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Novel Approaches in Pulmonary Fibrosis: Beyond the Fibroblast

Novel Approaches in Pulmonary Fibrosis: Beyond the Fibroblast

Tuesday, March 24, 2020, 8:30 AM - 5:00 PM

The New York Academy of Sciences, 7 World Trade Center, 250 Greenwich St Fl 40, New York

Presented By

Biochemical Pharmacology Discussion Group

The New York Academy of Sciences

 

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive lung disease with few treatment options. Research on IPF and other interstitial lung diseases has historically focused on fibroblasts and the importance of TGF-beta-driven epithelial to mesenchymal transition. Recently, new data have highlighted key roles for additional cell types including alveolar epithelial cells and endothelial cells in the development or maintenance of lung fibrosis. Moreover, cellular senescence and immune pathways have also been found to contribute to IPF pathogenesis. This symposium will discuss the emerging biological mechanisms underlying the etiology of pulmonary fibrosis and explore novel ways to remove, repair or regenerate damaged lung.

Call for Abstracts

Abstract submissions are invited for a poster session. For complete submission instructions, please visit our online portal. The deadline for abstract submission is Thursday, January 30, 2020.

Registration

Member
By 02/11/2020
$90
After 02/11/2020
$130
Nonmember Academia, Faculty, etc.
By 02/11/2020
$180
After 02/11/2020
$260
Nonmember Corporate, Other
By 02/11/2020
$250
After 02/11/2020
$350
Nonmember Not for Profit
By 02/11/2020
$180
After 02/11/2020
$260
Nonmember Student, Undergrad, Grad, Fellow
By 02/11/2020
$100
After 02/11/2020
$145
Member Student, Post-Doc, Fellow
By 02/11/2020
$50
After 02/11/2020
$70
Earlybird Registration:
13
days
left
Deadline:
1
days
left

Keynote Speaker

Oliver Eickelberg, MD

University of Colorado, Anschutz Medical Campus

Speakers

Megan Ballinger
Megan Ballinger, PhD

The Ohio State University

Stijn De Langhe
Stijn De Langhe, PhD

The University of Alabama at Birmingham School of Medicine

Wonder Puryear Drake
Wonder Puryear Drake

Vanderbilt University

Anjelica Gonzalez, PhD
Anjelica Gonzalez, PhD

Yale University

Louise Hecker, PhD
Louise Hecker, PhD

University of Arizona

Boris Hinz
Boris Hinz, PhD

University of Toronto

James Kirkland
James Kirkland, MD, PhD

Mayo Clinic

Ana Mora
Ana Mora, MD

University of Pittsburgh

Scientific Organizing Committee

Anthony V. Azzara, PhD

Bristol-Myers Squibb

Erica Herzog, MD, PhD

Yale University

Julia Kaufman, PhD

Boehringer Ingelheim

Chris Kitson, PhD

Bristol-Myers Squibb

Scott Macdonnell, PhD

Regeneron

Glenda Trujillo, PhD

Bristol-Myers Squibb

Sara Donnelly, PhD

The New York Academy of Sciences

Sonya Dougal, PhD

The New York Academy of Sciences

Tuesday

March 24, 2020

8:30 AM

Breakfast and Registration

9:00 AM

Introduction and Welcome Remarks

Speakers

Sara Donnelly, PhD
The New York Academy of Sciences
Erica Herzog, MD, PhD
Yale School of Medicine
9:15 AM

Keynote Address: Identifying Therapeutic Targets in Pulmonary Fibrosis

Speaker

Oliver Eickelberg
University of Colorado, Anschutz Medical Campus

Session 1: Epithelial Cells in Idiopathic Pulmonary Fibrosis

Session Chairperson
Anthony Azzara, PhD, Bristol-Myers Squibb
10:00 AM

Redox Imbalance in Pulmonary Fibrosis

Speaker

Louise Hecker, PhD
University of Arizona
10:30 AM

Networking Coffee Break

11:00 AM

Senolytics as Potential Disease Modifiers in Idiopathic Pulmonary Fibrosis

Speaker

James Kirkland, MD, PhD
Mayo Clinic

Aging processes such as cellular senescence may make a “root cause” contribution to chronic diseases. Senescent cells (SC) accumulate with aging and at sites of etiology of many chronic diseases. SC are resistant to apoptosis. SC can release factors that are pro-apoptotic, inflammatory, pro-fibrotic, cause stem cell dysfunction, and spread senescence, the senescence-associated secretory phenotype (SASP). Transplanting small numbers of SC into young mice, so that only 1/10,000 cells in recipients are transplanted SC, is sufficient to cause frailty, accelerated age-related disease onset, and early mortality.

