Innate Immune Response to Streptococcus iniae Infection in Zebrafish Larvae
Innate Immune Response to Streptococcus iniae Infection in Zebrafish Larvae
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DOI：
10.1128/iai.00642-12
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发表时间：
2013-01-01
影响因子：
3.1
通讯作者：
Huttenlocher, Anna
中科院分区：
文献类型：
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作者：
Harvie, Elizabeth A.;Green, Julie M.;Huttenlocher, Anna
海豚链球菌引起以脑膜炎和败血症为特征的全身感染。在这里，我们报告了一个S。海绵体感染。注射野生型S. iniae进入耳泡后24 h诱导致死性感染。相比之下，S.多糖荚膜缺陷的iniae突变体（cpsA突变体）在感染后24 h存活率大于90%，不致死。活体成像显示，中性粒细胞和巨噬细胞都被募集到突变型和野生型S。iniae并能够吞噬细菌。中性粒细胞和巨噬细胞的消耗损害了野生型S. iniae和cpsA突变体，表明白细胞是宿主生存的野生型和突变体细菌的存在下至关重要的。然而，中性粒细胞功能受损但巨噬细胞功能正常的斑马鱼幼虫对野生型细菌的易感性增加，但对cpsA突变体没有增加。综合这些发现，我们建立了一个S. iniae感染，并且已经发现，尽管中性粒细胞对于控制野生型S.因此，嗜中性粒细胞不是宿主防御cpsA突变体所必需的。
Streptococcus iniae causes systemic infection characterized by meningitis and sepsis. Here, we report a larval zebrafish model of S. iniae infection. Injection of wild-type S. iniae into the otic vesicle induced a lethal infection by 24 h postinfection. In contrast, an S. iniae mutant deficient in polysaccharide capsule (cpsA mutant) was not lethal, with greater than 90% survival at 24 h postinfection. Live imaging demonstrated that both neutrophils and macrophages were recruited to localized otic infection with mutant and wild-type S. iniae and were able to phagocytose bacteria. Depletion of neutrophils and macrophages impaired host survival following infection with wild-type S. iniae and the cpsA mutant, suggesting that leukocytes are critical for host survival in the presence of both the wild-type and mutant bacteria. However, zebrafish larvae with impaired neutrophil function but normal macrophage function had increased susceptibility to wild-type bacteria but not the cpsA mutant. Taking these findings together, we have developed a larval zebrafish model of S. iniae infection and have found that although neutrophils are important for controlling infection with wild-type S. iniae, neutrophils are not necessary for host defense against the cpsA mutant.