Genetic background affects susceptibility in nonfatal pneumococcal bronchopneumonia.

Preston, JA; Beagley, KW; Gibson, PG; Hansbro, PM

Genetic background affects susceptibility in nonfatal pneumococcal bronchopneumonia.

Preston, JA Beagley, KW Gibson, PG Hansbro, PM

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Publisher:: EUROPEAN RESPIRATORY SOC JOURNALS LTD
Publication Type:: Journal Article
Citation:: The European respiratory journal, 2004, 23, (2), pp. 224-231
Issue Date:: 2004-02

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Field	Value	Language
dc.contributor.author	Preston, JA
dc.contributor.author	Beagley, KW
dc.contributor.author	Gibson, PG
dc.contributor.author	Hansbro, PM
dc.date.accessioned	2020-12-22T22:41:06Z
dc.date.available	2020-12-22T22:41:06Z
dc.date.issued	2004-02
dc.identifier.citation	The European respiratory journal, 2004, 23, (2), pp. 224-231
dc.identifier.issn	0903-1936
dc.identifier.issn	1399-3003
dc.identifier.uri	http://hdl.handle.net/10453/144909
dc.description.abstract	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.
dc.format	Print
dc.language	eng
dc.publisher	EUROPEAN RESPIRATORY SOC JOURNALS LTD
dc.relation.ispartof	The European respiratory journal
dc.relation.isbasedon	10.1183/09031936.03.00081403
dc.rights	info:eu-repo/semantics/restrictedAccess
dc.subject	11 Medical and Health Sciences, 1116 Medical Physiology
dc.subject.classification	Respiratory System
dc.subject.mesh	Lung
dc.subject.mesh	Neutrophils
dc.subject.mesh	Lymphocytes
dc.subject.mesh	Animals
dc.subject.mesh	Mice, Inbred BALB C
dc.subject.mesh	Mice, Inbred C57BL
dc.subject.mesh	Humans
dc.subject.mesh	Mice
dc.subject.mesh	Pneumonia, Pneumococcal
dc.subject.mesh	Bronchopneumonia
dc.subject.mesh	Disease Models, Animal
dc.subject.mesh	Genetic Predisposition to Disease
dc.subject.mesh	Leukocyte Count
dc.subject.mesh	Colony Count, Microbial
dc.subject.mesh	Respiratory Burst
dc.subject.mesh	Phagocytosis
dc.subject.mesh	Genotype
dc.subject.mesh	Models, Genetic
dc.subject.mesh	Adult
dc.subject.mesh	Female
dc.subject.mesh	Adult
dc.subject.mesh	Animals
dc.subject.mesh	Bronchopneumonia
dc.subject.mesh	Colony Count, Microbial
dc.subject.mesh	Disease Models, Animal
dc.subject.mesh	Female
dc.subject.mesh	Genetic Predisposition to Disease
dc.subject.mesh	Genotype
dc.subject.mesh	Humans
dc.subject.mesh	Leukocyte Count
dc.subject.mesh	Lung
dc.subject.mesh	Lymphocytes
dc.subject.mesh	Mice
dc.subject.mesh	Mice, Inbred BALB C
dc.subject.mesh	Mice, Inbred C57BL
dc.subject.mesh	Models, Genetic
dc.subject.mesh	Neutrophils
dc.subject.mesh	Phagocytosis
dc.subject.mesh	Pneumonia, Pneumococcal
dc.subject.mesh	Respiratory Burst
dc.title	Genetic background affects susceptibility in nonfatal pneumococcal bronchopneumonia.
dc.type	Journal Article
utslib.citation.volume	23
utslib.location.activity	England
utslib.for	11 Medical and Health Sciences
utslib.for	1116 Medical Physiology
pubs.organisational-group	/University of Technology Sydney/Faculty of Science
pubs.organisational-group	/University of Technology Sydney/Faculty of Science/School of Life Sciences
pubs.organisational-group	/University of Technology Sydney
utslib.copyright.status	closed_access	*
dc.date.updated	2020-12-22T22:40:56Z
pubs.issue	2
pubs.publication-status	Published
pubs.volume	23
utslib.citation.issue	2

Abstract:

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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http://hdl.handle.net/10453/144909