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207 results on '"Hams, Emily"'

1. Itaconate and itaconate derivatives target JAK1 to suppress alternative activation of macrophages

Author

Runtsch, Marah C., Angiari, Stefano, Hooftman, Alexander, Wadhwa, Ridhima, Zhang, Yanling, Zheng, Yunan, Spina, Joseph S., Ruzek, Melanie C., Argiriadi, Maria A., McGettrick, Anne F., Mendez, Rui Santalla, Zotta, Alessia, Peace, Christian G., Walsh, Aoife, Chirillo, Roberta, Hams, Emily, Fallon, Padraic G., Jayaraman, Ranjith, Dua, Kamal, Brown, Alexandra C., Kim, Richard Y., Horvat, Jay C., Hansbro, Philip M., Wang, Chu, and O’Neill, Luke A.J.

Published
2022
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4. Cutting Edge: IL-25 Elicits Innate Lymphoid Type 2 and Type II NKT Cells That Regulate Obesity in Mice

Author

Hams, Emily, Locksley, Richard M, McKenzie, Andrew NJ, and Fallon, Padraic G

Subjects
Biochemistry and Cell Biology, Biomedical and Clinical Sciences, Biological Sciences, Obesity, Nutrition, Diabetes, Prevention, Aetiology, 2.1 Biological and endogenous factors, Cardiovascular, Stroke, Oral and gastrointestinal, Metabolic and endocrine, Adoptive Transfer, Animals, Cell Movement, Glucose, Homeodomain Proteins, Homeostasis, Immunity, Innate, Immunomodulation, Interleukin-13, Interleukins, Intra-Abdominal Fat, Lymphocyte Subsets, Macrophages, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Natural Killer T-Cells, Th2 Cells, Immunology, Biochemistry and cell biology
Abstract

The cellular composition of visceral adipose tissue (VAT) and release of cytokines by such cells within VAT has been implicated in regulating obesity and metabolic homeostasis. We show the importance of IL-25-responsive innate cells, which release the Th2 cytokine IL-13, in regulating weight and glucose homeostasis in mouse models of diet-induced obesity. Treating obese mice with IL-25 induces weight loss and improves glucose tolerance, and is associated with increased infiltration of innate lymphoid type 2 cells (ILC2), type I and type II NKT cells, eosinophils, and alternatively activated macrophages into the VAT. By depleting ILC2 in obese Rag1(-/-) mice, we observe exacerbated weight gain and glucose intolerance. Conversely, transferring ILC2 or type I or type II NKT cells into obese mice induces transient weight loss and stabilizes glucose homeostasis. Our data identify a mechanism whereby IL-25 eliciting IL-13-producing innate cells regulates inflammation in adipose tissue and prevents diet-induced obesity.

Published
2013

7. Regulation of acute inflamation by oncostatin M receptor-beta

Author

Hams, Emily

Subjects
616
Abstract

Although the interleukin (IL)-6 related cytokine Oncostatin M (OSM) affects a variety of inflammatory events associated with disease progression, the function of OSM in the face of an inflammatory challenge remains unclear. In this thesis a peritoneal model of inflammation, in association with in vitro studies using human primary cell lines, has been used to define the influence of OSM on chemokine-mediated leukocyte recruitment. When compared to wild type mice (WT) the induction of peritoneal inflammation in Oncostatin M receptor-beta deficient mice (OSMR-KO) resulted in enhanced monocytic cell trafficking, with no differences in neutrophil or lymphocyte recruitment observed, suggesting that OSM control of leukocyte recruitment is functionally distinct from that of IL-6. Subsequent in vitro studies and an in vivo appraisal of inflammatory chemokine expression following peritoneal inflammation inferred that OSM regulation of CCL5 might account for the observed difference in monocytic cell trafficking. The OSM-mediated control of CCL5 is clearly distinct from the actions of IL-6, which acts as a more prominent in vivo regulator of CCL2 expression than OSM. Mechanistically, these studies inferred a hitherto unidentified interplay between OSM-mediated STAT signalling and NF-kappaB activation. In this respect, EMSA analysis of nuclear extracts from peritoneal membranes isolated during course of the inflammatory response showed that OSMR-KO mice display an enhanced profile of NF-kappaB activation as compared to WT mice. Initial in vivo appraisal of the role of OSMRg-mediated signalling in repeated episodes of inflammation and associated tissue damage suggest that OSM continues to regulate monocytic cell trafficking throughout recurrent inflammatory episodes and does not play a significant role in inflammation-associated peritoneal tissue damage, again a finding clearly distinct from the observed effects of IL-6 in tissue injury. These findings suggest that activation of gp 130 by IL-6 and OSM trigger distinct inflammatory responses to affect individual aspects of leukocyte trafficking.

