title: Early transcriptional response of human monocyte-like THP-1 cells in response to Trichosporon asahii infection.
abstract: Trichosporon asahii is the major cause of invasive trichosporonosis, but little is known about the host immune response to this pathogen. In this study, the early transcriptional response of human monocyte-like THP-1 cells to T. asahii infection was evaluated using cDNA microarray and 1,315 differentially expressed genes were identified. The up-regulated genes were mostly involved in both innate and adaptive immune responses, as well as apoptosis and anti-apoptosis processes. Genes encoding the pro-inflammatory cytokines TNF-α, IL-1β, IL18 and IL-23α, along with the both C-C motif and C-X-C motif chemokines were strongly up-regulated, suggesting that THP-1 cells can mount a powerful inflammatory response to T. asahii infection. Genes encoding pattern recognition receptors were found up-regulated, such as dendritic cell-specific intercellular adhesion molecule 3-grabbing nonintegrin, cluster of differentiation 36 and the long pentraxin 3. Genes encoding members of the dual-spasticity phosphates family were up-regulated, and these genes were considered as a negative feedback mechanism to prevent excessive inflammatory response. The down-regulated genes in T. asahii-infected THP-1 cells were predominantly associated with cell cycle, mitosis, cell division and DNA repair. Thus, our study defines the early transcriptional response of monocyte-like THP-1 cells to T. asahii infection and provides a foundation for further investigations into the pathogenesis of T. asahii infection.
authors.affiliation: Department of Dermatology, General Hospital of Beijing Military Command, 5 Nanmencang, Dongcheng District, Beijing, 100700, China.
authors.forename: Lin
authors.initials: L
authors.lastname: Cong
authors.forename: Yong
authors.initials: Y
authors.lastname: Liao
authors.forename: Xuelian
authors.initials: X
authors.lastname: Lu
authors.forename: Zhikuan
authors.initials: Z
authors.lastname: Xia
authors.forename: Haitao
authors.initials: H
authors.lastname: Li
authors.forename: Rongya
authors.initials: R
authors.lastname: Yang
mesh_terms: D015703:Antigens, CD / Q000096:biosynthesis; D002097:C-Reactive Protein / Q000096:biosynthesis; D018955:CD36 Antigens / Q000096:biosynthesis; D015815:Cell Adhesion Molecules / Q000096:biosynthesis; D045744:Cell Line, Tumor; D004271:DNA, Fungal / Q000235:genetics; D054884:Host-Pathogen Interactions / Q000235:genetics / Q000276:immunology*; D006801:Humans; D020382:Interleukin-18 / Q000096:biosynthesis; D053583:Interleukin-1beta / Q000096:biosynthesis; D053760:Interleukin-23 Subunit p19 / Q000096:biosynthesis; D046228:Microarray Analysis; D008938:Mitosis / Q000235:genetics; D009000:Monocytes / Q000276:immunology*; D000683:Serum Amyloid P-Component / Q000096:biosynthesis; D014158:Transcription, Genetic / Q000235:genetics; D014250:Trichosporon / Q000276:immunology*; D060586:Trichosporonosis / Q000276:immunology* / Q000382:microbiology; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis; D000099153:Pentraxins
chemical_list: D015703:Antigens, CD; D002097:C-Reactive Protein; D018955:CD36 Antigens; D015815:Cell Adhesion Molecules; D004271:DNA, Fungal; D020382:Interleukin-18; D053583:Interleukin-1beta; D053760:Interleukin-23 Subunit p19; D000683:Serum Amyloid P-Component; D014409:Tumor Necrosis Factor-alpha; D000099153:Pentraxins; C483616:ICAM3 protein, human; C508585:IL1B protein, human; C508840:IL23A protein, human