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Genetic background affects susceptibility in nonfatal pneumococcal bronchopneumonia

¹ Discipline of Immunology & Microbiology, School of Biomedical Sciences, Faculty of Health, University of Newcastle, ² Respiratory and Sleep Medicine, Hunter Medical Research Institute, and School of Medical Practice, John Hunter Hospital, Newcastle, and ³ Vaccines, Immunity/Infection, Viruses and Asthma Group, Hunter Medical Research Institute, New Lambton, New South Wales, Australia

CORRESPONDENCE: P. Hansbro, Bacteriology Research Unit, Vaccines Immunity/Infection Viruses and Asthma, Discipline of Immunology & Microbiology, Level 3, David Maddison Clinical Sciences Building, Royal Newcastle Hospital, Newcastle, New South Wales, 2300, Australia. Fax: 61 249236814. E-mail: Philip.Hansbro@newcastle.edu.au

Keywords: genetic background, immune response, infection, nonfatal, pneumococcus, Streptococcus pneumoniae

Received: July 14, 2003
Accepted September 16, 2003

This work was funded by a Clive & Vera Ramaciotti Research Foundation Grant, the Respiratory SP&T funds, John Hunter Hospital, and the Hunter Medical Research Institute, Newcastle, Australia.

A nonfatal pneumococcal lung infection model was required to investigate immune responses during recovery, and the interaction of other diseases subsequent to infection. A murine model of nonfatal pneumococcal lung infection was developed and the effect of genetic background on susceptibility was determined in BALB/c and C57BL/6 mice.

Bacteria colonised the lungs and mice developed mild clinical illness with pathophysiology similar to human bronchopneumonia. Recovery was associated with immune cell influx, which cleared bacteria but induced tissue damage characteristic of pneumococcal bronchopneumonia.

After clearance, immune cell populations returned to normal and tissues appeared less inflamed. Although bacterial exposure and clearance were similar, the extent of immune cell influx and tissue damage differed significantly. Larger numbers of neutrophils and lymphocytes entered lung tissue and the affected area was greater in BALB/c compared with C57BL/6 mice.

An inflammatory basis for differences was determined with greater levels of phagocytosis and oxidative burst observed in BALB/c mice. C57BL/6 mice cleared the low inoculum with a reduced immune response; however, C57BL/6 mice are more susceptible to larger inocula, which overwhelms the immune system. These different susceptibilities result from a greater inflammatory response in BALB/c compared with C57BL/6 mice.

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