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Article ; Online: Community-acquired bacterial coinfections and COVID-19.

Patton, Michael John / Gaggar, Amit / Might, Matthew / Erdmann, Nathaniel / Orihuela, Carlos J / Harrod, Kevin S

2023 Volume 104, Issue 1, Page(s) 1–21

Language	English
Publishing date	2023-08-17
Publishing country	United States
Document type	Editorial
ZDB-ID	209902-0
ISSN	1522-1210 ; 0031-9333
ISSN (online)	1522-1210
ISSN	0031-9333
DOI	10.1152/physrev.00010.2023
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Article ; Online: Neutrophil elastase-dependent cleavage of LTA4H alters its aminopeptidase activity in cystic fibrosis.

Xu, Xin / Li, Jin-Dong / Green, Todd J / Wilson, Landon / Genschmer, Kristopher / Russell, Derek / Blalock, J Edwin / Gaggar, Amit

The European respiratory journal

2024 Volume 63, Issue 3

MeSH term(s)	Humans ; Leukocyte Elastase ; Cystic Fibrosis ; Proteolysis ; Aminopeptidases/genetics ; Neutrophils
Chemical Substances	Leukocyte Elastase (EC 3.4.21.37) ; Aminopeptidases (EC 3.4.11.-)
Language	English
Publishing date	2024-03-07
Publishing country	England
Document type	Letter
ZDB-ID	639359-7
ISSN	1399-3003 ; 0903-1936
ISSN (online)	1399-3003
ISSN	0903-1936
DOI	10.1183/13993003.01512-2023
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Article ; Online: What Lies beneath: Preformed Autoantibodies and Lung Transplantation.

Duncan, Steven R / Gaggar, Amit

American journal of respiratory cell and molecular biology

2019 Volume 60, Issue 6, Page(s) 613–614

MeSH term(s)	Autoantibodies/immunology ; Emphysema ; Humans ; Lung Transplantation ; Pulmonary Emphysema ; Reperfusion Injury
Chemical Substances	Autoantibodies
Language	English
Publishing date	2019-01-16
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	1025960-0
ISSN	1535-4989 ; 1044-1549
ISSN (online)	1535-4989
ISSN	1044-1549
DOI	10.1165/rcmb.2018-0415ED
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Article ; Online: Nontypeable Haemophilus influenzae Redox Recycling of Protein Thiols Promotes Resistance to Oxidative Killing and Bacterial Survival in Biofilms in a Smoke-Related Infection Model.

Hunt, Benjamin C / Xu, Xin / Gaggar, Amit / Swords, W Edward

mSphere

2022 Volume 7, Issue 1, Page(s) e0084721

Abstract: Smoke exposure is a risk factor for community-acquired pneumonia, which is typically caused by host-adapted airway opportunists like nontypeable Haemophilus influenzae (NTHi). Genomic analyses of NTHi revealed homologs of enzymes with predicted roles in ... ...

Abstract	Smoke exposure is a risk factor for community-acquired pneumonia, which is typically caused by host-adapted airway opportunists like nontypeable Haemophilus influenzae (NTHi). Genomic analyses of NTHi revealed homologs of enzymes with predicted roles in reduction of protein thiols, which can have key roles in oxidant resistance. Using a clinical NTHi isolate (NTHi 7P49H1), we generated isogenic mutants in which homologs of glutathione reductase (open reading frame NTHI 0251), thioredoxin-dependent thiol peroxidase (NTHI 0361), thiol peroxidase (NTHI 0907), thioredoxin reductase (NTHI 1327), and glutaredoxin/peroxiredoxin (NTHI 0705) were insertionally inactivated. Bacterial protein analyses revealed that protein oxidation after hydrogen peroxide treatment was elevated in all the mutant strains. Similarly, each of these mutants was less resistant to oxidative killing than the parental strain; these phenotypes were reversed by genetic complementation. Analysis of biofilm communities formed by the parental and mutant strains showed reduction in overall biofilm thickness and density and significant sensitization of bacteria within the biofilm structure to oxidative killing. Experimental respiratory infection of smoke-exposed mice with NTHi 7P49H1 showed significantly increased bacterial counts compared to control mice. Immunofluorescent staining of lung tissues showed NTHi communities on lung mucosae, interspersed with neutrophil extracellular traps; these bacteria had transcript profiles consistent with NTHi biofilms. In contrast, infection with the panel of NTHi mutants showed a significant decrease in bacterial load. Comparable results were observed in bactericidal assays with neutrophil extracellular traps
MeSH term(s)	Animals ; Anti-Bacterial Agents/metabolism ; Biofilms ; Haemophilus Infections/microbiology ; Haemophilus influenzae/genetics ; Mice ; Otitis Media/microbiology ; Oxidation-Reduction ; Oxidative Stress ; Peroxidases/metabolism ; Sulfhydryl Compounds/metabolism
Chemical Substances	Anti-Bacterial Agents ; Sulfhydryl Compounds ; Peroxidases (EC 1.11.1.-)
Language	English
Publishing date	2022-01-19
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	2379-5042
ISSN (online)	2379-5042
DOI	10.1128/msphere.00847-21
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Article ; Online: ADAM9: A Damaging Player in Chronic Obstructive Pulmonary Disease.