Published
2008

13. Discovery and multi-parametric optimization of a high-affinity antibody against interleukin-25 with neutralizing activity in a mouse model of skin inflammation

Author

Bone, Ruth, primary, Fennell, Brian J, additional, Tam, Amy, additional, Sheldon, Richard, additional, Nocka, Karl, additional, Varghese, Sreeja, additional, Chang, Chew Shun, additional, Hawerkamp, Heike C, additional, Yeow, Aoife, additional, Saunders, Sean P, additional, Hams, Emily, additional, Walsh, Patrick T, additional, Cunningham, Orla, additional, and Fallon, Padraic G, additional

Published
2022
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14. IL-25 and type 2 innate lymphoid cells induce pulmonary fibrosis

Author

Hams, Emily, Armstrong, Michelle E., Barlow, Jillian L., Saunders, Sean P., Schwartz, Christian, Cooke, Gordon, Fahy, Ruairi J., Crotty, Thomas B., Hirani, Nikhil, Flynn, Robin J., Voehringer, David, McKenzie, Andrew N. J., Donnelly, Seamas C., and Fallon, Padraic G.

Published
2014

17. Innate PD-L1 limits T cell–mediated adipose tissue inflammation and ameliorates diet-induced obesity

Author

Schwartz, Christian, primary, Schmidt, Viviane, additional, Deinzer, Andrea, additional, Hawerkamp, Heike C., additional, Hams, Emily, additional, Bayerlein, Jasmin, additional, Röger, Ole, additional, Bailer, Moritz, additional, Krautz, Christian, additional, El Gendy, Amr, additional, Elshafei, Moustafa, additional, Heneghan, Helen M., additional, Hogan, Andrew E., additional, O’Shea, Donal, additional, and Fallon, Padraic G., additional

Published
2022
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19. Itaconate is an anti-inflammatory metabolite that activates Nrf2 via alkylation of KEAP1

Author

Mills, Evanna L., Ryan, Dylan G., Prag, Hiran A., Dikovskaya, Dina, Menon, Deepthi, Zaslona, Zbigniew, Jedrychowski, Mark P., Costa, Ana S. H., Higgins, Maureen, Hams, Emily, Szpyt, John, Runtsch, Marah C., King, Martin S., McGouran, Joanna F., Fischer, Roman, Kessler, Benedikt M., McGettrick, Anne F., Hughes, Mark M., Carroll, Richard G., Booty, Lee M., Knatko, Elena V., Meakin, Paul J., Ashford, Michael L. J., Modis, Louise K., Brunori, Gino, Svin, Daniel C., Fallon, Padraic G., Caldwell, Stuart T., Kunji, Edmund R. S., Chouchani, Edward T., Frezza, Christian, Dinkova-Kostova, Albena T., Hartley, Richard C., Murphy, Michael P., and ONeill, Luke A.

Subjects
Metabolites -- Research, Physiological research, Activation analysis, Leucine zipper -- Research, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Author(s): Evanna L. Mills [1, 2, 3, 4]; Dylan G. Ryan [1]; Hiran A. Prag [5]; Dina Dikovskaya [6]; Deepthi Menon [1]; Zbigniew Zaslona [1]; Mark P. Jedrychowski [2, 3]; [...]

