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Your search keyword '"Thomas, Andrew M."' showing total 7 results
Start Over Author "Thomas, Andrew M." Publisher biomed central
7 results on '"Thomas, Andrew M."'

1. Total serum N-glycans associate with response to immune checkpoint inhibition therapy and survival in patients with advanced melanoma

Author

Visconti, Alessia, Rossi, Niccolò, Deriš, Helena, Lee, Karla A, Hanić, Maja, Trbojević-Akmačić, Irena, Thomas, Andrew M., Bolte, Laura A., Björk, Johannes R., Hooiveld-Noeken, Jahlisa S., Board, Ruth, Harland, Mark, Newton-Bishop, Julia, Harries, Mark, Sacco, Joseph J., Lorigan, Paul, Shaw, Heather M., de Vries, Elisabeth G.E., Fehrmann, Rudolf S.N., Weersma, Rinse K., Spector, Tim D., Nathan, Paul, Hospers, Geke A. P., Sasieni, Peter, Bataille, Veronique, Lauc, Gordan, and Falchi, Mario

Published
2023
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2. A probiotic has differential effects on allergic airway inflammation in A/J and C57BL/6 mice and is correlated with the gut microbiome

Author

Casaro, Mateus B., Thomas, Andrew M., Mendes, Eduardo, Fukumori, Claudio, Ribeiro, Willian R., Oliveira, Fernando A., Crisma, Amanda R., Murata, Gilson M., Bizzarro, Bruna, Sá-Nunes, Anderson, Setubal, Joao C., Mayer, Marcia P. A., Martins, Flaviano S., Vieira, Angélica T., Antiorio, Ana T. F. B., Tavares-de-Lima, Wothan, Camara, Niels O. S., Curi, Rui, Dias-Neto, Emmanuel, and Ferreira, Caroline M.

Published
2021
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3. Correction to: A probiotic has differential effects on allergic airway inflammation in A/J and C57BL/6 mice and is correlated with the gut microbiome

Author

Casaro, Mateus B., Thomas, Andrew M., Mendes, Eduardo, Fukumori, Claudio, Ribeiro, Willian R., Oliveira, Fernando A., Crisma, Amanda R., Murata, Gilson M., Bizzarro, Bruna, Sá-Nunes, Anderson, Setubal, Joao C., Mayer, Marcia P. A., Martins, Flaviano S., Vieira, Angélica T., Antiorio, Ana T. F. B., Tavares-de-Lima, Wothan, Camara, Niels O. S., Curi, Rui, Dias-Neto, Emmanuel, and Ferreira, Caroline M.

Published
2021
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4. Priming in response to pro-inflammatory cytokines is a feature of adult synovial but not dermal fibroblasts

Author

Crowley, Thomas, O'Neil, John D., Adams, Holly, Thomas, Andrew M., Filer, Andrew, Buckley, Christopher D., and Clark, Andrew R.

Subjects
Inflammation, musculoskeletal diseases, Interleukin-6, Blotting, Western, Synovial Membrane, NF-kappa B, Fluorescent Antibody Technique, Enzyme-Linked Immunosorbent Assay, Stromal memory, Fibroblasts, Synoviocytes, NF-κB, Arthritis, Rheumatoid, Fibroblast, Cytokines, Humans, Rheumatoid arthritis, Cytokine, Cells, Cultured, Research Article, Skin
Abstract

Background It has been hypothesized that chronic inflammatory diseases such as rheumatoid arthritis (RA) may be caused by a failure of negative feedback mechanisms. This study sought to examine negative feedback mechanisms in fibroblast-like synoviocytes (FLS), one of the most abundant cell types in the joint. We hypothesized that prior exposure of healthy FLS to an inflammatory stimulus would attenuate their responses to a second inflammatory stimulus, in the same way that negative feedback mechanisms desensitize macrophages to repeated stimulation by lipopolysaccharide. We further hypothesized that such negative feedback mechanisms would be defective in FLS derived from the joints in RA. Methods Synovial fibroblasts and dermal fibroblasts from non-inflamed joints and joints affected by RA and a fibroblast cell line from neonatal foreskin were stimulated twice with tumour necrosis factor (TNF) α or interleukin (IL)-1α, with a 24-h rest period between the two 24-h stimulations. Differences between response to the first and second dose of cytokine were examined by assessing secretion of inflammatory factors and intracellular signalling activity. Results FLS from both non-inflamed joints and joints affected by RA mounted an augmented response to re-stimulation. This response was site-specific, as primary dermal fibroblasts did not alter their response between doses. The fibroblast priming was also gene-specific and transient. Assessment of signalling events and nuclear localization showed prolonged activation of nuclear factor (NF)-κB during the second stimulation. Conclusion This study aimed to examine mechanisms of negative regulation of inflammatory responses in FLS. Instead, we found a pro-inflammatory stromal memory in FLS obtained from both non-inflamed joints and joints affected by RA. This suggests the joint is an area at high risk of chronic inflammation, and may provide a piece in the puzzle of how chronic inflammation is established in RA. Electronic supplementary material The online version of this article (doi:10.1186/s13075-017-1248-6) contains supplementary material, which is available to authorized users.

