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Article ; Online: The gift of preexisting immunity for developing an alternative vaccine strategy.

Tran, Kim A / Divangahi, Maziar

2023 Volume 133, Issue 23

Abstract: Despite the worldwide application of vaccination and other antiviral interventions, pulmonary viral infections remain a persistent threat to human health. The 1918 influenza pandemic killed more than 40 million people in just one year, and the SARS-CoV-2 ...

Abstract	Despite the worldwide application of vaccination and other antiviral interventions, pulmonary viral infections remain a persistent threat to human health. The 1918 influenza pandemic killed more than 40 million people in just one year, and the SARS-CoV-2 pandemic has killed more than 6.9 million people since 2019. While the current approved COVID-19 vaccines are administered parenterally and induce systemic immunity, they only prevent the progression to severe disease. Thus, other vaccine platforms are still needed for completely preventing the disease and subsequent transmission. In this issue of the JCI, Kawai et al. present an adjuvant-free subunit (RBD-HA) fusion vaccine, which produces robust IgG and IgA antibody responses against SARS-CoV-2, enriched within the nasal cavity, by using the host's preexisting immunity to influenza infection. This preclinical study has tremendous implications for future mucosal vaccine design and provides a roadmap for generating a safer and effective intranasal vaccine against pulmonary infections.
MeSH term(s)	Humans ; Influenza, Human/prevention & control ; COVID-19 Vaccines ; Antibodies, Viral ; Influenza Vaccines ; Administration, Intranasal ; Vaccination ; Immunity, Mucosal
Chemical Substances	COVID-19 Vaccines ; Antibodies, Viral ; Influenza Vaccines
Language	English
Publishing date	2023-12-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI174952
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Article ; Online: Author Correction: BCG immunization induces CX3CR1

Tran, Kim A / Pernet, Erwan / Sadeghi, Mina / Downey, Jeffrey / Chronopoulos, Julia / Lapshina, Elizabeth / Tsai, Oscar / Kaufmann, Eva / Ding, Jun / Divangahi, Maziar

Nature immunology

2024 Volume 25, Issue 3, Page(s) 578

Language	English
Publishing date	2024-01-30
Publishing country	United States
Document type	Published Erratum
ZDB-ID	2016987-5
ISSN	1529-2916 ; 1529-2908
ISSN (online)	1529-2916
ISSN	1529-2908
DOI	10.1038/s41590-024-01773-5
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Zs.A 5294: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: BCG immunization induces CX3CR1

Tran, Kim A / Pernet, Erwan / Sadeghi, Mina / Downey, Jeffrey / Chronopoulos, Julia / Lapshina, Elizabeth / Tsai, Oscar / Kaufmann, Eva / Ding, Jun / Divangahi, Maziar

Nature immunology

2024 Volume 25, Issue 3, Page(s) 418–431

Abstract: After a century of using the Bacillus Calmette-Guérin (BCG) vaccine, our understanding of its ability to provide protection against homologous (Mycobacterium tuberculosis) or heterologous (for example, influenza virus) infections remains limited. Here we ...

Abstract	After a century of using the Bacillus Calmette-Guérin (BCG) vaccine, our understanding of its ability to provide protection against homologous (Mycobacterium tuberculosis) or heterologous (for example, influenza virus) infections remains limited. Here we show that systemic (intravenous) BCG vaccination provides significant protection against subsequent influenza A virus infection in mice. We further demonstrate that the BCG-mediated cross-protection against influenza A virus is largely due to the enrichment of conventional CD4
MeSH term(s)	Animals ; Mice ; Administration, Intravenous ; BCG Vaccine/immunology ; Influenza A virus ; Memory T Cells ; Trained Immunity ; Vaccination ; Orthomyxoviridae Infections/immunology ; Orthomyxoviridae Infections/prevention & control
Chemical Substances	BCG Vaccine
Language	English
Publishing date	2024-01-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	2016987-5
ISSN	1529-2916 ; 1529-2908
ISSN (online)	1529-2916
ISSN	1529-2908
DOI	10.1038/s41590-023-01739-z
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Zs.A 5294: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Mitochondrial cyclophilin D promotes disease tolerance by licensing NK cell development and IL-22 production against influenza virus.

Downey, Jeffrey / Randolph, Haley E / Pernet, Erwan / Tran, Kim A / Khader, Shabaana A / King, Irah L / Barreiro, Luis B / Divangahi, Maziar

Cell reports

2022 Volume 39, Issue 12, Page(s) 110974

Abstract: Severity of pulmonary viral infections, including influenza A virus (IAV), is linked to excessive immunopathology, which impairs lung function. Thus, the same immune responses that limit viral replication can concomitantly cause lung damage that must be ... ...