Russell, Derek W / Gaggar, Amit

American journal of respiratory and critical care medicine

2018 Volume 198, Issue 12, Page(s) 1465–1466

MeSH term(s)	ADAM Proteins ; Disintegrins ; Humans ; Membrane Proteins ; Metalloproteases ; Pulmonary Disease, Chronic Obstructive
Chemical Substances	Disintegrins ; Membrane Proteins ; Metalloproteases (EC 3.4.-) ; ADAM Proteins (EC 3.4.24.-) ; ADAM9 protein, human (EC 3.4.24.-)
Language	English
Publishing date	2018-07-23
Publishing country	United States
Document type	Editorial ; Research Support, N.I.H., Extramural ; 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.201805-1012ED
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Article ; Online: The endothelial glycocalyx in critical illness: A pediatric perspective.

Richter, Robert P / Payne, Gregory A / Ambalavanan, Namasivayam / Gaggar, Amit / Richter, Jillian R

Matrix biology plus

2022 Volume 14, Page(s) 100106

Abstract: The vascular endothelium is the interface between circulating blood and end organs and thus has a critical role in preserving organ function. The endothelium is lined by a glycan-rich glycocalyx that uniquely contributes to endothelial function through ... ...

Abstract	The vascular endothelium is the interface between circulating blood and end organs and thus has a critical role in preserving organ function. The endothelium is lined by a glycan-rich glycocalyx that uniquely contributes to endothelial function through its regulation of leukocyte and platelet interactions with the vessel wall, vascular permeability, coagulation, and vasoreactivity. Degradation of the endothelial glycocalyx can thus promote vascular dysfunction, inflammation propagation, and organ injury. The endothelial glycocalyx and its role in vascular pathophysiology has gained increasing attention over the last decade. While studies characterizing vascular glycocalyx injury and its downstream consequences in a host of adult human diseases and in animal models has burgeoned, studies evaluating glycocalyx damage in pediatric diseases are relatively few. As children have unique physiology that differs from adults, significant knowledge gaps remain in our understanding of the causes and effects of endothelial glycocalyx disintegrity in pediatric critical illness. In this narrative literature overview, we offer a unique perspective on the role of the endothelial glycocalyx in pediatric critical illness, drawing from adult and preclinical data in addition to pediatric clinical experience to elucidate how marked derangement of the endothelial surface layer may contribute to aberrant vascular biology in children. By calling attention to this nascent field, we hope to increase research efforts to address important knowledge gaps in pediatric vascular biology that may inform the development of novel therapeutic strategies.
Language	English
Publishing date	2022-03-09
Publishing country	Netherlands
Document type	Journal Article
ISSN	2590-0285
ISSN (online)	2590-0285
DOI	10.1016/j.mbplus.2022.100106
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Article ; Online: Glycocalyx heparan sulfate cleavage promotes endothelial cell angiopoietin-2 expression by impairing shear stress-related AMPK/FoxO1 signaling.

Richter, Robert P / Ashtekar, Amit R / Zheng, Lei / Pretorius, Danielle / Kaushlendra, Tripathi / Sanderson, Ralph D / Gaggar, Amit / Richter, Jillian R

JCI insight

2022 Volume 7, Issue 15

Abstract: Angiopoietin-2 (Ang-2) is a key mediator of vascular disease during sepsis, and elevated plasma levels of Ang-2 are associated with organ injury scores and poor clinical outcomes. We have previously observed that biomarkers of endothelial glycocalyx (EG) ...