Published
2018
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22. Interleukin-6 Signaling Drives Fibrosis in Unresolved Inflammation

Author

Fielding, Ceri A., Jones, Gareth W., McLoughlin, Rachel M., McLeod, Louise, Hammond, Victoria J., Uceda, Javier, Williams, Anwen S., Lambie, Mark, Foster, Thomas L., Liao, Chia-Te, Rice, Christopher M., Greenhill, Claire J., Colmont, Chantal S., Hams, Emily, Coles, Barbara, Kift-Morgan, Ann, Newton, Zarabeth, Craig, Katherine J., Williams, John D., Williams, Geraint T., Davies, Simon J., Humphreys, Ian R., OʼDonnell, Valerie B., Taylor, Philip R., Jenkins, Brendan J., Topley, Nicholas, and Jones, Simon A.

Published
2014
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30. Cell Survival and Cytokine Release after Inflammasome Activation Is Regulated by the Toll-IL-1R Protein SARM

Author

Carty, Michael, primary, Kearney, Jay, additional, Shanahan, Katharine A., additional, Hams, Emily, additional, Sugisawa, Ryoichi, additional, Connolly, Dympna, additional, Doran, Ciara G., additional, Muñoz-Wolf, Natalia, additional, Gürtler, Claudia, additional, Fitzgerald, Katherine A., additional, Lavelle, Ed C., additional, Fallon, Padraic G., additional, and Bowie, Andrew G., additional

Published
2019
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31. Interleukin-17 receptor A maintains and protects the skin barrier to prevent allergic skin inflammation1

Author

Floudas, Achilleas, Saunders, Sean P., Moran, Tara, Schwartz, Christian, Hams, Emily, Fitzgerald, Denise C., Johnston, James A., Ogg, Graham S., McKenzie, Andrew N., Walsh, Patrick T., and Fallon, Padraic G.

Subjects
Receptors, Interleukin-17, integumentary system, Interleukins, Microbiota, Receptors, Antigen, T-Cell, gamma-delta, Filaggrin Proteins, Interleukin-33, Article, Dermatitis, Atopic, Disease Models, Animal, Mice, Th2 Cells, Gene Expression Regulation, Intermediate Filament Proteins, Thymic Stromal Lymphopoietin, Eosinophilia, Mutation, Animals, Cytokines, Dysbiosis, Homeostasis, Interleukin-5, Signal Transduction, Skin
Abstract

Atopic dermatitis (AD) is a common inflammatory skin disease affecting up to 20% of children and 3% of adults worldwide and is associated with dysregulation of the skin barrier. While type 2 responses are implicated in AD, emerging evidence indicates potential role for the IL-17A signalling axis in AD pathogenesis. In this study we show that in the filaggrin mutant mouse model of spontaneous AD, IL-17RA deficiency (Il17ra-/-) resulted in severe exacerbation of skin inflammation. Interestingly, Il17ra-/- mice without the filaggrin mutation also developed spontaneous progressive skin inflammation with eosinophilia, increased levels of thymic stromal lymphopoietin (TSLP) and IL-5 in the skin. Il17ra-/- mice have a defective skin barrier with altered filaggrin expression. The barrier dysregulation and spontaneous skin inflammation in Il17ra-/- mice was dependent on TSLP, but not the other alarmins IL-25 and IL-33. The associated skin inflammation was mediated by IL-5 expressing pathogenic effector (pe) Th2 cells and was independent of TCRγδ T cells and IL-22. An absence of IL-17RA in non-hematopoietic cells, but not in the hematopoietic cells, was required for the development of spontaneous skin inflammation. Skin microbiome dysbiosis developed in the absence of IL-17RA, with antibiotic intervention resulting in significant amelioration of skin inflammation and reductions in skin infiltrating peTh2 cells and TSLP. This study describes a previously unappreciated protective role for IL-17RA signalling in regulation of the skin barrier and maintenance of skin immune homeostasis.