Abstract	Severity of pulmonary viral infections, including influenza A virus (IAV), is linked to excessive immunopathology, which impairs lung function. Thus, the same immune responses that limit viral replication can concomitantly cause lung damage that must be countered by largely uncharacterized disease tolerance mechanisms. Here, we show that mitochondrial cyclophilin D (CypD) protects against IAV via disease tolerance. CypD
MeSH term(s)	Animals ; Peptidyl-Prolyl Isomerase F ; Humans ; Influenza A virus ; Influenza, Human ; Interleukins ; Killer Cells, Natural ; Mice ; Mice, Inbred C57BL ; Mitochondria/metabolism ; Orthomyxoviridae Infections ; Interleukin-22
Chemical Substances	Peptidyl-Prolyl Isomerase F ; Interleukins
Language	English
Publishing date	2022-06-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2022.110974
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Cardiac failure following inadvertent administration of high-dose epinephrine subcutaneously.

Tran, Kim A / Fraser, Douglas D / Hawrylyshyn, Krista / Norozi, Kambiz

Journal of pediatric intensive care

2018 Volume 1, Issue 4, Page(s) 221–225

Abstract: Our aim is to report the consequences of epinephrine toxicity leading to cardiac failure in a child and the successful management with dopamine and milrinone. A previously healthy 13-year-old girl undergoing a left tympanomastoidectomy was inadvertently ... ...

Abstract	Our aim is to report the consequences of epinephrine toxicity leading to cardiac failure in a child and the successful management with dopamine and milrinone. A previously healthy 13-year-old girl undergoing a left tympanomastoidectomy was inadvertently administered 10 mL of 1:1000 epinephrine subcutaneously (0.175 mg/kg) on the left post auricular region in lieu of lidocaine. She developed sudden supraventricular tachycardia, hypertension and flash pulmonary edema. She was initially treated with propofol, nitrogycerin and increased peak end-expiratory pressure. Within 4 h, she remained tachycardic, but was hypotensive with an increased central venous pressure. Electrocardiogram and echocardiogram investigations showed ST changes indicative of myocardial ischemia and globally reduced function, respectively. Dopamine infusion was administered, together with milrinone, resulting in a gradual improvement of cardiac function within 3 days. She was transitioned to enalapril and discharged home. This case highlights the clinical features of high dose epinephrine toxicity secondary to iatrogenic subcutaneous overdose followed by hypotension and pulmonary edema as a possible late effect of epinephrine and the successful management of secondary cardiac failure with administration of dopamine, milrinone and enalapril.
Language	English
Publishing date	2018-12-12
Publishing country	Germany
Document type	Journal Article
ISSN	2146-4618
ISSN	2146-4618
DOI	10.3233/PIC-12037
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Article ; Online: Characterization of the Clinical Evidence Supporting Repository Corticotropin Injection for FDA-Approved Indications: A Scoping Review.

Tran, Kim A / Harrod, Curtis / Bourdette, Dennis N / Cohen, David M / Deodhar, Atul A / Hartung, Daniel M

JAMA internal medicine

2021 Volume 182, Issue 2, Page(s) 206–217

Abstract: Importance: Repository corticotropin injection is an expensive medication that was approved in 1952 for the treatment of many inflammatory conditions. The clinical evidence supporting the use of repository corticotropin (hereinafter referred to as ... ...

