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Altered postnatal lung development in C3H/HeJ mice.

Venkatesh Sampath¹, Katy Davis, Albert P Senft

¹Division of Pulmonary Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio 45229, USA.

Pediatric Research

|October 27, 2006

Summary

C3H/HeJ mice exhibit enlarged air spaces in their lungs due to Gram-negative bacterial colonization. This early lung infection leads to chronic inflammation and lasting structural lung changes, impacting respiratory health.

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Area of Science:

Pulmonary biology
Microbiology
Immunology

Background:

C3H/HeJ mice show persistent increases in terminal air space area from early life.
This morphological change is not observed in control mouse strains like C3H/SnJ and C3H/OuJ.

Purpose of the Study:

To investigate the causes of altered lung development in C3H/HeJ mice.
To identify the role of bacterial colonization and inflammatory responses in lung morphology changes.

Main Methods:

Morphometric quantification of lung air space area.
Bacteriologic cultures of lung tissue to identify microbial colonization.
Analysis of inflammatory markers including macrophages, matrix metalloproteinase 12 (MMP-12), and cytokines (MCP-1, KC).
Investigated nuclear factor-kappaB (NF-kappaB) activation via Toll-like receptor 5 (TLR5) signaling.

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Main Results:

C3H/HeJ mice had a 50% increase in air space area by postnatal day 14 and a 2.3-fold increase by 2 months.
Predominant Gram-negative bacteria (Escherichia coli, Proteus mirabilis) were found in 13/14 C3H/HeJ mice but not in controls.
Increased macrophages, MMP-12, MCP-1, and KC levels were observed in C3H/HeJ mice.
P. mirabilis induced NF-kappaB activation in TLR5-transfected HEK 293 cells.

Conclusions:

Early Gram-negative bacterial colonization of the developing lung in C3H/HeJ mice is linked to permanent changes in lung morphology.
Toll-like receptor 4 (TLR4) signaling pathways are implicated in the association between bacterial colonization, chronic inflammation, and altered lung structure.