@article{mbs:/content/journal/jmm/10.1099/jmm.0.003293-0, author = "Loeffler, Juergen and Haddad, Ziad and Bonin, Michael and Romeike, Nele and Mezger, Markus and Schumacher, Ulrike and Kapp, Markus and Gebhardt, Florian and Grigoleit, Goetz-Ulrich and Stevanović, Stefan and Einsele, Hermann and Hebart, Holger", title = "Interaction analyses of human monocytes co-cultured with different forms of Aspergillus fumigatus", journal= "Journal of Medical Microbiology", year = "2009", volume = "58", number = "1", pages = "49-58", doi = "https://doi.org/10.1099/jmm.0.003293-0", url = "https://www.microbiologyresearch.org/content/journal/jmm/10.1099/jmm.0.003293-0", publisher = "Microbiology Society", issn = "1473-5644", type = "Journal Article", keywords = "SLR, signal log2 ratio", keywords = "IA, invasive aspergillosis", keywords = "IL, interleukin", keywords = "TLR, Toll-like receptor", keywords = "TNF, tumour necrosis factor", abstract = "Monocytes play a major role in the cellular defence against Aspergillus fumigatus in immunocompromised patients. To obtain a better understanding of the mechanisms involved in this interaction, phagocytosis and gene expression profiling of human monocytes was carried out after incubation with A. fumigatus resting, swollen and germinating conidia and hyphae (for 3, 6 and 9 h). The majority of monocytes phagocytosed up to three conidia during the first 3 h of incubation. Microarray analysis showed an increased expression level of immune-relevant genes, which was dependent on the germination state of the fungus and the incubation period. Among these genes, those encoding interleukin-8, macrophage inflammatory protein 3-α (CCL20) and monocyte chemotactic protein-1 (CCL2) were found to be potential key regulators involved in the A. fumigatus-induced immune response. In addition, A. fumigatus was found to be an inducer of the genes encoding urokinase type plasminogen activator (uPA), urokinase type plasminogen activator receptor (uPAR),plasminogen activator inhibitor (PAI), pentraxin-3 (PTX3) and intercellular adhesion molecule-1 (ICAM-1), which, in combination, may contribute to thrombosis and local lung tissue injury.", }