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5. Contributors

Author

Abadie, Valérie, primary, Abraham, Clara, additional, Adams, David H., additional, Agace, William W., additional, Alexander-Brett, Jennifer, additional, Alkhairy, Omar, additional, Ambite, Ines, additional, Anderson, Deborah J., additional, Artis, David, additional, Atmar, Robert L., additional, Aymeric, Laetitia, additional, Bachert, Claus, additional, Bakema, Jantine E., additional, Baker, Kristi, additional, Beagley, Kenneth W., additional, Befus, A.D., additional, Bemark, Mats, additional, Berin, M. Cecilia, additional, Berings, Margot, additional, Berzofsky, Jay A., additional, Bilej, Martin, additional, Biswas, Nabanita, additional, Blumberg, Richard S., additional, Bienenstock, John, additional, Bogdanos, Dimitrios, additional, Boirivant, Monica, additional, Boonnak, Kobporn, additional, Bracke, Ken R., additional, Brandtzaeg, Per, additional, Braun, Jonathan, additional, Bringer, Marie-Agnès, additional, Broadbent, Andrew J., additional, Bronson, Richard, additional, Brusselle, Guy G., additional, Bulmer, Judith N., additional, Butler, J.E., additional, Cardenas, Paul A., additional, Cebra, John J., additional, Cella, Marina, additional, Cerutti, Andrea, additional, Challacombe, Stephen J., additional, Chattha, Kuldeep, additional, Cheroutre, Hilde, additional, Chiba, Tsutomu, additional, Chorny, Alejo, additional, Clements, John D., additional, Colonna, Marco, additional, Cookson, William O.C., additional, Corbeil, Lynette B., additional, Corthésy, Blaise, additional, Cripps, Allan W., additional, van Crombruggen, Koen, additional, Pires da Cunha, Andre, additional, Cunningham-Rundles, Susanna, additional, Curtiss, Roy, additional, Darfeuille-Michaud, Arlette, additional, de Jonge, Wouter J., additional, Deban, Livija, additional, Denning, Timothy L., additional, Di Santo, James P., additional, Diefenbach, Andreas, additional, DiRita, Victor J., additional, Downey, Jordan, additional, Du, Ming-Qing, additional, Edelblum, Karen L., additional, van Egmond, Marjolein, additional, Epple, H.-J., additional, Fagarasan, Sidonia, additional, Fahey, John V., additional, Ferris, Michael J., additional, Fichtner-Feigl, Stefan, additional, Fidel, Paul L., additional, Flach, Melanie, additional, Flavell, Richard, additional, Fleit, Howard B., additional, Franchini, Genoveffa, additional, Freytag, Lucy C., additional, Fuchs, Anja, additional, Fujihashi, kohtaro, additional, Fuss, Ivan J., additional, Gagliani, Nicola, additional, Garcia, Marta Rodriguez, additional, Garrett, Wendy S., additional, Gershwin, M. Eric, additional, Gevaert, Philippe, additional, Gleeson, Maree, additional, Godaly, Gabriela, additional, Goldblum, Randall M., additional, Gour, Naina, additional, Gursel, Mayda, additional, Hajishengallis, George, additional, Hammad, Hamida, additional, Hammarström, Lennart, additional, Hänninen, Arno, additional, Hanson, Lars Å., additional, Hayday, Adrian, additional, Herzog, Ronit, additional, Hodgins, Douglas C., additional, Holgate, Stephen T., additional, Holmgren, Jan, additional, Holtzman, Michael J., additional, Hook, Edward W., additional, Huber, Samuel, additional, Hurwitz, Julia L., additional, Ivanyi, Juraj, additional, Iwasaki, Akiko, additional, Jabri, Bana, additional, Jackson, Susan, additional, Jacobs, Jonathan, additional, Jalkanen, Sirpa, additional, Janoff, Edward N., additional, Jerse, Ann E., additional, Jeyanathan, Mangalakumari, additional, Julian, Bruce A., additional, Kacskovics, Imre, additional, Kaetzel, Charlotte S., additional, Kaushic, Charu, additional, Kelsall, Brian L., additional, Kessans, Sarah, additional, Kesselring, Rebecca, additional, Kilian, Mogens, additional, Kiyono, Hiroshi, additional, Klinman, Dennis