Resilience to bacterial infection: difference between species could be due to proteins in serum.
Resilience to bacterial infection: difference between species could be due to proteins in serum.
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DOI：
10.1086/649557
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发表时间：
2010-01-15
期刊：
影响因子：
--
通讯作者：
Cavaillon JM
中科院分区：
文献类型：
--
作者：
Warren HS;Fitting C;Hoff E;Adib-Conquy M;Beasley-Topliffe L;Tesini B;Liang X;Valentine C;Hellman J;Hayden D;Cavaillon JM
脊椎动物对传染病的抵抗力和恢复力各不相同，调节这两个经常相反的保护过程之间的权衡的机制尚不清楚。物种对同等病原体负荷(恢复力)引起的破坏性炎症的敏感度的变异性使反映人类疾病的动物模型的使用复杂化。我们发现，在体外，巨噬细胞对炎症刺激的反应诱导促炎细胞因子的诱导，是由物种血清中的蛋白质调节的，与它们在体内对致死剂量的细菌脂多糖的弹性成反比，范围超过10,000倍。这一发现表明，血清中的蛋白质，而不是固有的细胞差异，可能在调节物种之间对微生物相关分子模式的弹性差异方面发挥作用。循环蛋白质作为关键分子的参与增加了人们对这一过程可能被操纵以创造更好的动物模型和潜在的新药物靶点的希望。
Vertebrates vary in resistance and resilience to infectious diseases, and the mechanisms regulating the trade-off between these two often opposing protective processes are not well understood. Variability in the sensitivity of species to induction of damaging inflammation in response to equivalent pathogen loads (resilience) complicates the use of animal models that reflect human disease. We found that induction of pro-inflammatory cytokines from macrophages in response to inflammatory stimuli in vitro is regulated by proteins in the sera of species in inverse proportion to their in vivo resilience to lethal doses of bacterial lipopolysaccharide over a range of 10,000-fold. This finding suggests that proteins in serum rather than intrinsic cellular differences may play a role in regulating variations in resilience to microbe-associated molecular patterns between species. Involvement of circulating proteins as key molecules raises hope that the process might be manipulated to create better animal models and potentially new drug targets.
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DOI：
10.1186/cc5055
发表时间：
2006
期刊：
Critical care (London, England)
影响因子：
--
作者：
Cavaillon JM;Adib-Conquy M
通讯作者：
Adib-Conquy M
影响因子：
3.1
作者：
GOLENBOCK, DT;WILL, JA;PROCTOR, RA
通讯作者：
PROCTOR, RA
影响因子：
3.8
作者：
Marie, C;Pitton, C;Cavaillon, JM
通讯作者：
Cavaillon, JM
影响因子：
4.4
作者：
Bagchi, Aranya;Herrup, Elizabeth A.;Hellman, Judith
通讯作者：
Hellman, Judith
影响因子：
6.4
作者：
MICHALEK, SM;MOORE, RN;MERGENHAGEN, SE
通讯作者：
MERGENHAGEN, SE