Published
2017

35. Perinatal Activation of the Interleukin-33 Pathway Promotes Type 2 Immunity in the Developing Lung

Author

de Kleer, Ismé M., primary, Kool, Mirjam, additional, de Bruijn, Marjolein J.W., additional, Willart, Monique, additional, van Moorleghem, Justine, additional, Schuijs, Martijn J., additional, Plantinga, Maud, additional, Beyaert, Rudi, additional, Hams, Emily, additional, Fallon, Padraic G., additional, Hammad, Hamida, additional, Hendriks, Rudi W., additional, and Lambrecht, Bart N., additional

Published
2016
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36. The PDGF-BB-SOX7 axis-modulated IL-33 in pericytes and stromal cells promotes metastasis through tumour-associated macrophages

Author

Yang, Yunlong, primary, Andersson, Patrik, additional, Hosaka, Kayoko, additional, Zhang, Yin, additional, Cao, Renhai, additional, Iwamoto, Hideki, additional, Yang, Xiaojuan, additional, Nakamura, Masaki, additional, Wang, Jian, additional, Zhuang, Rujie, additional, Morikawa, Hiromasa, additional, Xue, Yuan, additional, Braun, Harald, additional, Beyaert, Rudi, additional, Samani, Nilesh, additional, Nakae, Susumu, additional, Hams, Emily, additional, Dissing, Steen, additional, Fallon, Padraic G., additional, Langer, Robert, additional, and Cao, Yihai, additional

Published
2016
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39. Cutting Edge: Suppression of GM-CSF Expression in Murine and Human T Cells by IL-27:suppression of GM-CSF expression in murine and human T cells by IL-27

Author

Young, Andrew, Linehan, Eimear, Hams, Emily, O'Hara Hall, Aisling C., McClurg, Angela, Johnston, James A., Hunter, Christopher A., Fallon, Padraig G., and Fitzgerald, Denise C.

Subjects
SDG 3 - Good Health and Well-being, Immunology
Abstract

GM-CSF is a potent proinflammatory cytokine that plays a pathogenic role in the CNS inflammatory disease experimental autoimmune encephalomyelitis. As IL-27 alleviates experimental autoimmune encephalomyelitis, we hypothesized that IL-27 suppresses GM-CSF expression by T cells. We found that IL-27 suppressed GM-CSF expression in CD4+ and CD8+ T cells in splenocyte and purified T cell cultures. IL-27 suppressed GM-CSF in Th1, but not Th17, cells. IL-27 also suppressed GM-CSF expression by human T cells in nonpolarized and Th1- but not Th17-polarized PBMC cultures. In vivo, IL-27p28 deficiency resulted in increased GM-CSF expression by CNS-infiltrating T cells during Toxoplasma gondii infection. Although in vitro suppression of GM-CSF by IL-27 was independent of IL-2 suppression, IL-10 upregulation, or SOCS3 signaling, we observed that IL-27-driven suppression of GM-CSF was STAT1 dependent. Our findings demonstrate that IL-27 is a robust negative regulator of GM-CSF expression in T cells, which likely inhibits T cell pathogenicity in CNS inflammation.

Published
2012

40. Suppression of GM-CSF expression in murine and human T cells by IL-27

Author

Young, Andrew, Linehan, Eimear, Hams, Emily, O’Hara Hall, Aisling C., McClurg, Angela, Johnston, James A., Hunter, Christopher A., Fallon, Padraic G., and Fitzgerald, Denise C.

Subjects
Mice, Knockout, Interleukin-17, Cell Polarity, Granulocyte-Macrophage Colony-Stimulating Factor, Mice, Transgenic, Lymphocyte Activation, Article, Mice, Inbred C57BL, Mice, T-Lymphocyte Subsets, Immune Tolerance, Animals, Humans, Inflammation Mediators, Cells, Cultured, Toxoplasmosis
Abstract