M., additional, Korotkova, Marina, additional, Kronenberg, Mitchell, additional, Krysko, Olga, additional, Kurono, Yuichi, additional, Kverka, Miloslav, additional, Lambrecht, Bart N., additional, Lamm, Michael E., additional, Lantz, Olivier, additional, Lash, Gendie E., additional, Lavelle, E.C., additional, Lefrancois, Leo, additional, Leung, Patrick S.C., additional, Levine, Myron M., additional, Lim, David J., additional, Lippolis, John, additional, Louis, Nancy A., additional, Luster, Andrew D., additional, Lutay, Nataliya, additional, Lycke, Nils, additional, Macpherson, Andrew J., additional, Mantis, Nicholas J., additional, Marcotte, Harold, additional, Martin, David H., additional, Mason, Hugh S., additional, Massa, Helen M., additional, Matoba, Nobuyuki, additional, Mayer, Lloyd, additional, Maynard, Craig L., additional, McElrath, M. Juliana, additional, McEntee, C., additional, McGhee, Jerry R., additional, McGuckin, Michael A., additional, Mestecky, Jiri, additional, Mikhak, Zamaneh, additional, Miller, Robert D., additional, Moldoveanu, Zina, additional, Montgomery, Paul C., additional, Mor, Tsafrir, additional, Neurath, Markus F., additional, Neyt, Katrijn, additional, Nicholson, Lindsay K., additional, Novak, Jan, additional, Nowicki, Stella, additional, O’Hagan, D.T., additional, O’Sullivan, Nancy L., additional, Ogra, Pearay, additional, Orihuela, Carlos, additional, Ouellette, André J., additional, Owen, Robert L., additional, Pabst, Oliver, additional, Parkos, Charles A., additional, Parreño, Viviana, additional, Patel, Mickey V., additional, Perez-Novo, Claudina, additional, Perkins, Darren J., additional, Prussin, Calman, additional, Pudney, Jeffrey, additional, Raghavan, Sukanya, additional, Rainard, Pascal, additional, Ramani, Sasirekha, additional, Randall, Troy D., additional, Raska, Milan, additional, Renukaradhya, Gourapura J., additional, Rescigno, Maria, additional, Rosenthal, Kenneth L., additional, Rothenberg, Marc E., additional, Ruemmele, Frank M., additional, Russell, Michael W., additional, Saif, Linda J., additional, Salinas, Irene, additional, Salmi, Marko, additional, Salmon, Henri, additional, Sampson, Hugh A., additional, Sansonetti, Philippe, additional, Schneider, T., additional, Serafini, Nicolas, additional, Sharma, Dolly, additional, Shen, Zheng, additional, Shi, Hai Ning, additional, Shirlaw, Penelope J., additional, Shivhare, Sourima B., additional, Smith, Phillip D., additional, Smith, Patrick M., additional, Smith, Daniel J., additional, Smythies, Lesley E., additional, Spencer, Jo, additional, Strober, Warren, additional, Subbarao, Kanta, additional, Svanborg, Catharina, additional, Svennerholm, Ann-Mari, additional, Taubman, Martin A., additional, Telemo, Esbjörn, additional, Thornhill, Martin H., additional, Thornton, David J., additional, Thuenemann, Eva, additional, Tlaskalova-Hogenova, Helena, additional, Tristram, Debra, additional, Trivedi, Palak, additional, Tuomanen, Elaine, additional, Turanek, Jaroslav, additional, Turner, Jerrold R., additional, Underdown, Brian J., additional, van Helden, Mary J., additional, Veazey, Ronald S., additional, Verdu, Elena F., additional, Vlasova, Anastasia, additional, Vliagoftis, Harissios, additional, Vogel, Stefanie N., additional, Walker, W. Allan, additional, Wang, Xiaolei, additional, Watanabe, Tomohiro, additional, Weaver, Casey T., additional, Weiner, Howard L., additional, Wells, Jerry M., additional, Wen, Ting, additional, Whittum-Hudson, Judith, additional, Whitsett, Jeffrey A., additional, Williams, Ifor R., additional, Wills-Karp, Marsha, additional, Wira, Charles R., additional, Woof, Jenny M., additional, Wotherspoon, Andrew C., additional, Xing, Zhou, additional, Xu, Huanbin, additional, Zaph, Colby, additional, Zeissig, Sebastian, additional, and Zeitz, M., additional

