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Article: Blood Cholesterol and Triglycerides Associate with Right Ventricular Function in Pulmonary Hypertension.

Fakhry, Battoul / Peterson, Laura / Comhair, Suzy A A / Sharp, Jacqueline / Park, Margaret M / Tang, W H Wilson / Neumann, Donald R / DiFilippo, Frank P / Farha, Samar / Erzurum, Serpil C / Mulya, Anny

medRxiv : the preprint server for health sciences

2024

Abstract: Background: Blood lipids are dysregulated in pulmonary hypertension (PH). Lower high-density lipoproteins cholesterol (HDL-C) and low-density lipoproteins cholesterol (LDL-C) are associated with disease severity and death in PH. Right ventricle (RV) ... ...

Abstract	Background: Blood lipids are dysregulated in pulmonary hypertension (PH). Lower high-density lipoproteins cholesterol (HDL-C) and low-density lipoproteins cholesterol (LDL-C) are associated with disease severity and death in PH. Right ventricle (RV) dysfunction and failure are the major determinants of morbidity and mortality in PH. This study aims to test the hypothesis that dyslipidemia is associated with RV dysfunction in PH. Methods: We enrolled healthy control subjects (n=12) and individuals with PH (n=30) (age: 18-65 years old). Clinical characteristics, echocardiogram, 2-[18F] fluoro-2-deoxy-D-glucose positron emission tomography (PET) scan, blood lipids, including total cholesterol (TC), triglycerides (TG), lipoproteins (LDL-C and HDL-C), and N-terminal pro-B type Natriuretic Peptide (NT-proBNP) were determined. Results: Individuals with PH had lower HDL-C [PH, 41±12; control, 56±16 mg/dL, Conclusion: These findings confirm dyslipidemia is associated with worse right ventricular function in PH.
Language	English
Publishing date	2024-01-22
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.01.20.24301498
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Article ; Online: Hemoglobin resident in the lung epithelium is protective for smooth muscle soluble guanylate cyclase function.

Sumi, Mamta P / Tupta, Blair / Roychowdhury, Sanjoy / Comhair, Suzy / Asosingh, Kewal / Stuehr, Dennis J / Erzurum, Serpil C / Ghosh, Arnab

Redox biology

2023 Volume 63, Page(s) 102717

Abstract: Hemoglobin (Hb) present in the lung epithelium is of unknown significance. However Hb being an nitric oxide (NO) scavenger can bind to NO and reduce its deleterious effects. Hence we postulated an NO scavenging role for this lung Hb. Doing transwell co- ... ...

Abstract	Hemoglobin (Hb) present in the lung epithelium is of unknown significance. However Hb being an nitric oxide (NO) scavenger can bind to NO and reduce its deleterious effects. Hence we postulated an NO scavenging role for this lung Hb. Doing transwell co-culture with bronchial epithelial cells, A549/16-HBE (apical) and human airway smooth muscle cells (HASMCs as basal), we found that Hb can protect the smooth muscle soluble guanylyl cyclase (sGC) from excess NO. Inducing the apical A549/16-HBE cells with cytokines to trigger iNOS expression and NO generation caused a time dependent increase in SNO-sGC and this was accompanied with a concomitant drop in sGC-α1β1 heterodimerization. Silencing Hbαβ in the apical cells further increased the SNO on sGC with a faster drop in the sGC heterodimer and these effects were additive along with further silencing of thioredoxin 1 (Trx1). Since heme of Hb is critical for NO scavenging we determined the Hb heme in a mouse model of allergic asthma (OVA) and found that Hb in the inflammed OVA lungs was low in heme or heme-free relative to those of naïve lungs. Further we established a direct correlation between the status of the sGC heterodimer and the Hb heme from lung samples of human asthma, iPAH, COPD and cystic fibrosis. These findings present a new mechanism of protection of lung sGC by the epithelial Hb, and suggests that this protection maybe lost in asthma or COPD where lung Hb is unable to scavenge the NO due to it being heme-deprived.
MeSH term(s)	Mice ; Animals ; Humans ; Soluble Guanylyl Cyclase/genetics ; Soluble Guanylyl Cyclase/metabolism ; Guanylate Cyclase/genetics ; Nitric Oxide/metabolism ; Lung/metabolism ; Asthma/genetics ; Muscle, Smooth/metabolism ; Hemoglobins ; Heme/metabolism ; Epithelium/metabolism ; Pulmonary Disease, Chronic Obstructive
Chemical Substances	Soluble Guanylyl Cyclase (EC 4.6.1.2) ; Guanylate Cyclase (EC 4.6.1.2) ; Nitric Oxide (31C4KY9ESH) ; Hemoglobins ; Heme (42VZT0U6YR)
Language	English
Publishing date	2023-04-25
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2701011-9
ISSN	2213-2317 ; 2213-2317
ISSN (online)	2213-2317
ISSN	2213-2317
DOI	10.1016/j.redox.2023.102717
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Article ; Online: Mechanisms of Corticosteroid Resistance in Type 17 Asthma.

