Campbell D E, Kemp A S
Department of Immunology, Royal Children's Hospital, Melbourne, Australia.
Clin Exp Immunol. 1997 Feb;107(2):392-7. doi: 10.1111/j.1365-2249.1997.278-ce1172.x.
We have examined the cell-mediated immunity (CMI) to Staphylococcus aureus (S. aureus) and Staphylococcal enterotoxin B (SEB) in peripheral blood mononuclear cells (PBMC) from children with atopic dermatitis (AD) and from non-atopic child controls by measurement of proliferative responses and production of the cytokines IFN-gamma and IL-4. PBMC from children with AD showed significantly higher proliferative responses to both S. aureus (P < 0.01) and SEB (P < 0.05). Despite this enhanced proliferation, production of IFN-gamma in response to S. aureus (P < 0.001) and SEB (P < 0.01) from these PBMC was significantly diminished. In contrast, PBMC from children with AD were significantly more likely to produce IL-4 in response to S. aureus (P < 0.01). These findings demonstrate in vitro heightened CMI to S. aureus in children with AD, and implicate S. aureus as a potent inflammatory stimulant. Impaired IFN-gamma production to S. aureus in vivo may result in failure to eradicate S. aureus from skin. The organism's persistence on skin would contribute to inflammation by causing continued T cell activation and release of pro-inflammatory mediators.
我们通过测量增殖反应以及细胞因子IFN-γ和IL-4的产生,检测了特应性皮炎(AD)患儿和非特应性对照儿童外周血单个核细胞(PBMC)对金黄色葡萄球菌(S. aureus)和葡萄球菌肠毒素B(SEB)的细胞介导免疫(CMI)。AD患儿的PBMC对金黄色葡萄球菌(P < 0.01)和SEB(P < 0.05)均表现出显著更高的增殖反应。尽管增殖增强,但这些PBMC对金黄色葡萄球菌(P < 0.001)和SEB(P < 0.01)产生的IFN-γ却显著减少。相反,AD患儿的PBMC对金黄色葡萄球菌产生IL-4的可能性显著更高(P < 0.01)。这些发现表明,AD患儿体外对金黄色葡萄球菌的CMI增强,提示金黄色葡萄球菌是一种强效的炎症刺激物。体内对金黄色葡萄球菌的IFN-γ产生受损可能导致无法从皮肤清除金黄色葡萄球菌。该微生物在皮肤上的持续存在会通过持续激活T细胞和释放促炎介质而导致炎症。