The mucosa that lines the respiratory and gastrointestinal (GI) tracts is an important portal of entry for pathogens and provides the frontline of immune defense against HIV infection. Using the simian immunodeficiency virus (SIV) rhesus macaque model, we have performed a comparative analysis of host gene expression in the lung and GI mucosa in response to SIV infection and antiretroviral therapy.
Enhanced innate antiviral gene expression, IFN-α, and cytolytic responses are predictive of mucosal immune recovery during simian immunodeficiency virus infection.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Transcription profiling reveals potential mechanisms of dysbiosis in the oral microbiome of rhesus macaques with chronic untreated SIV infection.
Specimen part, Disease, Disease stage, Cell line, Treatment
View SamplesA majority of individuals infected with human immunodeficiency virus (HIV) have inadequate access to antiretroviral therapy and ultimately develop debilitating oral infections that often correlate with disease progression. Our study evaluates the potential of simian immunodeficiency virus (SIV) infected rhesus macaques to serve as a non-human primate model for oral manifestations of HIV disease.
Transcription profiling reveals potential mechanisms of dysbiosis in the oral microbiome of rhesus macaques with chronic untreated SIV infection.
Specimen part, Disease, Disease stage
View SamplesA majority of individuals infected with human immunodeficiency virus (HIV) have inadequate access to antiretroviral therapy and ultimately develop debilitating oral infections that often correlate with disease progression. Our study evaluates the potential of simian immunodeficiency virus (SIV) infected rhesus macaques to serve as a non-human primate model for oral manifestations of HIV disease.
Transcription profiling reveals potential mechanisms of dysbiosis in the oral microbiome of rhesus macaques with chronic untreated SIV infection.
Specimen part, Disease, Disease stage
View SamplesA majority of individuals infected with human immunodeficiency virus (HIV) have inadequate access to antiretroviral therapy and ultimately develop debilitating oral infections that often correlate with disease progression. Our study evaluates the impact of chronic exposure to the pro-inflammatory cytokine, interferon gamma, on the growth and barrier functions of the oral epithelium.
Transcription profiling reveals potential mechanisms of dysbiosis in the oral microbiome of rhesus macaques with chronic untreated SIV infection.
Cell line, Treatment
View SamplesThe mucosa that lines the gastrointestinal (GI) tracts is an important portal of entry for pathogens and provides the frontline of immune defense against HIV infection. Epithelial barrier dysfunction during HIV infection has largely been attributed to the rapid and severe depletion of CD4 T cells in the gastrointestinal (GI) tract. In this study, the poential role of small non-coding microRNA (miRNA) to contribute to epithelial dysfunction was investigated in the non-human primate SIV model and microarrays were utilized to determine changes in mucosal gene expression (non-miRNA) that could be correlated to miRNA modulatiolns.
Intestinal epithelial barrier disruption through altered mucosal microRNA expression in human immunodeficiency virus and simian immunodeficiency virus infections.
Specimen part
View SamplesThe study recapitulates, through in vitro micropatterned co-cultures, interactions between HIV-infected T-lymphocytes and intestinal epithelial cells in order to investigate the mechanisms underlying the disruption of normal epithelial cell and barrier function during HIV infection. The co-culture method simplifies observation/monitoring of the two cell types and is particularly suited for laser microdissection-based retrieval of the epithelial cells for downstream gene expressions studies.
Micropatterned co-cultures of T-lymphocytes and epithelial cells as a model of mucosal immune system.
Specimen part, Cell line, Treatment
View SamplesTo identify genes associated with citrus peel development and manifestation of peel disorders, we analyzed flavedo, albedo and juice sac tissues from five types of citrus fruit including, mandarin orange, navel orange, valencia orange, grapefruit and lemon.
Transcriptome and metabolome analysis of citrus fruit to elucidate puffing disorder.
Specimen part
View SamplesTo identify genes associated with citrus peel development and manifestation of peel disorders, we analyzed flavedo, albedo and juice sac tissues from navel orange displaying, and not displaying, the puff disorder.
Transcriptome and metabolome analysis of citrus fruit to elucidate puffing disorder.
Specimen part
View SamplesHuman intestinal macrophages contribute to tissue homeostasis in noninflamed mucosa through profound down-regulation of pro-inflammatory cytokine release. Here, we show that this down-regulation extends to Toll-like receptor (TLR)-induced cytokine release, as intestinal macrophages expressed TLR3-TLR9 but did not release cytokines in response to TLR-specific ligands. Likely contributing to this unique functional profile, intestinal macrophages expressed markedly down-regulated adapter proteins MyD88 and Toll interleukin receptor 1 domain-containing adapter-inducing interferon beta, which together mediate all TLR MyD88-dependent and -independent NF-kappaB signaling, did not phosphorylate NF-kappaB p65 or Smad-induced IkappaBalpha, and did not translocate NF-kappaB into the nucleus. Importantly, transforming growth factor-beta released from intestinal extracellular matrix (stroma) induced identical down-regulation in the NF-kappaB signaling and function of blood monocytes, the exclusive source of intestinal macrophages. Our findings implicate stromal transforming growth factor-beta-induced dysregulation of NF-kappaB proteins and Smad signaling in the differentiation of pro-inflammatory blood monocytes into noninflammatory intestinal macrophages.
Inflammation anergy in human intestinal macrophages is due to Smad-induced IkappaBalpha expression and NF-kappaB inactivation.
Specimen part
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