Published
2015
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9. sj-pdf-1-ini-10.1177_1753425920975082 - Supplemental material for cAMP levels regulate macrophage alternative activation marker expression

Author

Swamy Polumuri, Perkins, Darren J, and Vogel, Stefanie N

Subjects
FOS: Clinical medicine, 110306 Endocrinology
Abstract

Supplemental material, sj-pdf-1-ini-10.1177_1753425920975082 for cAMP levels regulate macrophage alternative activation marker expression by Swamy Polumuri, Darren J Perkins and Stefanie N Vogel in Innate Immunity

Published
2020
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11. A mouse model of human TLR4 D299G/T399I SNPs reveals mechanisms of altered LPS and pathogen responses

Author

Richard, Katharina, primary, Piepenbrink, Kurt H., additional, Shirey, Kari Ann, additional, Gopalakrishnan, Archana, additional, Nallar, Shreeram, additional, Prantner, Daniel J., additional, Perkins, Darren J., additional, Lai, Wendy, additional, Vlk, Alexandra, additional, Toshchakov, Vladimir Y., additional, Feng, Chiguang, additional, Fanaroff, Rachel, additional, Medvedev, Andrei E., additional, Blanco, Jorge C.G., additional, and Vogel, Stefanie N., additional

Published
2020
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12. Dissociation of TRIF bias and adjuvanticity

Author

Richard, Katharina, primary, Perkins, Darren J., additional, Harberts, Erin M., additional, Song, Yang, additional, Gopalakrishnan, Archana, additional, Shirey, Kari Ann, additional, Lai, Wendy, additional, Vlk, Alexandra, additional, Mahurkar, Anup, additional, Nallar, Shreeram, additional, Hawkins, Lynn D., additional, Ernst, Robert K., additional, and Vogel, Stefanie N., additional

Published
2020
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14. 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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15. cAMP levels regulate macrophage alternative activation marker expression.

Author

Polumuri, Swamy, Perkins, Darren J, and Vogel, Stefanie N

Subjects
*MACROPHAGE activation, *G protein coupled receptors, *GENES, *ADENYLATE cyclase, *MACROPHAGES
Abstract

The capacity for macrophages to polarize into distinct functional activation states (e.g., M1, M2) is critical to tune an inflammatory response to the relevant infection or injury. Alternative or M2 polarization of macrophages is most often achieved in vitro in response to IL-4/IL-13 and results in the transcriptional up-regulation of a constellation of characteristic M2 marker genes. In vivo, additional signals from the inflammatory milieu can further increase or decrease M2 marker expression. Particularly, activation of cAMP-generating G protein-coupled receptors is reported to increase M2 markers, but whether this is strictly dependent upon cAMP production is unclear. We report herein that increased cAMP alone can increase IL-4-dependent M2 marker expression through a PKA/C/EBPβ/CREB dependent pathway in murine macrophages. [ABSTRACT FROM AUTHOR]

Published
2021
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16. Type I interferon Licenses Enhanced Innate Recognition and Transcriptional Responses to Franciscella tularensis LVS

Author

Richard, Katharina, Vogel, Stefanie N., and Perkins, Darren J.

Subjects
Transcription, Genetic, Inflammasomes, Macrophages, Interleukin-1beta, Interferon-beta, Article, Immunity, Innate, Toll-Like Receptor 2, Mice, Inbred C57BL, Mice, RAW 264.7 Cells, Organ Specificity, Myeloid Differentiation Factor 88, Macrophages, Peritoneal, Animals, Humans, Francisella tularensis, Tularemia
Abstract

The innate inflammatory response to Francisella tularensis (Ft) in macrophages is significantly governed by the expression of type I interferons (IFN). Previously, the proteolytic processing and maturation of pro-IL-1β protein was shown to depend upon type I IFN expression. We show in this report that paracrine type I IFN can profoundly enhance innate recognition and TLR-dependent transcriptional responses to Ft infection upstream of its role in inflammasome regulation in both primary human monocyte-derived macrophages and primary murine peritoneal macrophages, but not murine bone marrow-derived macrophages. This type I IFN-enhanced response is synergistic with TLR2 transcriptional responses, partially TLR2-independent, but strictly MyD88-dependent.

