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32 results on '"Thanabalasuriar, Ajitha"'

1. Neonatal imprinting of alveolar macrophages via neutrophil-derived 12-HETE

Author

Pernet, Erwan, Sun, Sarah, Sarden, Nicole, Gona, Saideep, Nguyen, Angela, Khan, Nargis, Mawhinney, Martin, Tran, Kim A., Chronopoulos, Julia, Amberkar, Dnyandeo, Sadeghi, Mina, Grant, Alexandre, Wali, Shradha, Prevel, Renaud, Ding, Jun, Martin, James G., Thanabalasuriar, Ajitha, Yipp, Bryan G., Barreiro, Luis B., and Divangahi, Maziar

Published
2023
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4. Bispecific antibody targets multiple pseudomonas aeruginosa evasion mechanisms in the lung vasculature

Author

Thanabalasuriar, Ajitha, Surewaard, Bas G.J., Willson, Michelle E., Neupane, Arpan S., Stover, Charles K., Warrener, Paul, Wilson, George, Keller, Ashley E., Sellman, Bret R., DiGiandomenico, Antonio, and Kubes, Paul

Subjects
Antibodies -- Health aspects -- Analysis, Lung diseases -- Prevention, Pseudomonas aeruginosa -- Health aspects -- Analysis, Health care industry
Abstract

Pseudomonas aeruginosa is a major cause of severe infections that lead to bacteremia and high patient mortality. P. aeruginosa has evolved numerous evasion and subversion mechanisms that work in concert to overcome immune recognition and effector functions in hospitalized and immunosuppressed individuals. Here, we have used multilaser spinning-disk intravital microscopy to monitor the blood-borne stage in a murine bacteremic model of P. aeruginosa infection. P. aeruginosa adhered avidly to lung vasculature, where patrolling neutrophils and other immune cells were virtually blind to the pathogen's presence. This cloaking phenomenon was attributed to expression of Psl exopolysaccharide. Although an antiPsl mAb activated complement and enhanced neutrophil recognition of P. aeruginosa, neutrophil-mediated clearance of the pathogen was suboptimal owing to a second subversion mechanism, namely the type 3 secretion (T3S) injectisome. Indeed, T3S prevented phagosome acidification and resisted killing inside these compartments. Antibody-mediated inhibition of the T3S protein PcrV did not enhance bacterial phagocytosis but did enhance killing of the few bacteria ingested by neutrophils. A bispecific mAb targeting both Psl and PcrV enhanced neutrophil uptake of P. aeruginosa and also greatly increased inhibition of T3S function, allowing for phagosome acidification and bacterial killing. These data highlight the need to block multiple evasion and subversion mechanisms in tandem to kill P. aeruginosa., Introduction Pseudomonas aeruginosa is an important opportunistic bacterial pathogen that causes life-threatening infections in critically ill and immunocompromised individuals. It is one of the most common causes of Gram-negative pneumonia [...]

Published
2017
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8. PD-L1 + neutrophils contribute to injury-induced infection susceptibility

Author

Thanabalasuriar, Ajitha, primary, Chiang, Abby J., additional, Morehouse, Christopher, additional, Camara, Margarita, additional, Hawkins, Shonda, additional, Keller, Ashley E., additional, Koksal, Adem C., additional, Caceres, Carolina S., additional, Berlin, Aaron A., additional, Holoweckyj, Nicholas, additional, Takahashi, Virginia N., additional, Cheng, Lily, additional, de los Reyes, Melissa, additional, Pelletier, Mark, additional, Patera, Andriani C., additional, Sellman, Bret, additional, Hess, Sonja, additional, Marelli, Marcello, additional, Boo, Chelsea C., additional, Cohen, Taylor S., additional, and DiGiandomenico, Antonio, additional

Published
2021
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9. Patrolling Alveolar Macrophages Conceal Bacteria from the Immune System to Maintain Homeostasis

Author

Neupane, Arpan Sharma, primary, Willson, Michelle, additional, Chojnacki, Andrew Krzysztof, additional, Vargas E Silva Castanheira, Fernanda, additional, Morehouse, Christopher, additional, Carestia, Agostina, additional, Keller, Ashley Elaine, additional, Peiseler, Moritz, additional, DiGiandomenico, Antonio, additional, Kelly, Margaret Mary, additional, Amrein, Matthias, additional, Jenne, Craig, additional, Thanabalasuriar, Ajitha, additional, and Kubes, Paul, additional

Published
2020
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11. Dipeptidase-1 Is an Adhesion Receptor for Neutrophil Recruitment in Lungs and Liver

