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ZFIN ID: ZDB-PUB-121102-26
Innate Immune Response to Streptococcus iniae Infection in Zebrafish Larvae
Harvie, E.A., Green, J.M., Neely, M.N., and Huttenlocher, A.
Date: 2013
Source: Infection and Immunity   81(1): 110-121 (Journal)
Registered Authors: Huttenlocher, Anna, Neely, Melody N.
Keywords: none
MeSH Terms:
  • Animals
  • Bacterial Capsules/immunology
  • Bacterial Proteins/immunology
  • Immunity, Innate/immunology
  • Larva
  • Macrophages/immunology
  • Macrophages/microbiology
  • Myeloid Cells/immunology
  • Myeloid Cells/microbiology
  • Neutrophils/immunology
  • Neutrophils/microbiology
  • Phagocytosis/immunology
  • Streptococcal Infections/immunology*
  • Streptococcal Infections/microbiology
  • Streptococcus/immunology*
  • Zebrafish/immunology*
  • Zebrafish/microbiology*
PubMed: 23090960 Full text @ Infect. Immun.

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 hours post infection. In contrast, a S. iniae mutant deficient in polysaccharide capsule (cpsA) was not lethal, with greater than 90% survival at 24 hours post infection. 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. Taken 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.