Lacroix-Lamandé Sonia, Mancassola Roselyne, Auray Gaël, Bernardet Nelly, Laurent Fabrice
Laboratoire Contrôle et Immunologie des Maladies Entériques du Nouveau-né, INRA, UR1282, Infectiologie Animale et Santé Publique, F-37380 Nouzilly, France.
Microbes Infect. 2008 Apr;10(4):390-5. doi: 10.1016/j.micinf.2007.12.020. Epub 2008 Jan 9.
Chemokines play a critical role in immune cell trafficking and the transition from an innate to an acquired immune response. We analyzed host response in neonatal mice deficient in chemokine receptor CCR5 following infection with the intracellular protozoan parasite Cryptosporidium parvum. CCR5 neonatal mice had a higher parasite burden at the early stage of infection but eliminated the parasite as efficiently as their wild-type counterparts. The higher sensitivity of neonates at the beginning of infection was not due to an altered IFNgamma response. An increased CCR2-attracting chemokine response associated with the recruitment of CCR2-positive cells in the infected mucosa may have compensated for the absence of CCR5. A lack of CCR5 thus has an impact in the early stage of C. parvum infection in neonates, but this receptor is dispensable for subsequent parasite elimination.
趋化因子在免疫细胞运输以及从先天免疫反应向获得性免疫反应的转变过程中发挥着关键作用。我们分析了趋化因子受体CCR5缺陷的新生小鼠在感染细胞内原生动物寄生虫微小隐孢子虫后的宿主反应。CCR5缺陷的新生小鼠在感染早期寄生虫负荷较高，但清除寄生虫的效率与野生型小鼠相当。新生儿在感染初期较高的敏感性并非由于IFNγ反应改变所致。与感染黏膜中CCR2阳性细胞募集相关的CCR2趋化因子反应增强可能弥补了CCR5的缺失。因此，CCR5的缺乏对新生儿微小隐孢子虫感染的早期阶段有影响，但该受体对于随后清除寄生虫并非必需。
