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Article: Heterogeneity of Fibroblasts and Myofibroblasts in Pulmonary Fibrosis.

Habiel, David M / Hogaboam, Cory M

Current pathobiology reports

2017 Volume 5, Issue 2, Page(s) 101–110

Abstract: Purpose of review: Idiopathic Pulmonary Fibrosis (IPF) is the most common form of interstitial lung diseases of unknown eathiopathogenesis, mean survival of 3-5 years and limited therapeutics. Characterized by a loss of alveolar type II epithelial cells ...

Abstract	Purpose of review: Idiopathic Pulmonary Fibrosis (IPF) is the most common form of interstitial lung diseases of unknown eathiopathogenesis, mean survival of 3-5 years and limited therapeutics. Characterized by a loss of alveolar type II epithelial cells and aberrant activation of stromal cells, considerable effort was undertaken to characterize the origin and activation mechanisms of fibroblasts and myofibroblasts in IPF lungs. In this review, the origin and contribution of fibroblast and myofibroblasts in lung fibrosis will be summarized. Recent findings: Lineage tracing experiments suggested that interstitial lung fibroblasts and lipofibroblasts, pericytes and mesothelial cells differentiate into myofibroblasts. However, epithelial and bone marrow derived cells may give rise to collagen expressing fibroblasts but do not differentiate into myofibroblasts. Summary: There is great heterogeneity in fibroblasts and myofibroblasts in fibrotic lungs. Further, there is evidence for the expansion of pericyte derived myofibroblasts and loss of lipofibroblasts and lipofibroblast derived myofibroblasts in IPF.
Language	English
Publishing date	2017-05-02
Publishing country	United States
Document type	Journal Article
ISSN	2167-485X
ISSN	2167-485X
DOI	10.1007/s40139-017-0134-x
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Article ; Online: Reply to D'Alessandro-Gabazza et al.: Risks of Treating Idiopathic Pulmonary Fibrosis with a TAM Receptor Kinase Inhibitor.

Espindola, Milena S / Habiel, David M / Hogaboam, Cory M

American journal of respiratory and critical care medicine

2018 Volume 198, Issue 7, Page(s) 971–973

MeSH term(s)	Humans ; Idiopathic Pulmonary Fibrosis ; Protein Kinase Inhibitors
Chemical Substances	Protein Kinase Inhibitors
Language	English
Publishing date	2018-07-06
Publishing country	United States
Document type	Letter ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	1180953-x
ISSN	1535-4970 ; 0003-0805 ; 1073-449X
ISSN (online)	1535-4970
ISSN	0003-0805 ; 1073-449X
DOI	10.1164/rccm.201805-0972LE
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Article: Heterogeneity in fibroblast proliferation and survival in idiopathic pulmonary fibrosis.

Habiel, David M / Hogaboam, Cory

Frontiers in pharmacology

2014 Volume 5, Page(s) 2

Abstract: Idiopathic pulmonary fibrosis (IPF) is the most common form of interstitial lung disease characterized by the persistence of activated myofibroblasts resulting in excessive deposition of extracellular matrix proteins and profound tissue remodeling. ... ...

Abstract	Idiopathic pulmonary fibrosis (IPF) is the most common form of interstitial lung disease characterized by the persistence of activated myofibroblasts resulting in excessive deposition of extracellular matrix proteins and profound tissue remodeling. Myofibroblasts have been shown to arise from interstitial fibroblasts, epithelial to mesenchymal transition of type II alveolar epithelial cells, and the differentiation of recruited fibrocytes. There are many mechanisms that are utilized by these cells for survival, proliferation, and persistent activation including up-regulation of cytokines [i.e., Interleukin 6 (IL-6) and C-C motif chemokine ligand 21 (CCL21)], cytokine receptors [i.e., Interleukin 6Receptor 1 (IL-6R1), Glycoprotein 130 (gp130) and C-C Chemokine Receptor type 7 (CCR7)], and innate pattern recognition receptors [(PRRs; i.e., Toll Like Receptor 9 (TLR9)]. In this review, we will discuss the role of the cytokines IL-6 and CCL21, their receptors and the PRR, TLR9, in fibroblast recruitment, activation, survival, and differentiation into myofibroblasts in IPF.
Language	English
Publishing date	2014-01-23
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2587355-6
ISSN	1663-9812
ISSN	1663-9812
DOI	10.3389/fphar.2014.00002
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Article ; Online: Modeling Idiopathic Pulmonary Fibrosis in Humanized Severe Combined Immunodeficient Mice.

