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Your search keyword '"Kullberg, Bart-Jan"' showing total 8 results
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8 results on '"Kullberg, Bart-Jan"'

1. Cost-effectiveness of longer-term versus shorter-term provision of antibiotics in patients with persistent symptoms attributed to Lyme disease

Author

Berende, Anneleen, primary, Nieuwenhuis, Lisette, additional, ter Hofstede, Hadewych J. M., additional, Vos, Fidel J., additional, Vogelaar, Michiel L., additional, Tromp, Mirjam, additional, van Middendorp, Henriët, additional, Donders, A. Rogier T., additional, Evers, Andrea W. M., additional, Kullberg, Bart Jan, additional, and Adang, Eddy M. M., additional

Published
2018
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2. An integrative genomics approach identifies novel pathways that influence candidaemia susceptibility

Author

Matzaraki, Vasiliki, primary, Gresnigt, Mark S., additional, Jaeger, Martin, additional, Ricaño-Ponce, Isis, additional, Johnson, Melissa D., additional, Oosting, Marije, additional, Franke, Lude, additional, Withoff, Sebo, additional, Perfect, John R., additional, Joosten, Leo A. B., additional, Kullberg, Bart Jan, additional, van de Veerdonk, Frank L., additional, Jonkers, Iris, additional, Li, Yang, additional, Wijmenga, Cisca, additional, Netea, Mihai G., additional, and Kumar, Vinod, additional

Published
2017
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3. Voriconazole or Amphotericin B as Primary Therapy Yields Distinct Early Serum Galactomannan Trends Related to Outcomes in Invasive Aspergillosis

Author

Chai, Louis Yi Ann, primary, Kullberg, Bart Jan, additional, Earnest, Arul, additional, Johnson, Elizabeth M., additional, Teerenstra, Steven, additional, Vonk, Alieke G., additional, Schlamm, Haran T., additional, Herbrecht, Raoul, additional, Netea, Mihai G., additional, and Troke, Peter F., additional

Published
2014
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4. STAT1 Hyperphosphorylation and Defective IL12R/IL23R Signaling Underlie Defective Immunity in Autosomal Dominant Chronic Mucocutaneous Candidiasis

Author

Smeekens, Sanne P., primary, Plantinga, Theo S., additional, van de Veerdonk, Frank L., additional, Heinhuis, Bas, additional, Hoischen, Alexander, additional, Joosten, Leo A. B., additional, Arkwright, Peter D., additional, Gennery, Andrew, additional, Kullberg, Bart Jan, additional, Veltman, Joris A., additional, Lilic, Desa, additional, van der Meer, Jos W. M., additional, and Netea, Mihai G., additional

Published
2011
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8. Inflammasome-Independent Modulation of Cytokine Response by Autophagy in Human Cells.

Author

Crişn, Tania O., Plantinga, Theo S., van de Veerdonk, Frank L., Farcaş, Marius F., Stoffels, Monique, Kullberg, Bart-Jan, van der Meer, Jos W. M., Joosten, Leo A. B., and Netea, Mihai G.

Subjects
HUMAN cell culture, IMMUNOREGULATION, MOLECULAR immunology, CROHN'S disease, MACROPHAGES, PROTEIN kinases, PHOSPHORYLATION, LIGANDS (Biochemistry), CYTOKINES
Abstract

Autophagy is a cell housekeeping mechanism that has recently received attention in relation to its effects on the immune response. Genetic studies have identified candidate loci for Crohn's disease susceptibility among autophagy genes, while experiments in murine macrophages from ATG16L1 deficient mice have shown that disruption of autophagy increases processing of IL-1β and IL-18 through an inflammasome-dependent manner. Using complementary approaches either inducing or inhibiting autophagy, we describe modulatory effects of autophagy on proinflammatory cytokine production in human cells. Inhibition of basal autophagy in human peripheral blood mononuclear cells (PBMCs) significantly enhances IL- 1β after stimulation with TLR2 or TLR4 ligands, while at the same time reducing the production of TNFα. In line with this, induction of autophagy by starvation inhibited IL-1β production. These effects of autophagy were not exerted at the processing step, as inflammasome activation was not influenced. In contrast, the effect of autophagy on cytokine production was on transcription level, and possibly involving the inhibition of p38 mitogen activated protein kinase (MAPK) phosphorylation. In conclusion, autophagy modulates the secretion of proinflammatory cytokines in human cells through an inflammasome-independent pathway, and this is a novel mechanism that may be targeted in inflammatory diseases. [ABSTRACT FROM AUTHOR]

Published
2011
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