Abstract	Angiopoietin-2 (Ang-2) is a key mediator of vascular disease during sepsis, and elevated plasma levels of Ang-2 are associated with organ injury scores and poor clinical outcomes. We have previously observed that biomarkers of endothelial glycocalyx (EG) damage correlate with plasma Ang-2 levels, suggesting a potential mechanistic linkage between EG injury and Ang-2 expression during states of systemic inflammation. However, the cell signaling mechanisms regulating Ang-2 expression following EG damage are unknown. In the current study, we determined the temporal associations between plasma heparan sulfate (HS) levels as a marker of EG erosion and plasma Ang-2 levels in children with sepsis and in mouse models of sepsis. Second, we evaluated the role of shear stress-mediated 5'-adenosine monophosphate-activated protein kinase (AMPK) signaling in Ang-2 expression following enzymatic HS cleavage from the surface of human primary lung microvascular endothelial cells (HLMVECs). We found that plasma HS levels peaked before plasma Ang-2 levels in children and mice with sepsis. Further, we discovered that impaired AMPK signaling contributed to increased Ang-2 expression following HS cleavage from flow-conditioned HLMVECs, establishing a paradigm by which Ang-2 may be upregulated during sepsis.
MeSH term(s)	AMP-Activated Protein Kinases/metabolism ; Angiopoietin-2/metabolism ; Animals ; Biomarkers/metabolism ; Child ; Endothelial Cells/metabolism ; Forkhead Box Protein O1/metabolism ; Glycocalyx/metabolism ; Heparitin Sulfate/metabolism ; Humans ; Mice ; Sepsis ; Signal Transduction
Chemical Substances	Angiopoietin-2 ; Biomarkers ; FOXO1 protein, human ; Forkhead Box Protein O1 ; Foxo1 protein, mouse ; Heparitin Sulfate (9050-30-0) ; AMP-Activated Protein Kinases (EC 2.7.11.31)
Language	English
Publishing date	2022-08-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.155010
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Article ; Online: Therapeutic effect of two strategies directed at disruption of pathogenic neutrophil extracellular vesicles in a murine emphysema model.

Genschmer, Kristopher R / Madison, Matthew / Viera, Liliana / Margaroli, Camilla / Gaggar, Amit / Blalock, J Edwin / Russell, Derek W

American journal of physiology. Lung cellular and molecular physiology

2023 Volume 324, Issue 5, Page(s) L694–L699

Abstract: Chronic obstructive pulmonary disease (COPD) is characterized by lung extracellular matrix (ECM) remodeling that contributes to obstruction. This is driven, in part by extracellular vesicles (EVs) from activated neutrophils (PMNs), which express on their ...

Abstract	Chronic obstructive pulmonary disease (COPD) is characterized by lung extracellular matrix (ECM) remodeling that contributes to obstruction. This is driven, in part by extracellular vesicles (EVs) from activated neutrophils (PMNs), which express on their surface an α-1 antitrypsin (AAT) insensitive form of neutrophil elastase (NE). These EVs are predicted to bind to collagen fibers via Mac-1 integrins, during which time NE can enzymatically degrade the collagen. Protamine sulfate (PS), a cationic compound used safely for decades in humans, has been shown, in vitro, to dissociate this NE from the EV surface, rendering it AAT-sensitive. In addition, a nonapeptide inhibitor, MP-9, has been shown to prevent EV association with collagen. We sought to test whether PS, MP-9, or a combination of the two could effectively prevent NE+ EV-driven ECM remodeling in an animal COPD model. EVs were preincubated with PBS, protamine sulfate (25 μM), MP-9 (50 μM), or a combination of PS and MP-9. These were delivered intratracheally to anesthetized female 10- to 12-wk-old A/J mice for a 7-day time period. One group of mice was euthanized and lungs sectioned for morphometry, and the other group was used for live pulmonary function testing. The effect of alveolar destruction by activated neutrophil EVs was abrogated by pretreatment with PS or MP-9. However, in pulmonary function tests, only the PS groups (and combined PS/MP-9 groups) returned pulmonary function to near-control levels. These data presented here offer an insight into the effective use of PS in therapeutic setting for EV-derived alveolar damage.
MeSH term(s)	Humans ; Female ; Mice ; Animals ; Leukocyte Elastase/metabolism ; Neutrophils/metabolism ; Pulmonary Emphysema/metabolism ; Pulmonary Disease, Chronic Obstructive/metabolism ; Collagen/metabolism ; Emphysema ; Extracellular Vesicles/metabolism
Chemical Substances	Leukocyte Elastase (EC 3.4.21.37) ; Collagen (9007-34-5)
Language	English
Publishing date	2023-04-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1013184-x
ISSN	1522-1504 ; 1040-0605
ISSN (online)	1522-1504
ISSN	1040-0605
DOI	10.1152/ajplung.00057.2023
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Article: Characteristics and Determinants of Pulmonary Long COVID.

Patton, Michael John / Benson, Donald / Robison, Sarah W / Dhaval, Raval / Locy, Morgan L / Patel, Kinner / Grumley, Scott / Levitan, Emily B / Morris, Peter / Might, Matthew / Gaggar, Amit / Erdmann, Nathaniel

medRxiv : the preprint server for health sciences

2024

Abstract: Rationale: Persistent cough and dyspnea are prominent features of post-acute sequelae of SARS-CoV-2 (termed 'Long COVID'); however, physiologic measures and clinical features associated with these pulmonary symptoms remain poorly defined.: Objectives!# ...

