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Cryptogenic organizing pneumonia in Tomm5(-/-) mice.

P Vogel¹, R W Read, J E Rehg

¹Department of Pathology, St Jude Children's Research Hospital, Memphis, TN 38105, USA. peter.vogel@stjude.org

Veterinary Pathology

|June 13, 2012

Summary

Mitochondrial protein import is crucial. Tomm5 knockout mice unexpectedly developed lung fibrosis, mimicking human cryptogenic organizing pneumonia, highlighting the role of TOMM5 in lung health.

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Area of Science:

Mitochondrial biology
Genetics
Pulmonology

Background:

Mitochondrial proteins are synthesized in the cytosol and imported into mitochondria via the translocase of the outer mitochondrial membrane (TOMM) complex.
TOMM40 is a central component of the TOMM complex, with TOMM5 being a small associated subunit.

Purpose of the Study:

To investigate the in vivo function of TOMM5.
To characterize the phenotype of Tomm5 knockout mice.

Main Methods:

Generation and phenotyping of Tomm5 knockout mice.
Histopathological analysis of lung tissue.

Main Results:

Tomm5 knockout mice exhibited a lung-specific phenotype characterized by widespread intra-alveolar fibrosis.
Histopathology revealed lesions consistent with human cryptogenic organizing pneumonia (COP)/bronchiolitis obliterans organizing pneumonia (BOOP).
Lesions featured intraluminal fibrogenic buds and significant eosinophilic and macrophage infiltration.

Conclusions:

The study reveals an unexpected role for TOMM5 in maintaining lung homeostasis.
Tomm5 deficiency leads to lung fibrosis resembling human fibrotic lung diseases.
Histopathology is a valuable tool in high-throughput phenotyping for identifying novel disease models.