpoints were to relate different cytokines level productions and conditions.
We confirm the male over female increased cytokine productions already observed in adults. This is contrasting with numerous observations obtained in vivo about increased production of inflammatory markers in females (CRP, ESR and neutrophil counts), as we recently reported in children. Relative variations of the dimorphism according to stimulus, its concentration and cytokine type are discussed, presenting IL6 with a modulating function that could be more potent in males. TS subjects follow mostly the male pattern of reactivity, sustaining the role of some gene expression differing with X chromosome monosomy and disomy.
Persistence of the latter dimorphism throughout life casts doubts on its direct relationship with individual hormonal status, as already documented by others in vitro, and supports the need for alternative hypothesis, such as the influence of X chromosome gene products escaping X inactivation in females and absent in subjects with X monosomy (males, TS).
性别会影响炎症性疾病的临床表现和标志物。在许多慢性疾病中，女性并发症的频率更高，这表明持续的炎症反应可能会对靶向器官和功能造成更大的损害。
为了在细胞水平上研究性别二态性，我们评估了细胞因子（IL-1、IL-6、PGE-2 和 TNF-α）在健康青春期前儿童（男童和女童）和特纳综合征（TS）患者（XO 基因型）中的产生情况。我们使用 LPS（0.2 和 1ng/ml）和 Pokeweed 促分裂原（PWM）刺激 overnight 培养的全血样本，共采集了 57 名受试者：22 名女孩/26 名男孩（5-96 个月）和 9 名 TS 患者（6-15 岁）。主要结果是评估性别是否影响细胞因子的产生，这可能与 X 染色体单体有关。次要终点是研究不同细胞因子水平的产生和条件之间的关系。
我们证实了男性比女性产生细胞因子的增加，这与我们最近在儿童中报告的体内观察结果相矛盾，即女性炎症标志物（CRP、ESR 和中性粒细胞计数）的产生增加。我们讨论了根据刺激物、其浓度和细胞因子类型而变化的二态性的相对变化，IL6 具有调节功能，在男性中可能更有效。TS 患者的反应模式主要遵循男性模式，支持一些基因表达的差异与 X 染色体单体和三体有关。
这种二态性在整个生命周期中的持续存在，使人对其与个体激素状态的直接关系产生怀疑，正如其他人在体外已经证明的那样，这支持了需要替代假设的必要性，例如 X 染色体基因产物在女性中逃避 X 失活的影响，而在 X 单体的个体（男性，TS）中不存在。
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