GM-CSF is a potent proinflammatory cytokine that plays a pathogenic role in the CNS inflammatory disease experimental autoimmune encephalomyelitis. As IL-27 alleviates experimental autoimmune encephalomyelitis, we hypothesized that IL-27 suppresses GM-CSF expression by T cells. We found that IL-27 suppressed GM-CSF expression in CD4+ and CD8+ T cells in splenocyte and purified T cell cultures. IL-27 suppressed GM-CSF in Th1, but not Th17, cells. IL-27 also suppressed GM-CSF expression by human T cells in nonpolarized and Th1- but not Th17-polarized PBMC cultures. In vivo, IL-27p28 deficiency resulted in increased GM-CSF expression by CNS-infiltrating T cells during Toxoplasma gondii infection. Although in vitro suppression of GM-CSF by IL-27 was independent of IL-2 suppression, IL-10 upregulation, or SOCS3 signaling, we observed that IL-27-driven suppression of GM-CSF was STAT1 dependent. Our findings demonstrate that IL-27 is a robust negative regulator of GM-CSF expression in T cells, which likely inhibits T cell pathogenicity in CNS inflammation.

Published
2012

41. Interleukin-6 signaling drives fibrosis in unresolved inflammation

Author

Fielding, Ceri A., Jones, Gareth W., McLoughlin, Rachel M., McLeod, Louise, Hammond, Victoria J., Uceda, Javier, Williams, Anwen S., Lambie, Mark, Foster, Thomas L., Liao, Chia-Te, Rice, Christopher M., Greenhill, Claire J., Colmont, Chantal S., Hams, Emily, Coles, Barbara, Kift-Morgan, Ann, Newton, Zarabeth, Craig, Katherine J., Williams, John D., Williams, Geraint T., Davies, Simon J., Humphreys, Ian R., O’Donnell, Valerie B., Taylor, Philip R., Jenkins, Brendan J., Topley, Nicholas, and Jones, Simon A.

Subjects
Feedback, Physiological, Mice, Knockout, Interleukin-6, Immunology, Peritonitis, Th1 Cells, R1, Adoptive Transfer, Fibrosis, Article, Extracellular Matrix, Mice, Inbred C57BL, Disease Models, Animal, Interferon-gamma, Mice, Infectious Diseases, STAT1 Transcription Factor, Acute Disease, Chronic Disease, Immunology and Allergy, Animals, Humans, Peritoneum, Cells, Cultured, Signal Transduction
Abstract

Summary Fibrosis in response to tissue damage or persistent inflammation is a pathological hallmark of many chronic degenerative diseases. By using a model of acute peritoneal inflammation, we have examined how repeated inflammatory activation promotes fibrotic tissue injury. In this context, fibrosis was strictly dependent on interleukin-6 (IL-6). Repeat inflammation induced IL-6-mediated T helper 1 (Th1) cell effector commitment and the emergence of STAT1 (signal transducer and activator of transcription-1) activity within the peritoneal membrane. Fibrosis was not observed in mice lacking interferon-γ (IFN-γ), STAT1, or RAG-1. Here, IFN-γ and STAT1 signaling disrupted the turnover of extracellular matrix by metalloproteases. Whereas IL-6-deficient mice resisted fibrosis, transfer of polarized Th1 cells or inhibition of MMP activity reversed this outcome. Thus, IL-6 causes compromised tissue repair by shifting acute inflammation into a more chronic profibrotic state through induction of Th1 cell responses as a consequence of recurrent inflammation., Highlights • Repeated acute resolving inflammation leads to excessive tissue damage • IL-6 regulates profibrotic IFN-γ-secreting T cells • IFN-γ increases detrimental STAT1 signaling in stromal tissue • STAT1 activity alters homeostatic control of extracellular matrix to promote fibrosis

Published
2012

42. The hydroxylase inhibitor DMOG attenuates endotoxic shock via alternative activation of macrophages and IL-10 production by B-1 cells

Author

Hams, Emily, Saunders, Sean P., Cummins, Eoin P., O'Connor, Aisling, Tambuwala, Murtaza T., Gallagher, William M., Byrne, Annette, Compos-Torres, Antonio, Moynagh, Paul N., Jobin, Christian, Taylor, Cormac T, and Fallon, Padraic G.

