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Article ; Online: PTX3 in Granuloma Formation and Sarcoidosis: Helping Macrophages Accept a "Complement".

Ishikawa, Genta / Herzog, Erica L

American journal of respiratory and critical care medicine

2022 Volume 206, Issue 9, Page(s) 1064–1065

MeSH term(s)	Humans ; Macrophage Activation ; Sarcoidosis ; Macrophages/physiology ; Granuloma
Chemical Substances	PTX3 protein (148591-49-5)
Language	English
Publishing date	2022-07-12
Publishing country	United States
Document type	Editorial ; 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.202207-1277ED
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Article ; Online: Molecular Markers and the Promise of Precision Medicine for Interstitial Lung Disease.

Newton, Chad A / Herzog, Erica L

Clinics in chest medicine

2021 Volume 42, Issue 2, Page(s) 357–364

Abstract: Management of patients with interstitial lung disease (ILD) requires accurate classification. However, this process relies on subjective interpretation of nonspecific and overlapping clinical features that could hamper clinical care. The development and ... ...

Abstract	Management of patients with interstitial lung disease (ILD) requires accurate classification. However, this process relies on subjective interpretation of nonspecific and overlapping clinical features that could hamper clinical care. The development and implementation of objective biomarkers reflective of specific disease states could facilitate precision-based approaches based on patient-level biology to improve the health of ILD patients. Omics-based studies allow for the seemingly unbiased and highly efficient screening of candidate biomarkers and offer unprecedented opportunities for discovery. This review outlines representative major omics-based discoveries in a well-studied condition, idiopathic pulmonary fibrosis, to develop a roadmap to personalized medicine in ILD.
MeSH term(s)	Biomarkers ; Humans ; Idiopathic Pulmonary Fibrosis/diagnosis ; Lung Diseases, Interstitial/diagnosis ; Precision Medicine
Chemical Substances	Biomarkers
Language	English
Publishing date	2021-05-24
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	447455-7
ISSN	1557-8216 ; 0272-5231
ISSN (online)	1557-8216
ISSN	0272-5231
DOI	10.1016/j.ccm.2021.03.011
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Article ; Online: An Acute Exacerbation of Idiopathic Pulmonary Fibrosis After BNT162b2 mRNA COVID-19 Vaccination: A Case Report.

Ghincea, Alexander / Ryu, Changwan / Herzog, Erica L

Chest

2022 Volume 161, Issue 2, Page(s) e71–e73

Abstract: Idiopathic pulmonary fibrosis (IPF) is a fatal interstitial lung disease characterized by progressive scar tissue formation. An acute exacerbation of IPF (AE-IPF) is a clinically significant respiratory decompensation that accounts for a significant ... ...

Abstract	Idiopathic pulmonary fibrosis (IPF) is a fatal interstitial lung disease characterized by progressive scar tissue formation. An acute exacerbation of IPF (AE-IPF) is a clinically significant respiratory decompensation that accounts for a significant proportion of IPF-related morbidity and mortality. AE-IPF can be idiopathic or associated with pulmonary embolism, infection, aspiration, surgery, and drug toxicity. In this novel case report, we describe a potential association between AE-IPF and BNT162b2 mRNA COVID-19 vaccination that was successfully treated with a short course of glucocorticoids. While our aim is to raise awareness for this yet-to-be-described adverse event, immunization against vaccine-preventable disease remains widely recommended in vulnerable patients with chronic lung disease such as IPF.
MeSH term(s)	Aged ; BNT162 Vaccine/administration & dosage ; BNT162 Vaccine/adverse effects ; COVID-19/prevention & control ; COVID-19 Vaccines/administration & dosage ; COVID-19 Vaccines/adverse effects ; Disease Progression ; Drug Tapering/methods ; Glucocorticoids/administration & dosage ; Humans ; Idiopathic Pulmonary Fibrosis/diagnosis ; Idiopathic Pulmonary Fibrosis/physiopathology ; Idiopathic Pulmonary Fibrosis/therapy ; Lung/diagnostic imaging ; Male ; Methylprednisolone/administration & dosage ; Respiratory Insufficiency/diagnosis ; Respiratory Insufficiency/drug therapy ; Respiratory Insufficiency/etiology ; Risk Assessment/methods ; SARS-CoV-2 ; Tomography, X-Ray Computed/methods ; Treatment Outcome
Chemical Substances	COVID-19 Vaccines ; Glucocorticoids ; BNT162 Vaccine (N38TVC63NU) ; Methylprednisolone (X4W7ZR7023)
Language	English
Publishing date	2022-02-07
Publishing country	United States
Document type	Case Reports ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1032552-9
ISSN	1931-3543 ; 0012-3692
ISSN (online)	1931-3543
ISSN	0012-3692
DOI	10.1016/j.chest.2021.07.2160
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Article: Evolving Perspectives on Innate Immune Mechanisms of IPF.