We developed senolytics — drugs that selectively clear SC by inhibiting survival pathways that protect SC from apoptosis due to their SASP. Intermittent senolytic administration to mice alleviated bleomycininduced pulmonary fibrosis and many other conditions, including age- or diet-related cardiovascular dysfunction, liver fat and fibrosis in steatosis, radiation damage, cognitive dysfunction, and osteoporosis.

Senolytics delayed frailty, chronic diseases, and early death caused by transplanting SC. In old mice, senolytics improved physical function, delayed age-related diseases, and extended remaining lifespan 36%. In early clinical trials, senolytics reduced fat tissue SC in patients with diabetic kidney disease, decreased circulating SASP factors, and alleviated physical dysfunction in patients with idiopathic pulmonary fibrosis. Senolytics may hold promise for delaying, preventing, or treating age- and chronic disease-related disorders.

11:30 AM

Mitochondrial Dysfunction at the Crossroad of Aging and Lung Fibrosis

Speaker

Ana L. Mora, MD
University of Pittsburgh
12:00 PM

Role of Bronchial Epithelial Cells in Alveolar Epithelial Regeneration in Lung Fibrosis

Speaker

Stijn De Langhe, PhD
University of Alabama at Birmingham School of Medicine

Session 2: Data Blitz Talks

Session Chairperson
Anthony Azzara, PhD, Bristol-Myers Squibb
12:30 PM

Three Short Talks Selected From Submitted Abstracts

12:45 PM

Networking Lunch and Poster Session

Speakers

Odd number posters: 1:05pm - 1:40pm
Even number posters: 1:40pm - 2:15pm

Session 3: Immune Pathways in Idiopathic Pulmonary Fibrosis

Session Chairperson
Glenda Trujillo, PhD, Bristol-Myers Squibb
2:15 PM

PD-1 in Pulmonary Fibrosis

Speaker

Wonder P. Drake, PhD
Vanderbilt University
2:45 PM

Microvascular Targets in Fibrosis

Speaker

Anjelica Gonzalez, PhD
Yale University
3:15 PM

Networking Coffee Break

3:45 PM

Mechanisms Regulating the Recruitment of Monocyte-Derived Macrophages During Pulmonary Fibrosis

Speaker

Megan Ballinger, PhD
Ohio State University

Idiopathic pulmonary fibrosis is progressive lung disease disorder characterized by excessive collagen deposition. While other studies examine structural cells in the setting of IPF, our research focuses on the role of myeloid cells. Our data demonstrate that interleukin-1 receptor associated kinase (IRAK)-M, a negative regulator of Toll-like receptor signaling, was elevated in macrophages and monocytes from human IPF patients and murine macrophages after experimental fibrosis. In a murine model of bleomycin-induced pulmonary fibrosis, upregulation of IRAK-M contributes to the generation of a profibrotic macrophage. Recently, new work has determined that macrophage origin regulates their activation phenotype. In this study we investigated the role of IRAK-M in regulating monocyte trafficking and macrophage differentiation following bleomycin challenge. Using flow cytometry, we measured lung leukocytes after bleomycin challenge. There was no difference in the number of tissue resident alveolar macrophages between groups; however, there were increased monocyte–derived macrophages and inflammatory Ly6chi monocytes in the lungs of WT, but not IRAK-M−/− mice after bleomycin. Our data indicate that expression of IRAK-M regulates monocyte trafficking through the blood into the lungs resulting in more profibrotic macrophages. Understanding the mechanism by which monocytes traffic to the lungs is essential for the development of novel therapeutics.

Coauthors: Rose Viguna, Thomas Becket, Brenda Reader, David Weimar, Kristina Luikart, and John Christman, The Ohio State University Wexner College of Medicine.

4:15 PM

There Is Nothing Beyond the Fibroblast - On This Flat Earth

Speaker

Boris Hinz, PhD
University of Toronto
4:45 PM

Closing Remarks

Speaker

Julia Kauffman, PhD
Boehringer Ingelheim
4:50 PM

Networking Reception

5:50 PM

Adjourn