Abstract	Importance: Repository corticotropin injection is an expensive medication that was approved in 1952 for the treatment of many inflammatory conditions. The clinical evidence supporting the use of repository corticotropin (hereinafter referred to as corticotropin) has been weak, perhaps because its approval predated the modern review standards of the US Food and Drug Administration (FDA). Objective: To characterize the clinical evidence supporting the use of corticotropin for its FDA-approved indications. Evidence review: Studies were identified via electronic searches of Ovid MEDLINE, the Cumulative Index of Nursing and Allied Health Literature (CINAHL), and the Cochrane Central Register of Controlled Trials (CENTRAL) from database inception to May 12, 2021 (the MEDLINE search was updated on June 8, 2021). Bibliographies of retrieved articles were also reviewed through ClinicalTrials.gov, FDA documents, and the manufacturer's website. Search terms included HP Acthar, ACTH gel, repository corticotropin, and terms for specific diseases, such as multiple sclerosis, nephrotic syndrome, rheumatoid arthritis, and West syndrome (or spasms, infantile). The review included randomized clinical trials (RCTs), nonrandomized and single-arm clinical trials, and prospective cohort studies that compared corticotropin with an active comparator, placebo, or no treatment. Data were extracted by 1 reviewer and verified by a second. Disagreements were resolved through discussion. Studies were qualitatively synthesized by indication to summarize important design features and results. Findings: Of 1059 records screened, 203 full-text articles were assessed for eligibility. A total of 41 studies involving 2235 participants met inclusion criteria; of those, 11 involved infantile spasms, 10 involved multiple sclerosis (MS), 11 involved rheumatological conditions, 7 involved nephrotic syndrome, 1 involved ocular conditions, and 1 involved sarcoidosis. Overall, 19 studies either included a single arm or exclusively compared different corticotropin dosing strategies. The evidence was most robust for the treatment of infantile spasms and MS. The largest number of studies comparing corticotropin with an active agent (n = 4) or placebo (n = 5) pertained to MS, with almost all studies finding that corticotropin performed better than placebo but no different than corticosteroids. For the treatment of infantile spasms, 8 controlled studies were identified (6 were randomized); of those, only 1 small RCT found corticotropin to be significantly superior to corticosteroids. Studies of patients with other conditions (n = 20) frequently lacked a control group (n = 12), were placebo-controlled (n = 5), or exclusively examined different corticotropin dosing strategies (n = 2). Placebo-controlled RCTs of rheumatoid arthritis, ankylosing spondylitis, optic neuritis, systemic lupus erythematosus, and nephrotic syndrome were generally small and did not consistently demonstrate that corticotropin was superior to placebo. Blinded RCTs showed a similar or greater number of adverse effects with corticotropin relative to corticosteroids. Conclusions and relevance: In this scoping review, few RCTs supported the clinical benefit of corticotropin for most FDA-approved indications. Most RCTs found that corticotropin was not superior to corticosteroids for treating relapses of MS or infantile spasms.
MeSH term(s)	Adrenal Cortex Hormones/therapeutic use ; Adrenocorticotropic Hormone ; Arthritis, Rheumatoid/drug therapy ; Female ; Humans ; Male ; Multiple Sclerosis/drug therapy ; Nephrotic Syndrome/drug therapy ; Spasms, Infantile/drug therapy ; United States ; United States Food and Drug Administration
Chemical Substances	Adrenal Cortex Hormones ; Adrenocorticotropic Hormone (9002-60-2)
Language	English
Publishing date	2021-12-03
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2699338-7
ISSN	2168-6114 ; 2168-6106
ISSN (online)	2168-6114
ISSN	2168-6106
DOI	10.1001/jamainternmed.2021.7171
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Article ; Online: Virus-Induced Acute Respiratory Distress Syndrome Causes Cardiomyopathy Through Eliciting Inflammatory Responses in the Heart.

Circulation

2024

Abstract: Background: Viral infections can cause acute respiratory distress syndrome (ARDS), systemic inflammation, and secondary cardiovascular complications. Lung macrophage subsets change during ARDS, but the role of heart macrophages in cardiac injury during ... ...

Abstract	Background: Viral infections can cause acute respiratory distress syndrome (ARDS), systemic inflammation, and secondary cardiovascular complications. Lung macrophage subsets change during ARDS, but the role of heart macrophages in cardiac injury during viral ARDS remains unknown. Here we investigate how immune signals typical for viral ARDS affect cardiac macrophage subsets, cardiovascular health, and systemic inflammation. Methods: We assessed cardiac macrophage subsets using immunofluorescence histology of autopsy specimens from 21 patients with COVID-19 with SARS-CoV-2-associated ARDS and 33 patients who died from other causes. In mice, we compared cardiac immune cell dynamics after SARS-CoV-2 infection with ARDS induced by intratracheal instillation of Toll-like receptor ligands and an ACE2 (angiotensin-converting enzyme 2) inhibitor. Results: In humans, SARS-CoV-2 increased total cardiac macrophage counts and led to a higher proportion of CCR2 Conclusions: Our data suggest that viral ARDS promotes cardiac inflammation by expanding the CCR2
Language	English
Publishing date	2024-03-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	80099-5
ISSN	1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
ISSN (online)	1524-4539
ISSN	0009-7322 ; 0069-4193 ; 0065-8499
DOI	10.1161/CIRCULATIONAHA.123.066433
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Article ; Online: Neonatal imprinting of alveolar macrophages via neutrophil-derived 12-HETE.

Nature

2023 Volume 614, Issue 7948, Page(s) 530–538

Abstract: Resident-tissue macrophages (RTMs) arise from embryonic ... ...