Ishikawa, Genta / Liu, Angela / Herzog, Erica L

Frontiers in molecular biosciences

2021 Volume 8, Page(s) 676569

Abstract: While epithelial-fibroblast interactions are viewed as the primary drivers of Idiopathic Pulmonary Fibrosis (IPF), evidence gleaned from animal modeling and human studies implicates innate immunity as well. To provide perspective on this topic, this ... ...

Abstract	While epithelial-fibroblast interactions are viewed as the primary drivers of Idiopathic Pulmonary Fibrosis (IPF), evidence gleaned from animal modeling and human studies implicates innate immunity as well. To provide perspective on this topic, this review synthesizes the available data regarding the complex role of innate immunity in IPF. The role of substances present in the fibrotic microenvironment including pathogen associated molecular patterns (PAMPs) derived from invading or commensal microbes, and danger associated molecular patterns (DAMPs) derived from injured cells and tissues will be discussed along with the proposed contribution of innate immune populations such as macrophages, neutrophils, fibrocytes, myeloid suppressor cells, and innate lymphoid cells. Each component will be considered in the context of its relationship to environmental and genetic factors, disease outcomes, and potential therapies. We conclude with discussion of unanswered questions and opportunities for future study in this area.
Language	English
Publishing date	2021-08-09
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2814330-9
ISSN	2296-889X
ISSN	2296-889X
DOI	10.3389/fmolb.2021.676569
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Article ; Online: Evolving Perspectives on Innate Immune Mechanisms of IPF

Genta Ishikawa / Angela Liu / Erica L. Herzog

Frontiers in Molecular Biosciences, Vol

2021 Volume 8

Abstract	While epithelial-fibroblast interactions are viewed as the primary drivers of Idiopathic Pulmonary Fibrosis (IPF), evidence gleaned from animal modeling and human studies implicates innate immunity as well. To provide perspective on this topic, this review synthesizes the available data regarding the complex role of innate immunity in IPF. The role of substances present in the fibrotic microenvironment including pathogen associated molecular patterns (PAMPs) derived from invading or commensal microbes, and danger associated molecular patterns (DAMPs) derived from injured cells and tissues will be discussed along with the proposed contribution of innate immune populations such as macrophages, neutrophils, fibrocytes, myeloid suppressor cells, and innate lymphoid cells. Each component will be considered in the context of its relationship to environmental and genetic factors, disease outcomes, and potential therapies. We conclude with discussion of unanswered questions and opportunities for future study in this area.
Keywords	innate immunity ; macrophage ; pulmonary fibrosis ; microenvironment ; biomarker ; Biology (General) ; QH301-705.5
Subject code	616
Language	English
Publishing date	2021-08-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Emerging insights in sarcoidosis: moving forward through reverse translational research.

Liu, Angela / Sharma, Lokesh / Yan, Xiting / Dela Cruz, Charles S / Herzog, Erica L / Ryu, Changwan

American journal of physiology. Lung cellular and molecular physiology

2022 Volume 322, Issue 4, Page(s) L518–L525

Abstract: Sarcoidosis is a chronic granulomatous disease of unknown etiology that primarily affects the lungs. The development of stage IV or fibrotic lung disease accounts for a significant proportion of the morbidity and mortality attributable to sarcoidosis. ... ...