Published
2016

18. The Prostaglandin E2-EP3 Receptor Axis Regulates Anaplasma phagocytophilum-Mediated NLRC4 Inflammasome Activation

Author

Wang, Xiaowei, primary, Shaw, Dana K., additional, Hammond, Holly L., additional, Sutterwala, Fayyaz S., additional, Rayamajhi, Manira, additional, Shirey, Kari Ann, additional, Perkins, Darren J., additional, Bonventre, Joseph V., additional, Velayutham, Thangam S., additional, Evans, Sean M., additional, Rodino, Kyle G., additional, VieBrock, Lauren, additional, Scanlon, Karen M., additional, Carbonetti, Nicholas H., additional, Carlyon, Jason A., additional, Miao, Edward A., additional, McBride, Jere W., additional, Kotsyfakis, Michail, additional, and Pedra, Joao H. F., additional

Published
2016
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20. 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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23. Autocrine–paracrine prostaglandin E2signaling restricts TLR4 internalization and TRIF signaling

Author

Perkins, Darren J., Richard, Katharina, Hansen, Anne-Marie, Lai, Wendy, Nallar, Shreeram, Koller, Beverly, and Vogel, Stefanie N.

Abstract

The unique cell biology of Toll-like receptor 4 (TLR4) allows it to initiate two signal-transduction cascades: a signal dependent on the adaptors TIRAP (Mal) and MyD88 that begins at the cell surface and regulates proinflammatory cytokines, and a signal dependent on the adaptors TRAM and TRIF that begins in the endosomes and drives the production of type I interferons. Negative feedback circuits to limit TLR4 signals from both locations are necessary to balance the inflammatory response. We describe a negative feedback loop driven by autocrine–paracrine prostaglandin E2(PGE2) and the PGE2receptor EP4 that restricted TRIF-dependent signals and the induction of interferon-β through the regulation of TLR4 trafficking. Inhibition of PGE2production or antagonism of EP4 increased the rate at which TLR4 translocated to endosomes and amplified TRIF-dependent activation of the transcription factor IRF3 and caspase-8. This PGE2-driven mechanism restricted TLR4–TRIF signaling in vitro after infection of macrophages by the Gram-negative pathogens Escherichia colior Citrobacter rodentiumand protected mice against mortality induced by Salmonella enteritidisserovar Typhimurium. Thus, PGE2restricted TLR4–TRIF signaling specifically in response to lipopolysaccharide.

Published
2018
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26. The Prostaglandin E2-EP3 Receptor Axis Regulates Anaplasma phagocytophilum-Mediated NLRC4 Inflammasome Activation.

Author

Wang, Xiaowei, Shaw, Dana K., Hammond, Holly L., Sutterwala, Fayyaz S., Rayamajhi, Manira, Shirey, Kari Ann, Perkins, Darren J., Bonventre, Joseph V., Velayutham, Thangam S., Evans, Sean M., Rodino, Kyle G., VieBrock, Lauren, Scanlon, Karen M., Carbonetti, Nicholas H., Carlyon, Jason A., Miao, Edward A., McBride, Jere W., Kotsyfakis, Michail, and Pedra, Joao H. F.

Subjects
PROSTAGLANDIN receptors, ANAPLASMA phagocytophilum, INTRACELLULAR membranes, PHOSPHOLIPASES, INFLAMMASOMES
Abstract

Rickettsial agents are sensed by pattern recognition receptors but lack pathogen-associated molecular patterns commonly observed in facultative intracellular bacteria. Due to these molecular features, the order Rickettsiales can be used to uncover broader principles of bacterial immunity. Here, we used the bacterium Anaplasma phagocytophilum, the agent of human granulocytic anaplasmosis, to reveal a novel microbial surveillance system. Mechanistically, we discovered that upon A. phagocytophilum infection, cytosolic phospholipase A2 cleaves arachidonic acid from phospholipids, which is converted to the eicosanoid prostaglandin E2 (PGE2) via cyclooxygenase 2 (COX2) and the membrane associated prostaglandin E synthase-1 (mPGES-1). PGE2-EP3 receptor signaling leads to activation of the NLRC4 inflammasome and secretion of interleukin (IL)-1β and IL-18. Importantly, the receptor-interacting serine/threonine-protein kinase 2 (RIPK2) was identified as a major regulator of the immune response against A. phagocytophilum. Accordingly, mice lacking COX2 were more susceptible to A. phagocytophilum, had a defect in IL-18 secretion and exhibited splenomegaly and damage to the splenic architecture. Remarkably, Salmonella-induced NLRC4 inflammasome activation was not affected by either chemical inhibition or genetic ablation of genes associated with PGE2 biosynthesis and signaling. This divergence in immune circuitry was due to reduced levels of the PGE2-EP3 receptor during Salmonella infection when compared to A. phagocytophilum. Collectively, we reveal the existence of a functionally distinct NLRC4 inflammasome illustrated by the rickettsial agent A. phagocytophilum. [ABSTRACT FROM AUTHOR]