Abstract

Localized tissue hypoxia is a feature of infection and inflammation, resulting in the upregulation of the transcription factors HIF-1α and NF-κB via inhibition of oxygen sensing hydroxylase enzymes. Previous studies have demonstrated a beneficial role for the hydroxylase inhibitor dimethyloxallyl glycine (DMOG) in inflammatory conditions, including experimental colitis, by regulating the activity of HIF-1 and NF-κB. We have demonstrated in vivo that pre-treatment with DMOG attenuates systemic LPS-induced activation of the NF- κB pathway. Furthermore, mice treated with DMOG had significantly increased survival in LPS-induced shock. Conversely, in models of polymicrobial sepsis, DMOG exacerbates disease severity. DMOG treatment of mice promotes M2 polarization in macrophages within the peritoneal cavity, resulting in the downregulation of pro-inflammatory cytokines such as TNF α. In addition, in vivo DMOG treatment upregulates IL-10 expression, specifically in the peritoneal B-1 cell population. This study demonstrates cell type specific roles for hydroxylase inhibition in vivo and provides insight into the mechanism underlying the protection conveyed by DMOG in models of endotoxic shock.

Published
2011

43. Targeting Siglecs with a sialic acid–decorated nanoparticle abrogates inflammation

Author

Spence, Shaun, primary, Greene, Michelle K., additional, Fay, François, additional, Hams, Emily, additional, Saunders, Sean P., additional, Hamid, Umar, additional, Fitzgerald, Marianne, additional, Beck, Jonathan, additional, Bains, Baljinder K., additional, Smyth, Peter, additional, Themistou, Efrosyni, additional, Small, Donna M., additional, Schmid, Daniela, additional, O’Kane, Cecilia M., additional, Fitzgerald, Denise C., additional, Abdelghany, Sharif M., additional, Johnston, James A., additional, Fallon, Padraic G., additional, Burrows, James F., additional, McAuley, Daniel F., additional, Kissenpfennig, Adrien, additional, and Scott, Christopher J., additional

Published
2015
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46. 96

Author

Khan, Adnan R., primary, Hams, Emily, additional, Sparwasser, Tim, additional, Weaver, Casey T., additional, and Fallon, Padraic G., additional

Published
2014
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47. IL-18 Attenuates Experimental Choroidal Neovascularization as a Potential Therapy for Wet Age-Related Macular Degeneration

Author

Doyle, Sarah L., primary, Ozaki, Ema, additional, Brennan, Kiva, additional, Humphries, Marian M., additional, Mulfaul, Kelly, additional, Keaney, James, additional, Kenna, Paul F., additional, Maminishkis, Arvydas, additional, Kiang, Anna-Sophia, additional, Saunders, Sean P., additional, Hams, Emily, additional, Lavelle, Ed C., additional, Gardiner, Clair, additional, Fallon, Padraic G., additional, Adamson, Peter, additional, Humphries, Peter, additional, and Campbell, Matthew, additional

Published
2014
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48. Btk Regulates Macrophage Polarization in Response to Lipopolysaccharide

Author

Ní Gabhann, Joan, primary, Hams, Emily, additional, Smith, Siobhán, additional, Wynne, Claire, additional, Byrne, Jennifer C., additional, Brennan, Kiva, additional, Spence, Shaun, additional, Kissenpfennig, Adrien, additional, Johnston, James A., additional, Fallon, Padraic G., additional, and Jefferies, Caroline A., additional

Published
2014
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49. IL-25 and type 2 innate lymphoid cells induce pulmonary fibrosis

Author

Hams, Emily, primary, Armstrong, Michelle E., additional, Barlow, Jillian L., additional, Saunders, Sean P., additional, Schwartz, Christian, additional, Cooke, Gordon, additional, Fahy, Ruairi J., additional, Crotty, Thomas B., additional, Hirani, Nikhil, additional, Flynn, Robin J., additional, Voehringer, David, additional, McKenzie, Andrew N. J., additional, Donnelly, Seamas C., additional, and Fallon, Padraic G., additional

Published
2013
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50. 190

Author

Oliphant, Christopher J., primary, Wong, See Heng, additional, Walker, Jennifer A., additional, Hwang, You Yi, additional, Barlow, Jillian L., additional, Hams, Emily, additional, Fallon, Padraic G., additional, and McKenzie, Andrew N.J., additional

Published
2013
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