Filters
Technology
Platform
SRP154984
Homo sapiens
96 Downloadable Samples
Illumina HiSeq 4000
Description
Secondary bacterial pneumonia following influenza infection is a significant cause of mortality worldwide. Upper respiratory tract pneumococcal carriage is important as both determinants of disease and population transmission. The immunological mechanisms that contain pneumococcal carriage are well-studied in mice but remain unclear in humans. Loss of this control of carriage following influenza infection is associated with secondary bacterial pneumonia during seasonal and pandemic outbreaks. We used a human type 6B pneumococcal challenge model to show that carriage acquisition induces early degranulation of resident neutrophils and recruitment of monocytes to the nose. Monocyte function associated with clearance of pneumococcal carriage. Prior nasal infection with live attenuated influenza virus induced inflammation, impaired innate function and altered genome-wide nasal gene responses to pneumococcal carriage. Levels of the cytokine IP-10 promoted by viral infection at the time of pneumococcal encounter was positively associated with bacterial density. These findings provide novel insights in nasal immunity to pneumococcus and viral-bacterial interactions during co-infection. Overall design: 96 nasal samples from healthy volunteers experimentally challenged with pneumococcus, 3 days after receiving live attenuated influenza vaccine or tetravalent inactivated influenza vaccine underwent RNA-Sequencing. Nasal cells were collected at baseline (D-4) before vaccination, and at 5 days after vaccination (or 2 days after pneumococcal inoculation, D+2) and at 12 days after vaccination (or 9 days after pneumoocccal inoculation, D9)
Publication Title
Inflammation induced by influenza virus impairs human innate immune control of pneumococcus.
Sample Metadata Fields
Specimen part, Disease stage, Subject, Time
View Samples- Arabidopsis thaliana
- 18 Downloadable Samples
Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)
Description
Plants grown at high densities perceive a decrease in the red to far-red (R:FR) ratio of incoming light, resulting from absorption of red light by canopy leaves and reflection of far-red light from neighboring plants. These changes in light quality trigger a series of responses known collectively as the shade avoidance syndrome. During shade avoidance, stems elongate at the expense of leaf and storage organ expansion, there is reduced branching, and flowering is accelerated. We identified several loci in Arabidopsis, mutations in which lead to plants defective in multiple shade avoidance outputs. Here we describe SAV3, an aminotransferase, and show that SAV3 catalyzes the formation of indole-3-pyruvic acid (IPA) from L-tryptophan (L-Trp), the first step in a previously proposed, but uncharacterized, auxin biosynthetic pathway. This pathway can be rapidly deployed to biosynthesize auxin at the high levels required to initiate the multiple changes in body plan associated with shade avoidance.
Publication Title
Rapid synthesis of auxin via a new tryptophan-dependent pathway is required for shade avoidance in plants.
Sample Metadata Fields
Age, Specimen part
View Samples