Published
2016
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27. Type I interferon licenses enhanced innate recognition and transcriptional responses to Franciscella tularensislive vaccine strain

Author

Richard, Katharina, Vogel, Stefanie N, and Perkins, Darren J

Abstract

The innate inflammatory response to Francisella tularensis(Ft) in macrophages is significantly governed by the expression of type I interferon (IFN). Previously, the proteolytic processing and maturation of pro-IL-1β protein was shown to depend upon type I IFN expression. We show in this report that paracrine type I IFN can profoundly enhance innate recognition and TLR-dependent transcriptional responses to Ftinfection upstream of its role in inflammasome regulation in both primary human monocyte-derived macrophages and primary murine peritoneal macrophages but not murine bone marrow-derived macrophages. This type I IFN-enhanced response is synergistic with TLR2 transcriptional responses, partially TLR2-independent, but strictly MyD88-dependent.

Published
2016
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28. A mouse model of human TLR4 D299G/T399I SNPs reveals mechanisms of altered LPS and pathogen responses

Author

Richard, Katharina, Piepenbrink, Kurt H., Shirey, Kari Ann, Gopalakrishnan, Archana, Nallar, Shreeram, Prantner, Daniel J., Perkins, Darren J., Lai, Wendy, Vlk, Alexandra, Toshchakov, Vladimir Y., Feng, Chiguang, Fanaroff, Rachel, Medvedev, Andrei E., Blanco, Jorge C.G., and Vogel, Stefanie N.

Abstract

Two cosegregating single-nucleotide polymorphisms (SNPs) in human TLR4, an A896G transition at SNP rs4986790 (D299G) and a C1196T transition at SNP rs4986791 (T399I), have been associated with LPS hyporesponsiveness and differential susceptibility to many infectious or inflammatory diseases. However, many studies failed to confirm these associations, and transfection experiments resulted in conflicting conclusions about the impact of these SNPs on TLR4 signaling. Using advanced protein modeling from crystallographic data of human and murine TLR4, we identified homologous substitutions of these SNPs in murine Tlr4, engineered a knock-in strain expressing the D298G and N397I TLR4 SNPs homozygously, and characterized in vivo and in vitro responses to TLR4 ligands and infections in which TLR4 is implicated. Our data provide new insights into cellular and molecular mechanisms by which these SNPs decrease the TLR4 signaling efficiency and offer an experimental approach to confirm or refute human data possibly confounded by variables unrelated to the direct effects of the SNPs on TLR4 functionality.

Published
2021
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29. Improved Tolerability of a Salmonella entericaSerovar Typhimurium Live-Attenuated Vaccine Strain Achieved by Balancing Inflammatory Potential with Immunogenicity

Author

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

Abstract

A notable proportion of Salmonella-associated gastroenteritis in the United States is attributed to Salmonella entericaserovar Typhimurium. We have previously shown that live-attenuated S.

Published
2018
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30. 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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31. Quantitation of TLR4 Internalization in Response to LPS in Thioglycollate Elicited Peritoneal mouse Macrophages by Flow Cytometry.

Author

Richard K, Vogel SN, and Perkins DJ

Abstract

Internalization of cell surface Toll Like Receptor 4 (TLR4) is a convenient read-out to measure LPS dependent activation of the TRIF adaptor pathway. We here provide a protocol to quantify the LPS dependent internalization of TLR4 using thioglycollate-elicited peritoneal macrophages by flow cytometry.

Published
2019
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