Published
2018

6. Genomics and epidemiology for gastric adenocarcinomas (GE4GAC): a Brazilian initiative to study gastric cancer.

Author

Bartelli, Thais F., Senda de Abrantes, Lais L., Freitas, Helano C., Thomas, Andrew M., Silva, Jordana M., Albuquerque, Gabriela E., Araújo, Luiza F., Branco, Gabriela P., de Amorim, Maria G., Serpa, Marianna S., Takenaka, Isabella K. T. M., Souza, Deborah T., Monção, Lucas O., Moda, Bruno S., Valieris, Renan, Defelicibus, Alexandre, Borges, Rodrigo, Drummond, Rodrigo D., Alves, Francisco I. A., and Santos, Monize N. P.

Published
2019
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7. Rheumatoid synovial fluid interleukin-17-producing CD4 T cells have abundant tumor necrosis factor-alpha co-expression, but little interleukin-22 and interleukin-23R expression.

Author

Church LD, Filer AD, Hidalgo E, Howlett KA, Thomas AM, Rapecki S, Scheel-Toellner D, Buckley CD, and Raza K

Subjects
Arthritis, Rheumatoid metabolism, Cell Separation, Female, Flow Cytometry, Humans, Interleukins biosynthesis, Male, Middle Aged, Receptors, Interleukin biosynthesis, Synovial Fluid chemistry, Synovial Fluid metabolism, Th17 Cells metabolism, Interleukin-22, Arthritis, Rheumatoid immunology, Interleukin-17 biosynthesis, Synovial Fluid immunology, Th17 Cells immunology, Tumor Necrosis Factor-alpha biosynthesis
Abstract

Introduction: Th17 cells have been implicated in the pathogenesis of rheumatoid arthritis (RA). The aim of this study was to systematically analyse the phenotype, cytokine profile and frequency of interleukin-17 (IL-17) producing CD4-positive T cells in mononuclear cells isolated from peripheral blood, synovial fluid and synovial tissue of RA patients with established disease, and to correlate cell frequencies with disease activity., Methods: Flow cytometry was used to analyse the phenotype and cytokine production of mononuclear cells isolated from peripheral blood (PBMC) (n = 44), synovial fluid (SFMC) (n = 14) and synovium (SVMC) (n = 10) of RA patients and PBMC of healthy controls (n = 13)., Results: The frequency of IL-17-producing CD4 T cells was elevated in RA SFMC compared with RA PBMC (P = 0.04). However, the frequency of this population in RA SVMC was comparable to that in paired RA PBMC. The percentage of IL-17-producing CD4 T cells coexpressing tumor necrosis factor alpha (TNFα) was significantly increased in SFMC (P = 0.0068). The frequency of IFNγ-producing CD4 T cells was also significantly higher in SFMC than paired PBMC (P = 0.042). The majority of IL-17-producing CD4 T cells coexpressed IFNγ. IL-17-producing CD4 T cells in RA PBMC and SFMC exhibited very little IL-22 or IL-23R coexpression., Conclusions: These findings demonstrate a modest enrichment of IL-17-producing CD4 T cells in RA SFMC compared to PBMC. Th17 cells in SFMC produce more TNFα than their PBMC counterparts, but are not a significant source of IL-22 and do not express IL-23R. However, the percentage of CD4 T cells which produce IL-17 in the rheumatoid joint is low, suggesting that other cells may be alternative sources of IL-17 within the joints of RA patients.

Published
2010
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