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Exogenous leptin enhances markers of airway fibrosis in a mouse model of chronic allergic airways disease.

Publication ,  Journal Article
Ihrie, MD; McQuade, VL; Womble, JT; Hegde, A; McCravy, MS; Lacuesta, CVG; Tighe, RM; Que, LG; Walker, JKL; Ingram, JL
Published in: Respir Res
May 24, 2022

BACKGROUND: Asthma patients with comorbid obesity exhibit increased disease severity, in part, due to airway remodeling, which is also observed in mouse models of asthma and obesity. A mediator of remodeling that is increased in obesity is leptin. We hypothesized that in a mouse model of allergic airways disease, mice receiving exogenous leptin would display increased airway inflammation and fibrosis. METHODS: Five-week-old male and female C57BL/6J mice were challenged with intranasal house dust mite (HDM) allergen or saline 5 days per week for 6 weeks (n = 6-9 per sex, per group). Following each HDM exposure, mice received subcutaneous recombinant human leptin or saline. At 48 h after the final HDM challenge, lung mechanics were evaluated and the mice were sacrificed. Bronchoalveolar lavage was performed and differential cell counts were determined. Lung tissue was stained with Masson's trichrome, periodic acid-Schiff, and hematoxylin and eosin stains. Mouse lung fibroblasts were cultured, and whole lung mRNA was isolated. RESULTS: Leptin did not affect mouse body weight, but HDM+leptin increased baseline blood glucose. In mixed-sex groups, leptin increased mouse lung fibroblast invasiveness and increased lung Col1a1 mRNA expression. Total lung resistance and tissue damping were increased with HDM+leptin treatment, but not leptin or HDM alone. Female mice exhibited enhanced airway responsiveness to methacholine with HDM+leptin treatment, while leptin alone decreased total respiratory system resistance in male mice. CONCLUSIONS: In HDM-induced allergic airways disease, administration of exogenous leptin to mice enhanced lung resistance and increased markers of fibrosis, with differing effects between males and females.

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Published In

Respir Res

DOI

EISSN

1465-993X

Publication Date

May 24, 2022

Volume

23

Issue

1

Start / End Page

131

Location

England

Related Subject Headings

  • Respiratory System
  • RNA, Messenger
  • Pyroglyphidae
  • Pulmonary Fibrosis
  • Pulmonary Disease, Chronic Obstructive
  • Obesity
  • Mice, Inbred C57BL
  • Mice, Inbred BALB C
  • Mice
  • Male
 

Citation

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Ihrie, M. D., McQuade, V. L., Womble, J. T., Hegde, A., McCravy, M. S., Lacuesta, C. V. G., … Ingram, J. L. (2022). Exogenous leptin enhances markers of airway fibrosis in a mouse model of chronic allergic airways disease. Respir Res, 23(1), 131. https://doi.org/10.1186/s12931-022-02048-z
Ihrie, Mark D., Victoria L. McQuade, Jack T. Womble, Akhil Hegde, Matthew S. McCravy, Cyrus Victor G. Lacuesta, Robert M. Tighe, Loretta G. Que, Julia K. L. Walker, and Jennifer L. Ingram. “Exogenous leptin enhances markers of airway fibrosis in a mouse model of chronic allergic airways disease.Respir Res 23, no. 1 (May 24, 2022): 131. https://doi.org/10.1186/s12931-022-02048-z.
Ihrie MD, McQuade VL, Womble JT, Hegde A, McCravy MS, Lacuesta CVG, et al. Exogenous leptin enhances markers of airway fibrosis in a mouse model of chronic allergic airways disease. Respir Res. 2022 May 24;23(1):131.
Ihrie, Mark D., et al. “Exogenous leptin enhances markers of airway fibrosis in a mouse model of chronic allergic airways disease.Respir Res, vol. 23, no. 1, May 2022, p. 131. Pubmed, doi:10.1186/s12931-022-02048-z.
Ihrie MD, McQuade VL, Womble JT, Hegde A, McCravy MS, Lacuesta CVG, Tighe RM, Que LG, Walker JKL, Ingram JL. Exogenous leptin enhances markers of airway fibrosis in a mouse model of chronic allergic airways disease. Respir Res. 2022 May 24;23(1):131.

Published In

Respir Res

DOI

EISSN

1465-993X

Publication Date

May 24, 2022

Volume

23

Issue

1

Start / End Page

131

Location

England

Related Subject Headings

  • Respiratory System
  • RNA, Messenger
  • Pyroglyphidae
  • Pulmonary Fibrosis
  • Pulmonary Disease, Chronic Obstructive
  • Obesity
  • Mice, Inbred C57BL
  • Mice, Inbred BALB C
  • Mice
  • Male