Hong, Lingzi / Herjan, Tomasz / Bulek, Katarzyna / Xiao, Jianxin / Comhair, Suzy A A / Erzurum, Serpil C / Li, Xiaoxia / Liu, Caini

Journal of immunology (Baltimore, Md. : 1950)

2022 Volume 209, Issue 10, Page(s) 1860–1869

Abstract: IL-17A plays an important role in the pathogenesis of asthma, particularly the neutrophilic corticosteroid (CS)-resistant subtype of asthma. Clinical studies suggest that a subset of asthma patients, i.e., Th17/IL-17A-mediated (type 17) CS-resistant ... ...

Abstract	IL-17A plays an important role in the pathogenesis of asthma, particularly the neutrophilic corticosteroid (CS)-resistant subtype of asthma. Clinical studies suggest that a subset of asthma patients, i.e., Th17/IL-17A-mediated (type 17) CS-resistant neutrophilic asthma, may improve with Th17/IL-17A pathway blockade. However, little is known about the mechanisms underlying type 17 asthma and CS response. In this article, we show that blood levels of lipocalin-2 (LCN2) and serum amyloid A (SAA) levels are positively correlated with IL-17A levels and are not inhibited by high-dose CS usage in asthma patients. In airway cell culture systems, IL-17A induces these two secreted proteins, and their induction is enhanced by CS. Furthermore, plasma LCN2 and SAA levels are increased in mice on a preclinical type 17 asthma model, correlated to IL-17A levels, and are not reduced by glucocorticoid (GC). In the mechanistic studies, we identify CEBPB as the critical transcription factor responsible for the synergistic induction of LCN2 and SAA by IL-17A and GC. IL-17A and GC collaboratively regulate CEBPB at both transcriptional and posttranscriptional levels. The posttranscriptional regulation of CEBPB is mediated in part by Act1, the adaptor and RNA binding protein in IL-17A signaling, which directly binds CEBPB mRNA and inhibits its degradation. Overall, our findings suggest that blood LCN2 and SAA levels may be associated with a type 17 asthma subtype and provide insight into the molecular mechanism of the IL-17A-Act1/CEBPB axis on these CS-resistant genes.
MeSH term(s)	Mice ; Animals ; Interleukin-17/genetics ; Asthma/drug therapy ; Asthma/pathology ; Th17 Cells/pathology ; Signal Transduction ; Glucocorticoids
Chemical Substances	Interleukin-17 ; Glucocorticoids
Language	English
Publishing date	2022-11-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
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.2200288
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Article ; Online: Corrigendum to "Comparison of whole genome sequencing and targeted sequencing for mitochondrial DNA" [Mitochondrion 58 (2021) 303-310].

Chen, Ruoying / Aldred, Micheala A / Xu, Weiling / Zein, Joe / Bazeley, Peter / Comhair, Suzy A A / Meyers, Deborah A / Bleecker, Eugene R / Liu, Chunyu / Erzurum, Serpil C / Hu, Bo

Mitochondrion

2022 Volume 63, Page(s) 89

Language	English
Publishing date	2022-01-20
Publishing country	Netherlands
Document type	Published Erratum
ZDB-ID	2056923-3
ISSN	1872-8278 ; 1567-7249
ISSN (online)	1872-8278
ISSN	1567-7249
DOI	10.1016/j.mito.2022.01.004
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Article ; Online: Metabolomic Differences in Connective Tissue Disease-Associated Versus Idiopathic Pulmonary Arterial Hypertension in the PVDOMICS Cohort.

Simpson, Catherine E / Hemnes, Anna R / Griffiths, Megan / Grunig, Gabriele / Tang, W H Wilson / Garcia, Joe G N / Barnard, John / Comhair, Suzy A / Damico, Rachel L / Mathai, Stephen C / Hassoun, Paul M

Arthritis & rheumatology (Hoboken, N.J.)

2023 Volume 75, Issue 12, Page(s) 2240–2251

Abstract: Objective: Patients with connective tissue disease-associated pulmonary arterial hypertension (CTD-PAH) experience worse survival and derive less benefit from pulmonary vasodilator therapies than patients with idiopathic PAH (IPAH). We sought to ... ...