Abstract	Resident-tissue macrophages (RTMs) arise from embryonic precursors
MeSH term(s)	Animals ; Mice ; 12-Hydroxy-5,8,10,14-eicosatetraenoic Acid/metabolism ; Acute Lung Injury ; Animals, Newborn ; Arachidonate 12-Lipoxygenase/deficiency ; Arachidonate 15-Lipoxygenase/deficiency ; Cell Self Renewal ; COVID-19 ; Influenza A virus ; Lipopolysaccharides ; Lung/cytology ; Lung/virology ; Macrophages, Alveolar/cytology ; Macrophages, Alveolar/metabolism ; Neutrophils/metabolism ; Orthomyxoviridae Infections ; Prostaglandins E ; SARS-CoV-2 ; Disease Susceptibility
Chemical Substances	12-Hydroxy-5,8,10,14-eicosatetraenoic Acid (59985-28-3) ; Alox15 protein, mouse (EC 1.13.11.31) ; Arachidonate 12-Lipoxygenase (EC 1.13.11.31) ; Arachidonate 15-Lipoxygenase (EC 1.13.11.33) ; Lipopolysaccharides ; Prostaglandins E
Language	English
Publishing date	2023-01-04
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	120714-3
ISSN	1476-4687 ; 0028-0836
ISSN (online)	1476-4687
ISSN	0028-0836
DOI	10.1038/s41586-022-05660-7
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Article ; Online: BCG vaccination provides protection against IAV but not SARS-CoV-2.

Kaufmann, Eva / Khan, Nargis / Tran, Kim A / Ulndreaj, Antigona / Pernet, Erwan / Fontes, Ghislaine / Lupien, Andréanne / Desmeules, Patrice / McIntosh, Fiona / Abow, Amina / Moorlag, Simone J C F M / Debisarun, Priya / Mossman, Karen / Banerjee, Arinjay / Karo-Atar, Danielle / Sadeghi, Mina / Mubareka, Samira / Vinh, Donald C / King, Irah L /

Robbins, Clinton S / Behr, Marcel A / Netea, Mihai G / Joubert, Philippe / Divangahi, Maziar

Cell reports

2022 Volume 38, Issue 10, Page(s) 110502

Abstract: Since the vast majority of species solely rely on innate immunity for host defense, it stands to reason that a critical evolutionary trait like immunological memory evolved in this primitive branch of our immune system. There is ample evidence that ... ...

Abstract	Since the vast majority of species solely rely on innate immunity for host defense, it stands to reason that a critical evolutionary trait like immunological memory evolved in this primitive branch of our immune system. There is ample evidence that vaccines such as bacillus Calmette-Guérin (BCG) induce protective innate immune memory responses (trained immunity) against heterologous pathogens. Here we show that while BCG vaccination significantly reduces morbidity and mortality against influenza A virus (IAV), it fails to provide protection against severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). In contrast to IAV, SARS-CoV-2 infection leads to unique pulmonary vasculature damage facilitating viral dissemination to other organs, including the bone marrow (BM), a central site for BCG-mediated trained immunity. Finally, monocytes from BCG-vaccinated individuals mount an efficient cytokine response to IAV infection, while this response is minimal following SARS-CoV-2. Collectively, our data suggest that the protective capacity of BCG vaccination is contingent on viral pathogenesis and tissue tropism.
MeSH term(s)	BCG Vaccine ; COVID-19/prevention & control ; Humans ; Immunity, Innate ; Influenza A virus ; SARS-CoV-2 ; Vaccination
Chemical Substances	BCG Vaccine
Language	English
Publishing date	2022-02-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2022.110502
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Article: Cardiac failure following inadvertent administration of high-dose epinephrine subcutaneously

Tran, Kim A. / Fraser, Douglas D. / Hawrylyshyn, Krista / Norozi, Kambiz

Journal of Pediatric Intensive Care

2012 Volume 01, Issue 04, Page(s) 221–225

Abstract	Our aim is to report the consequences of epinephrine toxicity leading to cardiac failure in a child and the successful management with dopamine and milrinone. A previously healthy 13-year-old girl undergoing a left tympanomastoidectomy was inadvertently administered 10 mL of 1:1000 epinephrine subcutaneously (0.175 mg/kg) on the left post auricular region in lieu of lidocaine. She developed sudden supraventricular tachycardia, hypertension and flash pulmonary edema. She was initially treated with propofol, nitrogycerin and increased peak end-expiratory pressure. Within 4 h, she remained tachycardic, but was hypotensive with an increased central venous pressure. Electrocardiogram and echocardiogram investigations showed ST changes indicative of myocardial ischemia and globally reduced function, respectively. Dopamine infusion was administered, together with milrinone, resulting in a gradual improvement of cardiac function within 3 days. She was transitioned to enalapril and discharged home. This case highlights the clinical features of high dose epinephrine toxicity secondary to iatrogenic subcutaneous overdose followed by hypotension and pulmonary edema as a possible late effect of epinephrine and the successful management of secondary cardiac failure with administration of dopamine, milrinone and enalapril.
Keywords	Epinephrine ; drug toxicity ; dopamine ; milrinone ; myocardial ischemia ; pulmonary edema
Language	English
Publishing date	2012-12-01
Publisher	Georg Thieme Verlag KG
Publishing place	Stuttgart ; New York
Document type	Article
ISSN	2146-4626 ; 2146-4618
ISSN (online)	2146-4626
ISSN	2146-4618
DOI	10.3233/PIC-12037
Database	Thieme publisher's database

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