Habiel, David M / Espindola, Milena S / Coelho, Ana L / Hogaboam, Cory M

The American journal of pathology

2018 Volume 188, Issue 4, Page(s) 891–903

Abstract: Idiopathic pulmonary fibrosis (IPF) is a fibrotic lung disease of unknown etiopathogenesis with limited therapeutic options. IPF is characterized by an abundance of fibroblasts and loss of epithelial progenitors, which cumulates in unrelenting fibrotic ... ...

Abstract	Idiopathic pulmonary fibrosis (IPF) is a fibrotic lung disease of unknown etiopathogenesis with limited therapeutic options. IPF is characterized by an abundance of fibroblasts and loss of epithelial progenitors, which cumulates in unrelenting fibrotic lung remodeling and loss of normal oxygenation. IPF has been challenging to model in rodents; nonetheless, mouse models of lung fibrosis provide clues as to the natural progression of lung injury and remodeling, but many have not been useful in predicting efficacy of therapeutics in clinical IPF. We provide a detailed methodologic description of various iterations of humanized mouse models, initiated by the i.v. injection of cells from IPF lung biopsy or explants specimens into severe combined immunodeficiency (SCID)/beige or nonobese diabetic SCID γ mice. Unlike cells from normal lung samples, IPF cells promote persistent, nonresolving lung remodeling in SCID mice. Finally, we provide examples and discuss potential advantages and pitfalls of human-specific targeting approaches in a humanized SCID model of pulmonary fibrosis.
MeSH term(s)	Animals ; Antibodies, Neutralizing/pharmacology ; Benzylamines ; Cyclams ; Disease Models, Animal ; Fibroblasts/drug effects ; Fibroblasts/metabolism ; Fibroblasts/pathology ; Heterocyclic Compounds/pharmacology ; Heterocyclic Compounds/therapeutic use ; Humans ; Idiopathic Pulmonary Fibrosis/drug therapy ; Idiopathic Pulmonary Fibrosis/metabolism ; Idiopathic Pulmonary Fibrosis/pathology ; Interleukin-13/metabolism ; Lung/pathology ; Mice, SCID ; Phenotype ; Receptors, CXCR4/metabolism ; Receptors, Interleukin-4/metabolism
Chemical Substances	Antibodies, Neutralizing ; Benzylamines ; Cyclams ; Heterocyclic Compounds ; Interleukin-13 ; Receptors, CXCR4 ; Receptors, Interleukin-4 ; plerixafor (S915P5499N)
Language	English
Publishing date	2018-02-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2943-9
ISSN	1525-2191 ; 0002-9440
ISSN (online)	1525-2191
ISSN	0002-9440
DOI	10.1016/j.ajpath.2017.12.020
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Article ; Online: Quercetin Enhances Ligand-induced Apoptosis in Senescent Idiopathic Pulmonary Fibrosis Fibroblasts and Reduces Lung Fibrosis In Vivo.

Hohmann, Miriam S / Habiel, David M / Coelho, Ana L / Verri, Waldiceu A / Hogaboam, Cory M

American journal of respiratory cell and molecular biology

2018 Volume 60, Issue 1, Page(s) 28–40

Abstract: Although cellular senescence may be a protective mechanism in modulating proliferative capacity, fibroblast senescence is now recognized as a key pathogenic mechanism in idiopathic pulmonary fibrosis (IPF). In aged mice, abundance and persistence of ... ...