Abstract	Objective: Patients with connective tissue disease-associated pulmonary arterial hypertension (CTD-PAH) experience worse survival and derive less benefit from pulmonary vasodilator therapies than patients with idiopathic PAH (IPAH). We sought to identify differential metabolism in patients with CTD-PAH versus patients with IPAH that might underlie these observed clinical differences. Methods: Adult participants with CTD-PAH (n = 141) and IPAH (n = 165) from the Pulmonary Vascular Disease Phenomics (PVDOMICS) study were included. Detailed clinical phenotyping was performed at cohort enrollment, including broad-based global metabolomic profiling of plasma samples. Participants were followed prospectively for ascertainment of outcomes. Supervised and unsupervised machine learning algorithms and regression models were used to compare CTD-PAH versus IPAH metabolomic profiles and to measure metabolite-phenotype associations and interactions. Gradients across the pulmonary circulation were assessed using paired mixed venous and wedged samples in a subset of 115 participants. Results: Metabolomic profiles distinguished CTD-PAH from IPAH, with patients with CTD-PAH demonstrating aberrant lipid metabolism with lower circulating levels of sex steroid hormones and higher free fatty acids (FAs) and FA intermediates. Acylcholines were taken up by the right ventricular-pulmonary vascular (RV-PV) circulation, particularly in CTD-PAH, while free FAs and acylcarnitines were released. In both PAH subtypes, dysregulated lipid metabolites, among others, were associated with hemodynamic and RV measurements and with transplant-free survival. Conclusions: CTD-PAH is characterized by aberrant lipid metabolism that may signal shifted metabolic substrate utilization. Abnormalities in RV-PV FA metabolism may imply a reduced capacity for mitochondrial beta oxidation within the diseased pulmonary circulation.
MeSH term(s)	Adult ; Humans ; Familial Primary Pulmonary Hypertension ; Hypertension, Pulmonary/complications ; Phenomics ; Vasodilator Agents/therapeutic use ; Pulmonary Arterial Hypertension/complications ; Connective Tissue Diseases/complications
Chemical Substances	Vasodilator Agents
Language	English
Publishing date	2023-10-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2756371-6
ISSN	2326-5205 ; 2326-5191
ISSN (online)	2326-5205
ISSN	2326-5191
DOI	10.1002/art.42632
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Article ; Online: A Novel DNase Assay Reveals Low DNase Activity in Severe Asthma.

American journal of physiology. Lung cellular and molecular physiology

2024

Abstract: Secreted deoxyribonucleases (DNases), such as DNase-1 and DNase-IL3, degrade extracellular DNA, and endogenous DNases have roles in resolving airway inflammation and guarding against autoimmune responses to nucleotides. Subsets of patients with asthma ... ...

Abstract	Secreted deoxyribonucleases (DNases), such as DNase-1 and DNase-IL3, degrade extracellular DNA, and endogenous DNases have roles in resolving airway inflammation and guarding against autoimmune responses to nucleotides. Subsets of patients with asthma have high airway DNA levels, but information about DNase activity in health and in asthma is lacking. To characterize DNase activity in health and in asthma, we developed a novel kinetic assay using a Taqman probe sequence that is quickly cleaved by DNase-I to produce a large product signal. We used this kinetic assay to measure DNase activity in sputum from participants in the Severe Asthma Research Program (SARP)-3 (n=439) and from healthy controls (n=89). We found that DNase activity was lower than normal in asthma (78.7 RFU/min vs 120.4 RFU/min, p<0.0001). Compared to asthma patients with sputum DNase activity levels in the upper tertile activity levels, those in the lower tertile of sputum DNase activity were characterized clinically by more severe disease and pathologically by airway eosinophilia and airway mucus plugging. Carbamylation of DNase-I, a post translational modification that can be mediated by eosinophil peroxidase, inactivated DNase-I. In summary, a Taqman probe-based DNase activity assay uncovers low DNase activity in the asthma airway which is associated with more severe disease and airway mucus plugging and may be caused, at least in part, by eosinophil-mediated carbamylation.
Language	English
Publishing date	2024-04-23
Publishing country	United States
Document type	Journal Article
ZDB-ID	1013184-x
ISSN	1522-1504 ; 1040-0605
ISSN (online)	1522-1504
ISSN	1040-0605
DOI	10.1152/ajplung.00081.2024
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Article ; Online: Reply: To PMID 25488689.

Cowan, Douglas C / Taylor, D Robin / Comhair, Suzy A A

The Journal of allergy and clinical immunology

2015 Volume 136, Issue 2, Page(s) 515–516

MeSH term(s)	Adrenal Cortex Hormones/therapeutic use ; Asthma/diagnosis ; Asthma/drug therapy ; Female ; Humans ; Male ; Phenotype
Chemical Substances	Adrenal Cortex Hormones
Language	English
Publishing date	2015-08
Publishing country	United States
Document type	Comment ; Letter ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	121011-7
ISSN	1097-6825 ; 1085-8725 ; 0091-6749
ISSN (online)	1097-6825 ; 1085-8725
ISSN	0091-6749
DOI	10.1016/j.jaci.2015.04.038
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Book ; Thesis: Extracellular antioxidant response in oxidant mediated lung diseases