Author

Choudhury, Saurav Roy, primary, Babes, Liane, additional, Rahn, Jennifer J., additional, Ahn, Bo-Young, additional, Goring, Kimberly-Ann R., additional, King, Jennifer C., additional, Lau, Arthur, additional, Petri, Björn, additional, Hao, Xiaoguang, additional, Chojnacki, Andrew K., additional, Thanabalasuriar, Ajitha, additional, McAvoy, Erin F., additional, Tabariès, Sébastien, additional, Schraeder, Christoph, additional, Patel, Kamala D., additional, Siegel, Peter M., additional, Kopciuk, Karen A., additional, Schriemer, David C., additional, Muruve, Daniel A., additional, Kelly, Margaret M., additional, Yipp, Bryan G., additional, Kubes, Paul, additional, Robbins, Stephen M., additional, and Senger, Donna L., additional

Published
2019
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13. PD-L1+ neutrophils contribute to injury-induced infection susceptibility.

Author

Thanabalasuriar, Ajitha, Chiang, Abby J., Morehouse, Christopher, Camara, Margarita, Hawkins, Shonda, Keller, Ashley E., Koksal, Adem C., Caceres, Carolina S., Berlin, Aaron A., Holoweckyj, Nicholas, Takahashi, Virginia N., Cheng, Lily, de los Reyes, Melissa, Pelletier, Mark, Patera, Andriani C., Sellman, Bret, Hess, Sonja, Marelli, Marcello, Boo, Chelsea C., and Cohen, Taylor S.

Subjects
*NEUTROPHILS, *PSEUDOMONAS aeruginosa infections, *HAIR growth
Abstract

The article presents a study that explores the programmed death ligand 1 (PD-L1) neutrophils contribute to injury-induced infection susceptibility. It describes a rapid increase in neutrophil cell numbers in the lungs following induction of thermal injury. It provides evidence that injury promotes changes to neutrophils that are important for wound healing but contribute to infection susceptibility.

Published
2021
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15. Neutrophil Extracellular Traps Confine Pseudomonas aeruginosa Ocular Biofilms and Restrict Brain Invasion

Author

Thanabalasuriar, Ajitha, primary, Scott, Brittney Noelle Vivian, additional, Peiseler, Moritz, additional, Willson, Michelle Elizabeth, additional, Zeng, Zhutian, additional, Warrener, Paul, additional, Keller, Ashley Elaine, additional, Surewaard, Bas Gerardus Johannes, additional, Dozier, Elizabeth Ashley, additional, Korhonen, Juha Tapio, additional, Cheng, Lily I-ting, additional, Gadjeva, Mihaela, additional, Stover, C. Kendall, additional, DiGiandomenico, Antonio, additional, and Kubes, Paul, additional

Published
2019
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17. α-Toxin Induces Platelet Aggregation and Liver Injury during Staphylococcus aureus Sepsis

Author

Surewaard, Bas G.J., primary, Thanabalasuriar, Ajitha, additional, Zeng, Zhutian, additional, Tkaczyk, Christine, additional, Cohen, Taylor S., additional, Bardoel, Bart W., additional, Jorch, Selina K., additional, Deppermann, Carsten, additional, Bubeck Wardenburg, Juliane, additional, Davis, Rachelle P., additional, Jenne, Craig N., additional, Stover, Kendall C., additional, Sellman, Bret R., additional, and Kubes, Paul, additional

Published
2018
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19. Neonates, antibiotics and the microbiome

Author

Thanabalasuriar, Ajitha and Kubes, Paul

Subjects
Microbiota (Symbiotic organisms) -- Health aspects -- Research, Antibiotics -- Health aspects -- Usage -- Research, Infants (Newborn) -- Health aspects -- Research, Biological sciences, Health
Abstract

As babies leave their mothers' wombs, they are colonized by commensal bacteria. A new study shows that these microbes in a newborn's gut can promote an increase in circulating neutrophils that can guard the body from infections. Altering a neonate's gut microbiota with perinatal antibiotic treatment can impair neutrophils, leaving the newborn vulnerable to attack by harmful bacteria (pages 524-530)., Globally, around 4 million newborn babies die yearly due to sepsis (1). Prolonged use of antibiotics is currently under clinical practice in the interest of preventing early-onset sepsis in newborns [...]