Abstract	Although cellular senescence may be a protective mechanism in modulating proliferative capacity, fibroblast senescence is now recognized as a key pathogenic mechanism in idiopathic pulmonary fibrosis (IPF). In aged mice, abundance and persistence of apoptosis-resistant senescent fibroblasts play a central role in nonresolving lung fibrosis after bleomycin challenge. Therefore, we investigated whether quercetin can restore the susceptibility of senescent IPF fibroblasts to proapoptotic stimuli and mitigate bleomycin-induced pulmonary fibrosis in aged mice. Unlike senescent normal lung fibroblasts, IPF lung fibroblasts from patients with stable and rapidly progressing disease were highly resistant to Fas ligand (FasL)-induced and TNF-related apoptosis-inducing ligand (TRAIL)-induced apoptosis. Senescent IPF fibroblasts exhibited decreased expression of FasL and TRAIL receptors and caveolin-1, as well as increased AKT activation, compared with senescent normal lung fibroblasts. Although quercetin alone was not proapoptotic, it abolished the resistance to FasL- or TRAIL-induced apoptosis in IPF fibroblasts. Mechanistically, quercetin upregulated FasL receptor and caveolin-1 expression and modulated AKT activation. In vivo quercetin reversed bleomycin-induced pulmonary fibrosis and attenuated lethality, weight loss, and the expression of pulmonary senescence markers p21 and p19-ARF and senescence-associated secretory phenotype in aged mice. Collectively, these data indicate that quercetin reverses the resistance to death ligand-induced apoptosis by promoting FasL receptor and caveolin-1 expression and inhibiting AKT activation, thus mitigating the progression of established pulmonary fibrosis in aged mice. Therefore, quercetin may be a viable therapeutic option for IPF and other age-related diseases that progress with the accumulation of senescent fibroblasts.
MeSH term(s)	Animals ; Antibiotics, Antineoplastic/toxicity ; Antioxidants/pharmacology ; Apoptosis/drug effects ; Bleomycin/toxicity ; Cellular Senescence/drug effects ; Female ; Fibroblasts/drug effects ; Fibroblasts/pathology ; Humans ; Idiopathic Pulmonary Fibrosis/chemically induced ; Idiopathic Pulmonary Fibrosis/drug therapy ; Male ; Mice ; Mice, Inbred C57BL ; Quercetin/pharmacology
Chemical Substances	Antibiotics, Antineoplastic ; Antioxidants ; Bleomycin (11056-06-7) ; Quercetin (9IKM0I5T1E)
Language	English
Publishing date	2018-08-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1025960-0
ISSN	1535-4989 ; 1044-1549
ISSN (online)	1535-4989
ISSN	1044-1549
DOI	10.1165/rcmb.2017-0289OC
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Article ; Online: Differential Responses to Targeting Matrix Metalloproteinase 9 in Idiopathic Pulmonary Fibrosis.

Espindola, Milena S / Habiel, David M / Coelho, Ana Lucia / Stripp, Barry / Parks, William C / Oldham, Justin / Martinez, Fernando J / Noth, Imre / Lopez, David / Mikels-Vigdal, Amanda / Smith, Victoria / Hogaboam, Cory M

American journal of respiratory and critical care medicine

2020 Volume 203, Issue 4, Page(s) 458–470

Abstract: Rationale: ...