Abstract	Sarcoidosis is a chronic granulomatous disease of unknown etiology that primarily affects the lungs. The development of stage IV or fibrotic lung disease accounts for a significant proportion of the morbidity and mortality attributable to sarcoidosis. Further investigation into the active mechanisms of disease pathogenesis and fibrogenesis might illuminate fundamental mediators of injury and repair while providing new opportunities for clinical intervention. However, progress in sarcoidosis research has been hampered by the heterogeneity of clinical phenotypes and the lack of a consensus modeling system. Recently, reverse translational research, wherein observations made at the patient level catalyze hypothesis-driven research at the laboratory bench, has generated new discoveries regarding the immunopathogenic mechanisms of pulmonary granuloma formation, fibrogenesis, and disease model development. The purpose of this review is to highlight the promise and possibility of these novel investigative efforts.
MeSH term(s)	Granuloma/pathology ; Humans ; Lung/pathology ; Pulmonary Fibrosis/pathology ; Sarcoidosis/pathology ; Translational Research, Biomedical
Language	English
Publishing date	2022-02-23
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, U.S. Gov't, Non-P.H.S. ; 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.00266.2021
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Article: Mitochondrial DNA Sensing Pathogen Recognition Receptors in Systemic Sclerosis Associated Interstitial Lung Disease: A Review.

Ghincea, Alexander / Woo, Samuel / Yu, Sheeline / Pivarnik, Taylor / Fiorini, Vitoria / Herzog, Erica L / Ryu, Changwan

Current treatment options in rheumatology

2023 Volume 9, Issue 4, Page(s) 204–220

Abstract: Purpose of the review: Systemic sclerosis (SSc) is a condition of dermal and visceral scar formation characterized by immune dysregulation and inflammatory fibrosis. Approximately 90% of SSc patients develop interstitial lung disease (ILD), and it is ... ...

Abstract	Purpose of the review: Systemic sclerosis (SSc) is a condition of dermal and visceral scar formation characterized by immune dysregulation and inflammatory fibrosis. Approximately 90% of SSc patients develop interstitial lung disease (ILD), and it is the leading cause of morbidity and mortality. Further understanding of immune-mediated fibroproliferative mechanisms has the potential to catalyze novel treatment approaches in this difficult to treat disease. Recent findings: Recent advances have demonstrated the critical role of aberrant innate immune activation mediated by mitochondrial DNA (mtDNA) through interactions with toll-like receptor 9 (TLR9) and cytosolic cyclic guanosine monophosphate-adenosine monophosphate synthase (cGAS). Summary: In this review, we will discuss how the nature of the mtDNA, whether oxidized or mutated, and its mechanism of release, either intracellularly or extracellularly, can amplify fibrogenesis by activating TLR9 and cGAS, and the novel insights gained by interrogating these signaling pathways. Because the scope of this review is intended to generate hypotheses for future research, we conclude our discussion with several important unanswered questions.
Language	English
Publishing date	2023-08-08
Publishing country	Switzerland
Document type	Journal Article
ISSN	2198-6002
ISSN	2198-6002
DOI	10.1007/s40674-023-00211-1
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Article ; Online: TGF-β1 Drives Integrin-Dependent Pericyte Migration and Microvascular Destabilization in Fibrotic Disease.

Pellowe, Amanda S / Wu, Michelle J / Kang, Tae-Yun / Chung, Tracy D / Ledesma-Mendoza, Adrian / Herzog, Erica / Levchenko, Andre / Odell, Ian / Varga, John / Gonzalez, Anjelica L

The American journal of pathology

2024

Abstract: Interactions between endothelial cells (ECs) and mural pericytes (PCs) are critical to maintaining the stability and function of the microvascular wall. Abnormal interactions between these two cell types are a hallmark of progressive fibrotic diseases ... ...

