Literature DB >> 25144860

An in situ, in vivo murine model for the study of laryngotracheal stenosis.

Alexander T Hillel1, Daryan Namba1, Dacheng Ding1, Vinciya Pandian1, Jennifer H Elisseeff2, Maureen R Horton3.   

Abstract

IMPORTANCE: Laryngotracheal stenosis (LTS) lacks an ideal animal model to study its unique wound-healing pathophysiology and the effect of interventions.
OBJECTIVE: To present an in vivo, in situ mouse model of LTS that can be used to investigate its pathophysiology, mechanisms, and interventions for treatment. DESIGN, SETTING, AND
SUBJECTS: Prospective controlled animal study performed at an academic animal research facility on 87 C57BL/6 mice.
INTERVENTIONS: Experimental mice (n = 40) underwent bleomycin-coated wire-brush injury to the larynx and trachea, while mechanical injury controls (n = 32) underwent phosphate-buffered saline-coated wire-brush injury. Normal controls (n = 9) underwent no intervention, and mock surgery controls (n = 6) underwent anterior transcervical tracheal exposure only. Laryngotracheal complexes were harvested at days 7, 14, and 21 after injury. At the respective time points, mice in the chemomechanical and mechanical injury groups were killed, and their laryngotracheal complexes were harvested for histologic analysis. Normal and mock surgery controls were killed and then underwent histologic analysis. MAIN OUTCOMES AND MEASURES: The primary outcome measure was lamina propria thickness.
RESULTS: The chemomechanical injury group maintained a significant increase in lamina propria thickness through day 21 compared with uninjured controls at day 7 (82.7 vs 41.8 μm; P<.05), day 14 (93.5 vs 26.0 μm; P<.05), and day 21 (91.2 vs 40.8 μm; P<.05). Compared with the mechanical injury group, the chemomechanical injury group demonstrated a significantly increased thickness at 21 days (91.2 vs 33.7 μm; P<.05). CONCLUSIONS AND RELEVANCE: Chemomechanical initiation of fibrosis in situ creates a viable mouse model of LTS that incorporates the physiologic circulatory supply and airflow. This small-animal model may be used to investigate the pathogenesis and inflammatory mechanisms of iatrogenic LTS and test therapeutic interventions to reverse or reduce the development of fibrosis.

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Mesh:

Year:  2014        PMID: 25144860     DOI: 10.1001/jamaoto.2014.1663

Source DB:  PubMed          Journal:  JAMA Otolaryngol Head Neck Surg        ISSN: 2168-6181            Impact factor:   6.223


  15 in total

1.  Fibroblasts in Hypoxic Conditions Mimic Laryngotracheal Stenosis.

Authors:  Linda X Yin; Kevin M Motz; Idris Samad; Madhavi Duvvuri; Michael Murphy; Dacheng Ding; Alexander T Hillel
Journal:  Otolaryngol Head Neck Surg       Date:  2017-03-28       Impact factor: 3.497

2.  Metabolic variations in normal and fibrotic human laryngotracheal-derived fibroblasts: A Warburg-like effect.

Authors:  Garret Ma; Idris Samad; Kevin Motz; Linda X Yin; Madhavi V Duvvuri; Dacheng Ding; Daryan R Namba; Jennifer H Elisseeff; Maureen R Horton; Alexander T Hillel
Journal:  Laryngoscope       Date:  2016-09-01       Impact factor: 3.325

3.  Rapamycin inhibits human laryngotracheal stenosis-derived fibroblast proliferation, metabolism, and function in vitro.

Authors:  Daryan R Namba; Garret Ma; Idris Samad; Dacheng Ding; Vinciya Pandian; Jonathan D Powell; Maureen R Horton; Alexander T Hillel
Journal:  Otolaryngol Head Neck Surg       Date:  2015-03-09       Impact factor: 3.497

4.  Targeting metabolic abnormalities to reverse fibrosis in iatrogenic laryngotracheal stenosis.

Authors:  Michael K Murphy; Kevin M Motz; Dacheng Ding; Linda Yin; Madhavi Duvvuri; Michael Feeley; Alexander T Hillel
Journal:  Laryngoscope       Date:  2017-09-20       Impact factor: 3.325

5.  T-Helper 2 Lymphocyte Immunophenotype Is Associated With Iatrogenic Laryngotracheal Stenosis.

Authors:  Alexander T Hillel; Dacheng Ding; Idris Samad; Michael K Murphy; Kevin Motz
Journal:  Laryngoscope       Date:  2018-11-13       Impact factor: 3.325

6.  Pathologic Fibroblasts in Idiopathic Subglottic Stenosis Amplify Local Inflammatory Signals.

Authors:  Robert J Morrison; Nicolas-George Katsantonis; Kevin M Motz; Alexander T Hillel; C Gaelyn Garrett; James L Netterville; Christopher T Wootten; Susan M Majka; Timothy S Blackwell; Wonder P Drake; Alexander Gelbard
Journal:  Otolaryngol Head Neck Surg       Date:  2018-10-16       Impact factor: 3.497

7.  Engineering an immunomodulatory drug-eluting stent to treat laryngotracheal stenosis.

Authors:  Madhavi Duvvuri; Kevin Motz; Michael Murphy; Michael Feeley; Dacheng Ding; Andrew Lee; Jennifer H Elisseeff; Alexander T Hillel
Journal:  Biomater Sci       Date:  2019-04-23       Impact factor: 6.843

8.  Dysregulated Macrophages Are Present in Bleomycin-Induced Murine Laryngotracheal Stenosis.

Authors:  Alexander T Hillel; Idris Samad; Garret Ma; Dacheng Ding; Kaitlyn Sadtler; Jonathan D Powell; Andrew P Lane; Maureen R Horton
Journal:  Otolaryngol Head Neck Surg       Date:  2015-06-17       Impact factor: 3.497

9.  Design of a Biocompatible Drug-Eluting Tracheal Stent in Mice with Laryngotracheal Stenosis.

Authors:  Madhavi Duvvuri; Kevin Motz; Hsiu-Wen Tsai; Ioan Lina; Dacheng Ding; Andrew Lee; Alexander T Hillel
Journal:  J Vis Exp       Date:  2020-01-21       Impact factor: 1.355

10.  Glutamine Inhibition Reduces Iatrogenic Laryngotracheal Stenosis.

Authors:  Hsiu-Wen Tsai; Ioan Lina; Kevin M Motz; Liam Chung; Dacheng Ding; Michael K Murphy; Michael Feeley; Jennifer H Elisseeff; Alexander T Hillel
Journal:  Laryngoscope       Date:  2021-01-12       Impact factor: 2.970

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