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Your search keyword '"Samantha D Crane"' showing total 3 results
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3 results on '"Samantha D Crane"'

1. SARS-CoV-2 Infection Causes Heightened Disease Severity and Mortality in a Mouse Model of Down Syndrome

Author

Roger D. Pechous, Priyangi A. Malaviarachchi, Zhuo Xing, Avrium Douglas, Samantha D. Crane, Hayley M. Theriot, Zijing Zhang, Alireza Ghaffarieh, Lu Huang, Y. Eugene Yu, and Xuming Zhang

Subjects
SARS-CoV-2, COVID-19, Down syndrome, mouse model, pathogenesis, Biology (General), QH301-705.5
Abstract

Recent epidemiological studies suggest that individuals with Down syndrome are more susceptible to SARS-CoV-2 infection and have higher rates of hospitalization and mortality than the general population. However, the main drivers behind these disparate health outcomes remain unknown. Herein, we performed experimental infections with SARS-CoV-2 in a well-established mouse model of Down syndrome. We observed similar SARS-CoV-2 replication kinetics and dissemination in the primary and secondary organs between mice with and without Down syndrome, suggesting that both groups have similar susceptibilities to SARS-CoV-2 infection. However, Down syndrome mice exhibited more severe disease as defined by clinical features including symptoms, weight loss, pulmonary function, and survival of mice. We found that increased disease severity in Down syndrome mice could not be attributed solely to increased infectivity or a more dramatic pro-inflammatory response to infection. Rather, results from RNA sequencing suggested that differences in the expression of genes from other physiological pathways, such as deficient oxidative phosphorylation, cardiopulmonary dysfunction, and deficient mucociliary clearance in the lungs may also contribute to heightened disease severity and mortality in Down syndrome mice following SARS-CoV-2 infection.

Published
2024
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2. A Dual Role for the Plasminogen Activator Protease During the Preinflammatory Phase of Primary Pneumonic Plague

Author

Srijon Kaushik Banerjee, Samantha D Crane, and Roger D. Pechous

Subjects
0301 basic medicine, Pneumonic plague, Yersinia pestis, medicine.medical_treatment, 030106 microbiology, Biology, Bubonic plague, Bacterial Adhesion, Virulence factor, Microbiology, Major Articles and Brief Reports, Mice, Plasminogen Activators, 03 medical and health sciences, stomatognathic system, medicine, Animals, Humans, Immunology and Allergy, Lung, Pathogen, Plague, Protease, Virulence, respiratory system, biology.organism_classification, medicine.disease, Mice, Inbred C57BL, Bacterial adhesin, Disease Models, Animal, 030104 developmental biology, Infectious Diseases, Host-Pathogen Interactions, Cytokines, lipids (amino acids, peptides, and proteins), Female, Plasminogen activator
Abstract

Early after inhalation, Yersinia pestis replicates to high numbers in the airways in the absence of disease symptoms or notable inflammatory responses to cause primary pneumonic plague. The plasminogen activator protease (Pla) is a critical Y. pestis virulence factor that is important for early bacterial growth in the lung via an unknown mechanism. In this article, we define a dual role for Pla in the initial stages of pulmonary infection. We show that Pla functions as an adhesin independent of its proteolytic function to suppress early neutrophil influx into the lungs, and that Pla enzymatic activity contributes to bacterial resistance to neutrophil-mediated bacterial killing. Our results suggest that the fate of Y. pestis infection of the lung is decided extremely early during infection and that Pla plays a dual role to tilt the balance in favor of the pathogen.

Published
2020

3. The Yersinia pestis GTPase BipA Promotes Pathogenesis of Primary Pneumonic Plague

Author

William E. Goldman, Kara R. Eichelberger, Samantha D Crane, Richard C. Kurten, Srijon Kaushik Banerjee, and Roger D. Pechous

Subjects
Pneumonic plague, Virulence Factors, Yersinia pestis, Immunology, Virulence, Yersinia, medicine.disease_cause, Microbiology, Bubonic plague, Virulence factor, GTP Phosphohydrolases, Mice, Bacterial Proteins, medicine, Animals, Humans, Pathogen, Plague, biology, Pseudomonas aeruginosa, pathogenesis, medicine.disease, biology.organism_classification, Molecular Pathogenesis, Mice, Inbred C57BL, Disease Models, Animal, Infectious Diseases, Models, Animal, Female, Parasitology, pneumonic plague, bacterial GTPases
Abstract

Yersinia pestis is a highly virulent pathogen and the causative agent of bubonic, septicemic, and pneumonic plague. Primary pneumonic plague caused by inhalation of respiratory droplets contaminated with Y. pestis is nearly 100% lethal within 4 to 7 days without antibiotic intervention., Yersinia pestis is a highly virulent pathogen and the causative agent of bubonic, septicemic, and pneumonic plague. Primary pneumonic plague caused by inhalation of respiratory droplets contaminated with Y. pestis is nearly 100% lethal within 4 to 7 days without antibiotic intervention. Pneumonic plague progresses in two phases, beginning with extensive bacterial replication in the lung with minimal host responsiveness, followed by the abrupt onset of a lethal proinflammatory response. The precise mechanisms by which Y. pestis is able to colonize the lung and survive two very distinct disease phases remain largely unknown. To date, a few bacterial virulence factors, including the Ysc type 3 secretion system, are known to contribute to the pathogenesis of primary pneumonic plague. The bacterial GTPase BipA has been shown to regulate expression of virulence factors in a number of Gram-negative bacteria, including Pseudomonas aeruginosa, Escherichia coli, and Salmonella enterica serovar Typhi. However, the role of BipA in Y. pestis has yet to be investigated. Here, we show that BipA is a Y. pestis virulence factor that promotes defense against early neutrophil-mediated bacterial killing in the lung. This work identifies a novel Y. pestis virulence factor and highlights the importance of early bacterial/neutrophil interactions in the lung during primary pneumonic plague.

Published
2021

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