Published
2014

23. R-Spondin 2 signalling mediates susceptibility to fatal infectious diarrhoea

Author

Papapietro, Olivier, primary, Teatero, Sarah, additional, Thanabalasuriar, Ajitha, additional, Yuki, Kyoko E., additional, Diez, Eduardo, additional, Zhu, Lei, additional, Kang, Eugene, additional, Dhillon, Sandeep, additional, Muise, Aleixo M., additional, Durocher, Yves, additional, Marcinkiewicz, Martin M., additional, Malo, Danielle, additional, and Gruenheid, Samantha, additional

Published
2013
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29. The Bacterial Virulence Factor NleA Inhibits Cellular Protein Secretion by Disrupting Mammalian COPII Function

Author

Kim, Jinoh, primary, Thanabalasuriar, Ajitha, additional, Chaworth-Musters, Tessa, additional, Fromme, J. Chris, additional, Frey, Elizabeth A., additional, Lario, Paula I., additional, Metalnikov, Pavel, additional, Rizg, Keyrillos, additional, Thomas, Nikhil A., additional, Lee, Sau Fung, additional, Hartland, Elizabeth L., additional, Hardwidge, Philip R., additional, Pawson, Tony, additional, Strynadka, Natalie C., additional, Finlay, B. Brett, additional, Schekman, Randy, additional, and Gruenheid, Samantha, additional

Published
2007
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30. The bacterial virulence factor NleA is required for the disruption of intestinal tight junctions by enteropathogenic Escherichia coli.

Author

Thanabalasuriar, Ajitha, Koutsouris, Athanasia, Weflen, Andrew, Mimee, Mark, Hecht, Gail, and Gruenheid, Samantha

Subjects
*ESCHERICHIA coli, *EPITHELIAL cells, *SMALL intestine, *PROTEINS, *INTESTINES, *CELLS
Abstract

Enteropathogenic Escherichia coli (EPEC) is a diarrhoeal pathogen that adheres to epithelial cells of the small intestine and uses a type III secretion system to inject effector proteins into host cells. EPEC infection leads to disruption of host intestinal tight junctions that are important for maintaining intestinal barrier function. This disruption is dependent on the bacterial type III secretion system, as well as the translocated effectors EspF and Map. Here we show that a third type III translocated bacterial effector protein, NleA, is also involved in tight junction disruption during EPEC infection. Using the drug Brefeldin A, we demonstrate that the effect of NleA on tight junction integrity is related to its inhibition of host cell protein trafficking through COPII-dependent pathways. These results suggest that NleA's striking effect on virulence is mediated, at least in part, via its role in disruption of intestinal barrier function. [ABSTRACT FROM AUTHOR]

Published
2010
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31. The bacterial virulence factor NleA's involvement in intestinal tight junction disruption during Enteropathogenic E. coliinfection is independent of its putative PDZ binding domain

Author

Thanabalasuriar, Ajitha, Koutsouris, Athanasia, Hecht, Gail, and Gruenheid, Samantha

Abstract

Enteropathogenic Escherichia coli(EPEC) is an enteric pathogen able to cause severe diarrhea. Once adhered to the small intestine, EPEC disrupts tight junctions that are important for intestinal barrier function. This disruption is dependent on the bacterial type III secretion system, as well as the translocated effectors EspF and Map. Recently we have shown that a third type III translocated bacterial effector protein, NleA, is also involved in tight junction disruption during EPEC infection. NleA has a predicted PDZ-binding domain at its C-terminus which is proposed to be involved in protein interactions with PDZ domain containing proteins. Since several PDZ-domain-containing proteins localize to tight junctions, we hypothesized that the PDZ-binding domain of NleA might be important for its role in tight junction disruption. However, here we show that a molecular variant of NleA lacking the PDZ-binding domain behaves indistinguishably from the wild-type protein with respect to disruption of tight junctions.

Published
2010
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32. Intravital Microscopy for Imaging and Live Cell Tracking of Alveolar Macrophages in Real Time.

Author

Kwak A and Thanabalasuriar A

Subjects
Animals, Mice, Lung cytology, Host-Pathogen Interactions, Macrophages, Alveolar cytology, Intravital Microscopy methods, Cell Tracking methods
Abstract

Classic in vitro coculture assays of pathogens with host cells have contributed significantly to our understanding of the intracellular lifestyle of several pathogens. Coculture assays with pathogens and eukaryotic cells can be analyzed through various techniques including plating for colony-forming units (CFU), confocal microscopy, and flow cytometry. However, findings from in vitro assays require validation in an in vivo model. Several physiological conditions can influence host-pathogen interactions, which cannot easily be mimicked in vitro. Intravital microscopy (IVM) is emerging as a powerful tool for studying host-pathogen interactions by enabling in vivo imaging of living organisms. As a result, IVM has significantly enhanced the understanding of infection mediated by diverse pathogens. The versatility of IVM has also allowed for the imaging of various organs as sites of local infection. This chapter specifically focuses on IVM conducted on the lung for elucidating pulmonary immune response, primarily involving alveolar macrophages, to pathogens. Additionally, in this chapter we outline the protocol for lung IVM that utilizes a thoracic suction window to stabilize the lung for acquiring stable images., (© 2024. The Author(s), under exclusive license to Springer Science+Business Media, LLC, part of Springer Nature.)

Published
2024
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