Abstract	Rationale: Persistent cough and dyspnea are prominent features of post-acute sequelae of SARS-CoV-2 (termed 'Long COVID'); however, physiologic measures and clinical features associated with these pulmonary symptoms remain poorly defined. Objectives: Using longitudinal pulmonary function testing (PFTs) and CT imaging, this study aimed to identify the characteristics and determinants of pulmonary Long COVID. Methods: The University of Alabama at Birmingham Pulmonary Long COVID cohort was utilized to characterize lung defects in patients with persistent pulmonary symptoms after resolution primary COVID infection. Longitudinal PFTs including total lung capacity (TLC) and diffusion limitation of carbon monoxide (DLCO) were used to evaluate restriction and diffusion impairment over time in this cohort. Analysis of chest CT imaging was used to phenotype the pulmonary Long COVID pathology. Risk factors linked to development of pulmonary Long COVID were estimated using univariate and multivariate logistic regression models. Measurements and main results: Longitudinal evaluation 929 patients with post-COVID pulmonary symptoms revealed diffusion impairment (DLCO ≤80%) and restriction (TLC ≤80%) in 51% of the cohort (n=479). In multivariable logistic regression analysis (adjusted odds ratio; aOR, 95% confidence interval [CI]), invasive mechanical ventilation during primary infection conferred the greatest increased odds of developing pulmonary Long COVID with diffusion impaired restriction (aOR=10.9 [4.09-28.6]). Finally, a sub-analysis of CT imaging identified evidence of fibrosis in this population. Conclusions: Persistent diffusion impaired restriction was identified as a key feature of pulmonary Long COVID. Subsequent clinical trials should leverage combined symptomatic and quantitative PFT measurements for more targeted enrollment of pulmonary Long COVID patients.
Language	English
Publishing date	2024-02-14
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.02.13.24302781
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Article ; Online: Characteristics and Determinants of Pulmonary Long COVID.

Patton, Michael John / Benson, Donald / Robison, Sarah W / Raval, Dhaval / Locy, Morgan L / Patel, Kinner / Grumley, Scott / Levitan, Emily B / Morris, Peter / Might, Matthew / Gaggar, Amit / Erdmann, Nathaniel

JCI insight

2024

Abstract: BACKGROUNDPersistent cough and dyspnea are prominent features of post-acute sequelae of SARS-CoV-2 (also termed 'Long COVID'); however, physiologic measures and clinical features associated with these pulmonary symptoms remain poorly defined. Using ... ...

Abstract	BACKGROUNDPersistent cough and dyspnea are prominent features of post-acute sequelae of SARS-CoV-2 (also termed 'Long COVID'); however, physiologic measures and clinical features associated with these pulmonary symptoms remain poorly defined. Using longitudinal pulmonary function testing (PFTs) and CT imaging, this study aimed to identify the characteristics and determinants of pulmonary Long COVID.METHODSThis single-center retrospective study included 1,097 patients with clinically defined Long COVID characterized by persistent pulmonary symptoms (dyspnea, cough, and chest discomfort) lasting for ≥1 month after resolution of primary COVID infection.RESULTSAfter exclusion, a total of 929 patients with post-COVID pulmonary symptoms and PFTs were stratified diffusion impairment and restriction as measured by percent predicted diffusion capacity for carbon monoxide (DLCO) and total lung capacity (TLC). Dyspnea was the predominant symptom in the cohort (78%) and had similar prevalence regardless of degree of diffusion impairment or restriction. Longitudinal evaluation revealed diffusion impairment (DLCO ≤80%) and pulmonary restriction (TLC ≤80%) in 51% of the cohort overall (n=479). In multivariable logistic regression analysis (adjusted odds ratio; aOR, 95% confidence interval [CI]), invasive mechanical ventilation during primary infection conferred the greatest increased odds of developing pulmonary Long COVID with diffusion impairment and restriction (aOR=10.9 [4.09-28.6]). Finally, a sub-analysis of CT imaging identified radiographic evidence of fibrosis in this patient population.CONCLUSIONSLongitudinal PFT measurements in patients with prolonged pulmonary symptoms after SARS-CoV-2 infection revealed persistent diffusion impaired restriction as a key feature of pulmonary Long COVID. These results emphasize the importance of incorporating PFTs into routine clinical practice for evaluation of patients with prolonged pulmonary symptoms after resolution of SARS-CoV-2. Subsequent clinical trials should leverage combined symptomatic and quantitative PFT measurements for more targeted enrollment of pulmonary Long COVID patients.FUNDINGThis work was supported by the National Institute of Allergy and Infectious Diseases (AI156898, K08AI129705), the National Heart, Lung, and Blood Institute (HL153113, OTA21-015E, HL149944), and the COVID-19 Urgent Research Response Fund established by the Hugh Kaul Precision Medicine Network at the University of Alabama at Birmingham.
Language	English
Publishing date	2024-04-23
Publishing country	United States
Document type	Journal Article
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.177518
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