Abstract	Rationale:
MeSH term(s)	Animals ; Antibodies, Monoclonal, Humanized/metabolism ; Antibodies, Monoclonal, Humanized/therapeutic use ; California/epidemiology ; Epithelial Cells/drug effects ; Female ; Gene Expression Regulation/drug effects ; Humans ; Idiopathic Pulmonary Fibrosis/drug therapy ; Idiopathic Pulmonary Fibrosis/epidemiology ; Idiopathic Pulmonary Fibrosis/genetics ; Idiopathic Pulmonary Fibrosis/physiopathology ; Matrix Metalloproteinase 9/drug effects ; Matrix Metalloproteinase 9/genetics ; Matrix Metalloproteinase 9/metabolism ; Mice ; Michigan/epidemiology ; Models, Animal ; Proteomics ; United States
Chemical Substances	Antibodies, Monoclonal, Humanized ; Matrix Metalloproteinase 9 (EC 3.4.24.35)
Language	English
Publishing date	2020-10-14
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1180953-x
ISSN	1535-4970 ; 0003-0805 ; 1073-449X
ISSN (online)	1535-4970
ISSN	0003-0805 ; 1073-449X
DOI	10.1164/rccm.201910-1977OC
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Article ; Online: Characterization of CD28

Habiel, David M / Espindola, Milena S / Kitson, Chris / Azzara, Anthony V / Coelho, Ana Lucia / Stripp, Barry / Hogaboam, Cory M

Mucosal immunology

2018 Volume 12, Issue 1, Page(s) 212–222

Abstract: Idiopathic pulmonary fibrosis (IPF) is a fibrotic lung disease, with unknown etiopathogenesis and suboptimal therapeutic options. Previous reports have shown that increased T-cell numbers and ... ...

Abstract	Idiopathic pulmonary fibrosis (IPF) is a fibrotic lung disease, with unknown etiopathogenesis and suboptimal therapeutic options. Previous reports have shown that increased T-cell numbers and CD28
MeSH term(s)	Airway Remodeling ; Animals ; Antibodies, Monoclonal/metabolism ; CD28 Antigens/metabolism ; CD8-Positive T-Lymphocytes/immunology ; CTLA-4 Antigen/immunology ; CTLA-4 Antigen/metabolism ; Cell Separation ; Cells, Cultured ; Flow Cytometry ; Humans ; Idiopathic Pulmonary Fibrosis/immunology ; Immunophenotyping ; Lung/pathology ; Mice ; Mice, SCID ; Programmed Cell Death 1 Receptor/immunology ; Programmed Cell Death 1 Receptor/metabolism ; T-Lymphocyte Subsets/immunology
Chemical Substances	Antibodies, Monoclonal ; CD28 Antigens ; CTLA-4 Antigen ; Ctla4 protein, mouse ; Pdcd1 protein, mouse ; Programmed Cell Death 1 Receptor
Language	English
Publishing date	2018-10-12
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2411370-0
ISSN	1935-3456 ; 1933-0219
ISSN (online)	1935-3456
ISSN	1933-0219
DOI	10.1038/s41385-018-0082-8
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Article ; Online: Axl receptor blockade protects from invasive pulmonary aspergillosis in mice.

Shibata, Takehiko / Habiel, David M / Coelho, Ana Lucia / Hogaboam, Cory M

Journal of immunology (Baltimore, Md. : 1950)

2014 Volume 193, Issue 7, Page(s) 3559–3565

Abstract: Aspergillus fumigatus is a sporulating fungus found ubiquitously in the environment, which is quickly contained in the immunocompetent host but can cause lethal invasive aspergillosis in the immunocompromised host. We have recently demonstrated that Axl ( ...