Armande Comhair, Suzy Ans

redox regulation of the glutathione system and superoxide dismutase

2001

Author's details	door Suzy Ans Armande Comhair
Language	English ; Dutch
Size	146 S. : Ill., graph. Darst.
Publishing country	Netherlands
Document type	Book ; Thesis
Thesis / German Habilitation thesis	Nijmegen, Univ., Diss., 2001
Note	Zsfassung in niederländ. Sprache
HBZ-ID	HT013243372
ISBN	90-9013953-2 ; 978-90-9013953-1
Database	Catalogue ZB MED Medicine, Health

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Article ; Online: Assessing the clinico-immunological profile of patients with obesity and chronic rhinosinusitis.

Chaaban, Mohamad R / Asosingh, Kewal / Comhair, Suzy / Hoying, David

International forum of allergy & rhinology

2023

Abstract: Background: No studies have investigated the systemic and local sinonasal profile of obesity-related chronic rhinosinusitis (CRS), despite its observed association in recent retrospective studies. The objectives of our study were to assess the impact of ...

Abstract	Background: No studies have investigated the systemic and local sinonasal profile of obesity-related chronic rhinosinusitis (CRS), despite its observed association in recent retrospective studies. The objectives of our study were to assess the impact of obesity on the clinical and cytokine profile of patients with CRS and evaluate treatment response with functional endoscopic sinus surgery. Methods: This was a prospective observational study at the Cleveland Clinic that included patients with CRS (n = 54) between December 2021 and September 2022. Data collection included demographics, body mass index (BMI), comorbidities, baseline sinonasal outcome test scores, baseline radiologic scores (Lund-Mackay), postoperative sinonasal outcome test scores (at 3-4 months), and local and systemic alarmins/T-helper cytokines. Results: Out of the 54 CRS patients, there were 20 CRS patients without nasal polyps (37%) and 34 with nasal polyps (63%). Patients were categorized based on obesity (BMI ≥ 30 kg/m Conclusions: In conclusion, patients with obese CRS and nasal polyps displayed diminished levels of intranasal alarmins and reduced intranasal eotaxin-3. These results potentially imply the presence of a unique, obese type 2-low CRS phenotype that warrants further exploration.
Language	English
Publishing date	2023-11-23
Publishing country	United States
Document type	Journal Article
ZDB-ID	2625826-2
ISSN	2042-6984 ; 2042-6976
ISSN (online)	2042-6984
ISSN	2042-6976
DOI	10.1002/alr.23304
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Article ; Online: CCL5 is a potential bridge between type 1 and type 2 inflammation in asthma.

The Journal of allergy and clinical immunology

2023 Volume 152, Issue 1, Page(s) 94–106.e12

Abstract: Background: Type 1 (T1) inflammation (marked by IFN-γ expression) is now consistently identified in subsets of asthma cohorts, but how it contributes to disease remains unclear.: Objective: We sought to understand the role of CCL5 in asthmatic T1 ... ...

Abstract	Background: Type 1 (T1) inflammation (marked by IFN-γ expression) is now consistently identified in subsets of asthma cohorts, but how it contributes to disease remains unclear. Objective: We sought to understand the role of CCL5 in asthmatic T1 inflammation and how it interacts with both T1 and type 2 (T2) inflammation. Methods: CCL5, CXCL9, and CXCL10 messenger RNA expression from sputum bulk RNA sequencing, as well as clinical and inflammatory data were obtained from the Severe Asthma Research Program III (SARP III). CCL5 and IFNG expression from bronchoalveolar lavage cell bulk RNA sequencing was obtained from the Immune Mechanisms in Severe Asthma (IMSA) cohort and expression related to previously identified immune cell profiles. The role of CCL5 in tissue-resident memory T-cell (TRM) reactivation was evaluated in a T1 Results: Sputum CCL5 expression strongly correlated with T1 chemokines (P < .001 for CXCL9 and CXCL10), consistent with a role in T1 inflammation. CCL5 Conclusion: CCL5 appears to contribute to TRM-related T1 neutrophilic inflammation in asthma while paradoxically also correlating with T2 inflammation and with sputum eosinophilia.
MeSH term(s)	Animals ; Humans ; Mice ; Asthma ; Chemokine CCL5/genetics ; Chemokine CCL5/metabolism ; Chemokines/metabolism ; Eosinophils ; Inflammation/metabolism ; Neutrophils ; Sputum
Chemical Substances	CCL5 protein, human ; Chemokine CCL5 ; Chemokines
Language	English
Publishing date	2023-03-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	121011-7
ISSN	1097-6825 ; 1085-8725 ; 0091-6749
ISSN (online)	1097-6825 ; 1085-8725
ISSN	0091-6749
DOI	10.1016/j.jaci.2023.02.028
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