Abstract	Interactions between endothelial cells (ECs) and mural pericytes (PCs) are critical to maintaining the stability and function of the microvascular wall. Abnormal interactions between these two cell types are a hallmark of progressive fibrotic diseases such as systemic sclerosis (also known as scleroderma). However, the role that PCs play in signaling microvascular dysfunction remains underexplored. It is hypothesized that integrin-matrix interactions contribute to PC migration from the vascular wall and conversion into interstitial myofibroblasts. Using pro-inflammatory tumor necrosis factor α (TNFα) or a fibrotic growth factor [transforming growth factor β1 (TGF-β1)], human PC inflammatory and fibrotic phenotypes were evaluated by assessing their migration, matrix deposition, integrin expression, and subsequent effects on endothelial dysfunction. Both TNFα and TGF-β1 treatment altered integrin expression and matrix protein deposition, but only fibrotic TGF-β1 drove PC migration in an integrin-dependent manner. In addition, integrin-dependent PC migration was correlated to changes in EC angiopoietin-2 levels, a marker of vascular instability. Finally, there was evidence of changes in vascular stability corresponding to disease state in human systemic sclerosis skin. This work shows that TNFα and TGF-β1 induce changes in PC integrin expression and matrix deposition that facilitate migration and reduce vascular stability, providing evidence that microvascular destabilization can be an early indicator of tissue fibrosis.
Language	English
Publishing date	2024-03-26
Publishing country	United States
Document type	Journal Article
ZDB-ID	2943-9
ISSN	1525-2191 ; 0002-9440
ISSN (online)	1525-2191
ISSN	0002-9440
DOI	10.1016/j.ajpath.2024.02.021
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Article ; Online: Regulatory T Cells in Idiopathic Pulmonary Fibrosis: Too Much of a Good Thing?

Moore, Meagan W / Herzog, Erica L

The American journal of pathology

2016 Volume 186, Issue 8, Page(s) 1978–1981

Abstract: This commentary highlights the article by Birjandi et al showing that alterations in regulatory T cells can exacerbate lung fibrosis. ...

Abstract	This commentary highlights the article by Birjandi et al showing that alterations in regulatory T cells can exacerbate lung fibrosis.
MeSH term(s)	Humans ; Idiopathic Pulmonary Fibrosis ; Pulmonary Fibrosis ; T-Lymphocytes, Regulatory
Language	English
Publishing date	2016-06-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Comment
ZDB-ID	2943-9
ISSN	1525-2191 ; 0002-9440
ISSN (online)	1525-2191
ISSN	0002-9440
DOI	10.1016/j.ajpath.2016.06.002
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Article ; Online: Integrated computational and experimental pipeline for quantifying local cell-matrix interactions.

Xiao, Hugh / Nguyen, Ryan Y / LaRanger, Ryan / Herzog, Erica L / Mak, Michael

Scientific reports

2021 Volume 11, Issue 1, Page(s) 16465

Abstract: Cellular interactions with the extracellular matrix (ECM) play a key role in modulating biological processes. While studies have identified key molecular factors of these interactions, the mechanical regulation associated with these interactions is not ... ...

Abstract	Cellular interactions with the extracellular matrix (ECM) play a key role in modulating biological processes. While studies have identified key molecular factors of these interactions, the mechanical regulation associated with these interactions is not well characterized. To address this, we present an image analysis platform to analyze time-dependent dynamics observed in lung fibroblasts embedded in a 3D collagen matrix. Combining drug studies with quantitative analysis of cell-matrix interactions, our results are able to provide cellular level quantitative insights for mechanical and biophysical phenomena relevant to cell-ECM interactions. This system overall represents an initial pipeline for understanding cell mechanics in a 3D collagen gel and their implications in a physiologically relevant context.
MeSH term(s)	Algorithms ; Cell Communication ; Cells, Cultured ; Collagen/metabolism ; Extracellular Matrix/physiology ; Humans ; Lung/cytology ; Lung/metabolism
Chemical Substances	Collagen (9007-34-5)
Language	English
Publishing date	2021-08-12
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-021-95935-2
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