Abstract	Aspergillus fumigatus is a sporulating fungus found ubiquitously in the environment, which is quickly contained in the immunocompetent host but can cause lethal invasive aspergillosis in the immunocompromised host. We have recently demonstrated that Axl (one member of the Tyro3, Axl, Mertk receptor family) is a key regulator of antiviral immune responses in the lung. In this study, we investigated the role of Axl in antifungal immunity in a model of invasive pulmonary aspergillosis (IPA). In this model, Aspergillus fumigatus conidia were administered into the lungs of neutrophil-depleted mice, and the mice were monitored for survival, lung inflammatory response, and fungal clearance. The lethal effect of IPA was significantly reduced in anti-Axl mAb-treated mice compared with IgG control-treated mice. Targeting Axl significantly inhibited pulmonary inflammation, including the expression of IL-1β, IL-6, TNF-α, and chitinase-like proteins in whole lung. Further, anti-Axl mAb treatment significantly increased M1 macrophages that highly expressed inducible NO synthase and decreased M2 macrophages that expressed Arginase 1 and were found in inflammatory zone protein (Fizz1). More importantly, anti-Axl mAb treatment significantly increased the number of IFN-γ-producing T cells and NK cells compared with the IgG control group during IPA. Together, our results demonstrate that the Axl mAb treatment is protective during invasive aspergillosis in neutropenic mice. Collectively, these data suggest a potential deleterious role for Axl during primary immune responses directed against A. fumigatus and novel therapeutic strategy for IPA.
MeSH term(s)	Animals ; Antibodies, Monoclonal/immunology ; Antibodies, Monoclonal/pharmacology ; Aspergillosis, Allergic Bronchopulmonary/immunology ; Aspergillosis, Allergic Bronchopulmonary/pathology ; Aspergillosis, Allergic Bronchopulmonary/prevention & control ; Aspergillus fumigatus/immunology ; Cytokines/immunology ; Disease Models, Animal ; Female ; Intercellular Signaling Peptides and Proteins/immunology ; Killer Cells, Natural/immunology ; Killer Cells, Natural/pathology ; Macrophages, Alveolar/immunology ; Macrophages, Alveolar/pathology ; Mice ; Nitric Oxide Synthase Type II/immunology ; Proto-Oncogene Proteins/antagonists & inhibitors ; Proto-Oncogene Proteins/immunology ; Receptor Protein-Tyrosine Kinases/antagonists & inhibitors ; Receptor Protein-Tyrosine Kinases/immunology ; T-Lymphocytes/immunology ; T-Lymphocytes/pathology
Chemical Substances	Antibodies, Monoclonal ; Cytokines ; Intercellular Signaling Peptides and Proteins ; Proto-Oncogene Proteins ; Retnla protein, mouse ; Nitric Oxide Synthase Type II (EC 1.14.13.39) ; Nos2 protein, mouse (EC 1.14.13.39) ; Receptor Protein-Tyrosine Kinases (EC 2.7.10.1) ; axl receptor tyrosine kinase (EC 2.7.10.1)
Language	English
Publishing date	2014-10-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1401258
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Article ; Online: CCR10+ epithelial cells from idiopathic pulmonary fibrosis lungs drive remodeling.

Habiel, David M / Espindola, Milena S / Jones, Isabelle C / Coelho, Ana Lucia / Stripp, Barry / Hogaboam, Cory M

JCI insight

2018 Volume 3, Issue 16

Abstract: Idiopathic pulmonary fibrosis (IPF) is a devastating fibrotic lung disease of unknown etiology and limited therapeutic options. In this report, we characterize what we believe is a novel CCR10+ epithelial cell population in IPF lungs. There was a ... ...

