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Your search keyword '"Perkins, Darren J."' showing total 6 results
Start Over Author "Perkins, Darren J." Publisher american society for microbiology
6 results on '"Perkins, Darren J."'

3. Improved Tolerability of a Salmonella enterica Serovar Typhimurium Live-Attenuated Vaccine Strain Achieved by Balancing Inflammatory Potential with Immunogenicity

Author

Higginson, Ellen E., primary, Ramachandran, Girish, additional, Panda, Aruna, additional, Shipley, Steven T., additional, Kriel, Edwin H., additional, DeTolla, Louis J., additional, Lipsky, Michael, additional, Perkins, Darren J., additional, Salerno-Goncalves, Rosangela, additional, Sztein, Marcelo B., additional, Pasetti, Marcela F., additional, Levine, Myron M., additional, and Tennant, Sharon M., additional

Published
2018
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4. The Tick Protein Sialostatin L2 Binds to Annexin A2 and Inhibits NLRC4-Mediated Inflammasome Activation

Author

Wang, Xiaowei, primary, Shaw, Dana K., additional, Sakhon, Olivia S., additional, Snyder, Greg A., additional, Sundberg, Eric J., additional, Santambrogio, Laura, additional, Sutterwala, Fayyaz S., additional, Dumler, J. Stephen, additional, Shirey, Kari Ann, additional, Perkins, Darren J., additional, Richard, Katharina, additional, Chagas, Andrezza C., additional, Calvo, Eric, additional, Kopecký, Jan, additional, Kotsyfakis, Michail, additional, and Pedra, Joao H. F., additional

Published
2016
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6. ER-transiting bacterial toxins amplify STING innate immune responses and elicit ER stress.

Author

Schlenker C, Richard K, Skobelkina S, Mathena RP, and Perkins DJ

Subjects
Animals, Mice, Signal Transduction, Endoplasmic Reticulum metabolism, Endoplasmic Reticulum immunology, Macrophages immunology, Macrophages metabolism, Mice, Inbred C57BL, Humans, Immunity, Innate, Endoplasmic Reticulum Stress immunology, Membrane Proteins metabolism, Membrane Proteins immunology, Bacterial Toxins immunology, Bacterial Toxins metabolism
Abstract

The cGAS/STING sensor system drives innate immune responses to intracellular microbial double-stranded DNA (dsDNA) and bacterial cyclic nucleotide second messengers (e.g., c-di-AMP). STING-dependent cell-intrinsic responses can increase resistance to microbial infection and speed pathogen clearance. Correspondingly, STING activation and signaling are known to be targeted for suppression by effectors from several bacterial pathogens. Whether STING responses are also positively regulated through sensing of specific bacterial effectors is less clear. We find that STING activation through dsDNA, by its canonical ligand 2'-3' cGAMP, or the small molecule DMXAA is potentiated following intracellular delivery of the AB 5 toxin family member pertussis toxin from Bordetella pertussis or the B subunit of cholera toxin from Vibrio cholerae . Entry of pertussis toxin or cholera toxin B into mouse macrophages triggers markers of endoplasmic reticulum (ER) stress and enhances ligand-dependent STING responses at the level of STING receptor activation in a manner that is independent of toxin enzymatic activity. Our results provide an example in which STING responses integrate information about the presence of relevant ER-transiting bacterial toxins into the innate inflammatory response and may help to explain the in vivo adjuvant effects of catalytically inactive toxins., Competing Interests: The authors declare no conflict of interest.

Published
2024
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