ZFIN ID: ZDB-PUB-130402-2
Looking within the zebrafish to understand the tuberculous granuloma
Ramakrishnan, L.
Date: 2013
Source: Advances in experimental medicine and biology   783: 251-266 (Chapter)
Registered Authors: Ramakrishnan, Lalita
Keywords: tubercles, tuberculous granuloma, mycobacterium tuberculosis, macrophages, necrosis, mycobacterium marinum, zebrafish, tumor necrosis factor, mycobacterium bovis bacillus Calmette-Guerin (BCG) vaccine strain, neutrophils, cell death, host matrix metalloproteinase 9 (MMP9), apoptosis, mycobacteria
MeSH Terms:
  • Animals
  • Antigens, Bacterial/physiology
  • Apoptosis
  • BCG Vaccine/immunology
  • Bacterial Proteins/physiology
  • Disease Models, Animal*
  • Disease Resistance
  • Enzyme Induction
  • Humans
  • Immune Evasion/immunology*
  • Larva
  • Macrophages/microbiology
  • Matrix Metalloproteinase 9/physiology
  • Mycobacterium Infections, Nontuberculous/immunology
  • Mycobacterium Infections, Nontuberculous/pathology
  • Mycobacterium Infections, Nontuberculous/veterinary*
  • Mycobacterium marinum/growth & development
  • Mycobacterium marinum/immunology*
  • Mycobacterium marinum/pathogenicity
  • Mycobacterium tuberculosis/growth & development
  • Mycobacterium tuberculosis/immunology
  • Mycobacterium tuberculosis/pathogenicity
  • Necrosis
  • Tuberculoma/immunology
  • Tuberculoma/microbiology
  • Tuberculoma/pathology*
  • Virulence
  • Zebrafish/growth & development
  • Zebrafish/immunology*
  • Zebrafish Proteins/physiology
PubMed: 23468113 Full text @ Adv. Exp. Med. Biol.
ABSTRACT

Tuberculosis is characterized by the formation of complex immune cell aggregates called granulomas, which for nearly a century have been viewed as critical host-beneficial structures to restrict bacterial growth and spread. A different view has now emerged from real-time visualization of granuloma formation and its consequences in the optically transparent and genetically tractable zebrafish larva. Pathogenic mycobacteria have developed mechanisms to use host granulomas for their expansion and dissemination, at least during the innate phases of infection. Host processes that are intended to be beneficial—death of infected macrophages and their subsequent phagocytosis by macrophages that are newly recruited to the growing granuloma—are harnessed by mycobacteria for their own benefit. Mycobacteria can also render the granuloma a safe-haven in the more advanced stages of infection. An understanding of the host and bacterial pathways involved in tuberculous granuloma formation may suggest new ways to combat mycobacterial infection.

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