Abstract	Idiopathic pulmonary fibrosis (IPF) is a devastating fibrotic lung disease of unknown etiology and limited therapeutic options. In this report, we characterize what we believe is a novel CCR10+ epithelial cell population in IPF lungs. There was a significant increase in the percentage of CCR10+ epithelial cells in IPF relative to normal lung explants and their numbers significantly correlated to lung remodeling in humanized NSG mice. Cultured CCR10-enriched IPF epithelial cells promoted IPF lung fibroblast invasion and collagen 1 secretion. Single-cell RNA sequencing analysis showed distinct CCR10+ epithelial cell populations enriched for inflammatory and profibrotic transcripts. Consistently, cultured IPF but not normal epithelial cells induced lung remodeling in humanized NSG mice, where the number of CCR10+ IPF, but not normal, epithelial cells correlated with hydroxyproline concentration in the remodeled NSG lungs. A subset of IPF CCR10hi epithelial cells coexpress EphA3 and ephrin A signaling induces the expression of CCR10 by these cells. Finally, EphA3+CCR10hi epithelial cells induce more consistent lung remodeling in NSG mice relative to EphA3-CCR10lo epithelial cells. Our results suggest that targeting epithelial cells, highly expressing CCR10, may be beneficial in IPF.
MeSH term(s)	Airway Remodeling/immunology ; Animals ; Cell Line ; Disease Models, Animal ; Epithelial Cells/immunology ; Epithelial Cells/metabolism ; Epithelial Cells/transplantation ; Female ; Fibrosis ; Humans ; Idiopathic Pulmonary Fibrosis/immunology ; Idiopathic Pulmonary Fibrosis/pathology ; Lung/cytology ; Lung/immunology ; Lung/pathology ; Mice ; Mice, Inbred NOD ; Receptors, CCR10/metabolism ; Respiratory Mucosa/cytology ; Respiratory Mucosa/immunology ; Respiratory Mucosa/pathology ; Specific Pathogen-Free Organisms ; Transplantation Chimera
Chemical Substances	CCR10 protein, human ; Ccr10 protein, mouse ; Receptors, CCR10
Language	English
Publishing date	2018-08-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Video-Audio Media
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.122211
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Article ; Online: Inhibition of the stem cell factor 248 isoform attenuates the development of pulmonary remodeling disease.

Rasky, Andrew / Habiel, David M / Morris, Susan / Schaller, Matthew / Moore, Bethany B / Phan, Sem / Kunkel, Steven L / Phillips, Martin / Hogaboam, Cory / Lukacs, Nicholas W

American journal of physiology. Lung cellular and molecular physiology

2019 Volume 318, Issue 1, Page(s) L200–L211

Abstract: Stem cell factor (SCF) and its receptor c-kit have been implicated in inflammation, tissue remodeling, and fibrosis. Ingenuity Integrated Pathway Analysis of gene expression array data sets showed an upregulation of SCF transcripts in idiopathic ... ...

Abstract	Stem cell factor (SCF) and its receptor c-kit have been implicated in inflammation, tissue remodeling, and fibrosis. Ingenuity Integrated Pathway Analysis of gene expression array data sets showed an upregulation of SCF transcripts in idiopathic pulmonary fibrosis (IPF) lung biopsies compared with tissue from nonfibrotic lungs that are further increased in rapid progressive disease. SCF248, a cleavable isoform of SCF, was abundantly and preferentially expressed in human lung fibroblasts and fibrotic mouse lungs relative to the SCF220 isoform. In fibroblast-mast cell coculture studies, blockade of SCF248 using a novel isoform-specific anti-SCF248 monoclonal antibody (anti-SCF248), attenuated the expression of
MeSH term(s)	Animals ; Bleomycin/pharmacology ; Cell Count/methods ; Cells, Cultured ; Coculture Techniques/methods ; Female ; Fibroblasts/drug effects ; Fibroblasts/metabolism ; Fibrosis/drug therapy ; Fibrosis/metabolism ; Humans ; Idiopathic Pulmonary Fibrosis/drug therapy ; Idiopathic Pulmonary Fibrosis/metabolism ; Lung/drug effects ; Lung/metabolism ; Mast Cells/drug effects ; Mast Cells/metabolism ; Mice ; Mice, Inbred C57BL ; Protein Isoforms/metabolism ; Signal Transduction/drug effects ; Stem Cell Factor/metabolism ; Up-Regulation/drug effects
Chemical Substances	Protein Isoforms ; Stem Cell Factor ; Bleomycin (11056-06-7)
Language	English
Publishing date	2019-11-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1013184-x
ISSN	1522-1504 ; 1040-0605
ISSN (online)	1522-1504
ISSN	1040-0605
DOI	10.1152/ajplung.00114.2019
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