Macrophage Migration Inhibitory Factor (MIF) Inhibition in a Murine Model of Bleomycin-Induced Pulmonary Fibrosis

Int J Mol Sci. 2018 Dec 18;19(12):4105. doi: 10.3390/ijms19124105.

Abstract

Background: Pulmonary hypertension (PH) is a common complication of idiopathic pulmonary fibrosis (IPF) that significantly contributes to morbidity and mortality. Macrophage migration inhibitory factor (MIF) is a critical factor in vascular remodeling of the pulmonary circulation.

Objectives: We tested the effects of two small molecules targeting MIF on bleomycin (BLM)-induced collagen deposition, PH, and vascular remodeling in mouse lungs.

Methods: We examined the distribution pattern of MIF, CD74, and CXCR4 in the lungs of patients with IPF-PH and the lungs of BLM-injected mice. Then, treatments were realized with (S,R)-3-(4-hydroxyphenyl)-4,5-dihydro-5-isoxazole acetic acid methyl ester (ISO-1) and N-(3-hydroxy-4-fluorobenzyl)-5 trifluoromethylbenzoxazol-2-thione 31 (20 mg/kg/day per os for 3 weeks) started 24 h after an intratracheal BLM administration.

Results: More intense immunoreactivity was noted for MIF, CD74, and CXCR4 in lungs from IPF-PH patients and BLM-injected mice. Furthermore, we found that treatments of BLM-injected mice with ISO-1 or compound 31 attenuated lung collagen deposition and right ventricular systolic pressure increase. Additionally, reduced pulmonary inflammatory infiltration and pulmonary arterial muscularization were observed in the lungs of BLM-injected mice treated with ISO-1 or compound 31.

Conclusions: Treatments with ISO-1 or compound 31 attenuates BLM-induced inflammation and fibrosis in lung, and prevents PH development in mice, suggesting that MIF is an important factor for IPF-PH development.

Keywords: idiopathic pulmonary fibrosis associated with pulmonary hypertension (IPF-PH); macrophage migration inhibitory factor; molecular target; pulmonary vascular remodeling.

MeSH terms

  • Animals
  • Antigens, Differentiation, B-Lymphocyte / genetics
  • Bleomycin / toxicity
  • Disease Models, Animal
  • Female
  • Histocompatibility Antigens Class II / genetics
  • Humans
  • Hypertension, Pulmonary / chemically induced
  • Hypertension, Pulmonary / drug therapy*
  • Hypertension, Pulmonary / genetics
  • Hypertension, Pulmonary / pathology
  • Idiopathic Pulmonary Fibrosis / chemically induced
  • Idiopathic Pulmonary Fibrosis / drug therapy*
  • Idiopathic Pulmonary Fibrosis / genetics
  • Idiopathic Pulmonary Fibrosis / pathology
  • Inflammation / chemically induced
  • Inflammation / drug therapy*
  • Inflammation / genetics
  • Inflammation / pathology
  • Intramolecular Oxidoreductases / genetics*
  • Isoxazoles / administration & dosage
  • Lung / drug effects
  • Lung / metabolism
  • Lung / pathology
  • Macrophage Migration-Inhibitory Factors / genetics*
  • Male
  • Mice
  • Receptors, CXCR4 / genetics
  • Vascular Remodeling / drug effects
  • Vascular Remodeling / genetics

Substances

  • 3-(4-hydroxyphenyl)-4,5-dihydro-5-isoxazoleacetic acid methyl ester
  • Antigens, Differentiation, B-Lymphocyte
  • CXCR4 protein, human
  • Histocompatibility Antigens Class II
  • Isoxazoles
  • Macrophage Migration-Inhibitory Factors
  • Receptors, CXCR4
  • invariant chain
  • Bleomycin
  • Intramolecular Oxidoreductases
  • MIF protein, human