Murine models of pulmonary fibrosis.

@article{Moore2008MurineMO,
  title={Murine models of pulmonary fibrosis.},
  author={Bethany B. Moore and Cory M. Hogaboam},
  journal={American journal of physiology. Lung cellular and molecular physiology},
  year={2008},
  volume={294 2},
  pages={
          L152-60
        }
}
  • B. MooreC. Hogaboam
  • Published 1 February 2008
  • Biology, Medicine
  • American journal of physiology. Lung cellular and molecular physiology
Human pulmonary fibrosis is characterized by alveolar epithelial cell injury, areas of type II cell hyperplasia, accumulation of fibroblasts and myofibroblasts, and the deposition of extracellular matrix proteins. The result is a progressive loss of normal lung architecture and impairment in gas exchange. Pertinent features of the human disease include temporal heterogeneity of the fibrotic lesions, progressive nature of the disease, development of fibrotic foci, and in some patients, a rapid… 

Tables from this paper

Molecular and cellular mechanisms of pulmonary fibrosis

Three broad areas which have been explored that may be responsible for the combination of altered lung fibroblasts, loss of alveolar epithelial cells, and excessive accumulation of ECM are discussed: inflammation and immune mechanisms, oxidative stress and oxidative signaling, and procoagulant mechanisms.

Experimental mouse model of Bleomycin-induced Pulmonary Fibrosis

This model is presented as a reference for studies on the pulmonary fibrosis with different cellular and molecular markers such as by total protein concentration, total cell count, immune cell differential count, and the expression of pro-inflammatory mediators.

Animal Models of Pulmonary Fibrosis.

This chapter discusses the application of two of the most commonly employed direct lung instillation models, namely, the induction of pulmonary fibrosis with bleomycin or fluorescein isothiocyanate (FITC) and methods to induce fibrosis in aged mice using murine gamma-herpesvirus (γHV-68).

Irreversibility of Pulmonary Fibrosis

The underlying pathogenesis of irreversible pulmonary fibrosis is focused on from the above aspects as well as preclinical disease models, and directions for future studies are suggested.

Idiopathic Pulmonary Fibrosis: A Disorder of Epithelial Cell Dysfunction

Although the nature of injurious events and processes involved in aberrant repair of the alveolar epithelium are not well understood, ongoing investigations provide hope to better understand mechanisms by which AECs maintain homeostasis or contribute to fibrosis.

Animal models of fibrotic lung disease.

Each of the models reviewed in this report offers a powerful tool for studying some aspect of fibrotic lung disease and has a much better understanding of the fact that the aged lung has increased susceptibility to fibrosis.

Experimental Models of Pulmonary Fibrosis and their Translational Potential

The characteristics of the most frequently used animal models of fibrosis, including the limitations of their use are reviewed, to allow preclinical testing of novel treatment approaches or their combinations in the laboratory conditions before their use in the clinical practice.

Modeling pulmonary fibrosis with bleomycin

The characteristics of the bleomycin animal model, the most commonly used model of pulmonary fibrosis, are summarized, highlighting recent advances it has led us to despite its disadvantages.
...

Mechanisms and mediators of pulmonary fibrosis.

The development of effective therapies will require the understanding of the complex interplay of the various mediators and the mechanisms of remodeling.

A novel model for human interstitial lung disease: Hapten‐driven lung fibrosis in rodents

A novel model of chronic pulmonary fibrosis in rodents induced by a single intratracheal instillation of a well‐characterized fluorescent haptenic antigen, fluorescein isothiocyanate, which results in an acute inflammatory response involving a granulocytic infiltrate, which disappears over a week and is replaced by a chronic mononuclear infiltrate in which T lymphocytes predominate.

Fibrosis of the lung and other tissues: new concepts in pathogenesis and treatment.

Data will be provided to support the role of Type 2 cytokines in the pathogenesis of fibrosis and novel therapeutic options based on inhibiting these pathways will be described.

Expression of a tumor necrosis factor-alpha transgene in murine lung causes lymphocytic and fibrosing alveolitis. A mouse model of progressive pulmonary fibrosis.

Pulmonary pathology in the SP-C T NF-alpha mice bears a striking resemblance to human idiopathic pulmonary fibrosis, in which increased expression of TNF-alpha in type II epithelial cells has also been noted.

Lung infection with gamma-herpesvirus induces progressive pulmonary fibrosis in Th2-biased mice.

  • A. MoraC. Woods A. Stecenko
  • Medicine, Biology
    American journal of physiology. Lung cellular and molecular physiology
  • 2005
Chronic herpesvirus pulmonary infection in IFN-gammaR-/- mice causes progressive pulmonary fibrosis and many of the pathological features seen in IPF.

Protection from Pulmonary Fibrosis in the Absence of CCR2 Signaling1

It is demonstrated that CCR2−/− mice are protected from fibrosis in both the FITC and bleomycin pulmonary fibrosis models, and the protection is not explained by differences in acute lung injury, or the magnitude or composition of inflammatory cells.

A role for C‐C chemokines in fibrotic lung disease

Results indicate that MIP‐1α expression is mediated by alveolar macrophage‐derived tumor necrosis factor, identifying an important cytokine pathway in the initiation of pulmonary fibrosis and providing direct evidence for its involvement in fibrotic pathology.

Repression of Bleomycin-Induced Pneumopathy by TNF

It is demonstrated that in TNF-deficient mice, challenge via airways with murine, but not human rTNF, efficiently eliminated inflammatory cells from the bronchoalveolar space by apoptosis, and thus promoted tissue repair of damaged lungs.

Induction of lung fibrosis in the mouse by intratracheal instillation of fluorescein isothiocyanate is not T-cell-dependent.

...