Lipoteichoic acid (LTA), a cell wall component of gram-positive bacteria, up-regulates inflammatory cytokine production through the toll-like receptor 2 (TLR2) signaling pathway, and also contributes to anti-inflammatory responses against immune cells stimulated by lipopolysaccharides. In the current study, we examined the effects of LTAs isolated from Staphylococcus aureus (aLTA) and Lactobacillus plantarum (pLTA) on the aggravation and alleviation of atopic dermatitis (AD). aLTA strongly induced CCL2 production in THP-1 cells. CCL2 was regulated by the TLR2 pathway including the activation of IRAK2, NF-κB and JNK. CCL2 induced Th2 polarization of CD4+T cells through induction of interleukin (IL)-2, −4, and −5 and inhibition of interferon-gamma (IFN-γ). CCL2 levels and immunoglobulin E (IgE) production were increased in aLTA-injected mice. On the other hand, pLTA moderately affected CCL2 production and it inhibited aLTA-mediated CCL2 production. The serum levels of CCL2 and IgE were inhibited by pLTA pre-injection followed by aLTA reinjection, which resulted in the alleviation of irritant contact dermatitis (ICD) symptoms. Our results suggest that S. aureus infection causes an increase in CCL2 production, and may exacerbate atopic dermatitis (AD)-like symptoms through the excessive IgE production. Alternatively, pLTA alleviated AD-like symptoms by inhibiting aLTA-induced CCL2 and IgE production.

脂蛋白磷酸（LTA）是革兰氏阳性细菌的细胞壁成分，它通过toll样受体2（TLR2）信号传导途径上调炎症细胞因子的产生，并且还有助于抵抗由脂多糖刺激的免疫细胞的抗炎反应。在本研究中，我们研究了从金黄色葡萄球菌（aLTA）和植物乳杆菌分离的LTA的作用（pLTA）对特应性皮炎（AD）的加重和缓解。aLTA在THP-1细胞中强烈诱导CCL2产生。CCL2受TLR2途径调控，包括IRAK2，NF-κB和JNK的激活。CCL2通过诱导白介素（IL）-2，-4和-5以及抑制干扰素-γ（IFN-γ）诱导CD4 + T细胞的Th2极化。在注射了ALTA的小鼠中，CCL2水平和免疫球蛋白E（IgE）的产生增加了。另一方面，pLTA适度影响了CCL2的产生，并抑制了aLTA介导的CCL2的产生。预先注射pLTA，然后再注射aLTA，可抑制CCL2和IgE的血清水平，从而减轻刺激性接触性皮炎（ICD）症状。我们的结果表明金黄色葡萄球菌感染会导致CCL2产生增加，并可能因IgE产生过多而加剧特应性皮炎（AD）样症状。或者，pLTA通过抑制aLTA诱导的CCL2和IgE产生来缓解AD样症状。