PT - JOURNAL ARTICLE AU - J.A. Preston AU - K.W. Beagley AU - P.G. Gibson AU - P.M. Hansbro TI - Genetic background affects susceptibility in nonfatal pneumococcal bronchopneumonia AID - 10.1183/09031936.03.00081403 DP - 2004 Feb 01 TA - European Respiratory Journal PG - 224--231 VI - 23 IP - 2 4099 - http://erj.ersjournals.com/content/23/2/224.short 4100 - http://erj.ersjournals.com/content/23/2/224.full SO - Eur Respir J2004 Feb 01; 23 AB - 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. 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.