Transcription profiling by array to investigate the response of mice colon samples when infected by a H3N2 influenza virus.
ABSTRACT: To study the impact of influenza infection on gene expression changes in the colon, mice were intra-nasally infected with 30 plaque forming units of the mouse-adapted H3N2 IAV strain Scotland/20/1974. PBS-treated mice served as controls. The colons were collected 7 days post-infection.
Project description:Severe bacterial (pneumococcal) infections are commonly associated with influenza and are significant contributors to the excess morbidity and mortality of influenza. Disruption of lung tissue integrity during influenza participates in bacterial pulmonary colonization and dissemination out of the lungs. Interleukin (IL)-22 has gained considerable interest in anti-inflammatory and anti-infection immunotherapy over the last decade. In the current study, we investigated the effect of exogenous IL-22 delivery on the outcome of bacterial superinfection post-influenza. Our data show that exogenous treatment of influenza-infected mice with recombinant IL-22 reduces bacterial dissemination out of the lungs but is without effect on pulmonary bacterial burden. We describe an IL-22 specific gene signature in the lung tissue of IAV-infected (and naïve) mice that might explain the observed effects. Indeed, exogenous IL-22 modulates gene expression profile in a way suggesting a reinforcement of tissue integrity. Our results open the way to alternative approaches for limiting post-influenza bacterial superinfection, particularly systemic bacterial invasion.
Project description:Mice were infected intranasally with 1.5x10E5 PFU and total RNA were extracted from mice lungs at day 3. RNA samples were extracted from mice lung infected or not by influenza virus.
Project description:The gene expression profile of neonatal versus adult lung, 2 days after an RSV or mock infection was analyzed using whole mouse genome agilent microarrays. Total lung RNA were extracted, labeled with Cy3 and hybridized on Agilent G4122F slides. We used 4 biological replicates per condition.
Project description:This transcriptomic study aims to identify genes differentially expressed after cellular therapy of muscular dystrophy dogs (GRMD) by MuStem cells, in order to identify the cellular mechanisms parallel to skeletal muscle remodeling.
Project description:Array analysis of total lung RNAs from female BALB/c mice collected at 12, 48 and 96 h post-infection with highly and less virulent influenza A (H3N2) viruses. Viruses (designated as LVI and HVI) were derived from influenza strain virus A/Aichi/2/68 (Aichi68). LVI is Aichi68 propagated in eggs, and HVI is mouse adapted Aichi68. Infection: lung homogenate (mock), LVI and HVI; time of sample collection: 12, 48 and 96 h post-infection; two biological replicates for each group.
Project description:The genome of the western honey bee (Apis mellifera) harbours ten different major royal jelly protein genes (mrjp1-10) which originate from a single-copy precursor via gene duplication. The evolutionary fate of duplicated genes is eventually determined over time as to result in loss due to pseudogenization, or in preservation due to neo- or sub-functionalization. Both fates were already observed in the mrjp gene cluster, as only mrjp1 - 9 are expressed, whereas mrjp10 was pseudogenized and represents an incomplete gene copy. In contrast, MRJP1 underwent neofunctionalization and developed an essential function within the food jelly of queen larvae, to guaranty the survival of the whole colony. We here show combining quantitative real time PCR with quantitative mass spectrometry that expression of most mrjps (mrjp1-5 and 7) shows an age dependent pattern in worker hypopharyngeal glands as well as in brains. Expression increases after hatching until the nurse bee period and is followed by a decrease in older workers that forage for different plant products. Mrjp6 expression deviates considerably from the expression profiles of the other mrjps and transcript abundance does not correlate with protein amount. Thus, either mrjp6 does fulfil a total different function or it might be on its way to pseudogenization. Furthermore, a tissue-specific function of the proteins MRJP8 and 9 in the hypopharyngeal glands and the brain can be excluded, suggesting a more general physiological than a nutritive function for both gene products.
Project description:Influenza A viruses cause epidemics and pandemics with damaging health and economic impacts. Alike any obligate intracellular pathogen, IAVs hijack host cell machinery and energetic resources to multiply within, and eventually exit, the host. Increased fatty acid and cholesterol synthesis, as well as increased glucose metabolism have been identified as the major metabolic changes induced by infection. Besides these effects on metabolism, IAV infection also triggers a variety of innate defense mechanisms within the host cell. Although mainly defined as a virus of the respiratory tract, with airway epithelial cells being its prime cellular habitat, complications outside the site of infection have also been reported. However, whether influenza on its own may impact on endocrine tissues and, thereby, lead to metabolic complications, has never been investigated. Here, we compared the response of preadipocytes and adipocytes to IAV infection, in terms of transcriptomic profiles and bioenergetics. The results showed that IAV triggers a browning adipogenesis process, leading to metabolic reprogramming of the adipose tissue resulting in long-lasting alterations of body metabolism. We conclude that the adipose tissue might be an undervalued organ in influenza pathophysiology.
Project description:Analysis of gene expression in macrophages infected with influenza A virus or Mock and treated with the VX-787 to investigate the effects VX-787 have on transcriptional response in human macrophages. Human macrophages were infected with influenza A/WSN/1933(H1N1) or A/Udorn/307/72(H3N2) viruses, or non-infected (Mock). 10nM VX-787 was treated to WSN, Udorn or Mock infected cells, repectively.
Project description:Influenza A virus (IAV) predisposes individuals to secondary infections with the bacterium Streptococcus pneumoniae (the pneumococcus). Infections may manifest as pneumonia, sepsis, meningitis or otitis media (OM). It remains controversial as to whether secondary pneumococcal disease is due to the induction of an aberrant immune response or IAV induced immunosuppression. Moreover, as the majority of studies have been performed in the context of pneumococcal pneumonia, it remains unclear how far these findings can be extrapolated to other pneumococcal disease phenotypes. Here, we demonstrate that the viral hemagglutinin (HA) mediates bacterial OM by inducing a pro-inflammatory response in the middle ear cavity in a replication-dependent manner. Importantly, our findings show that it is the inflammatory response that mediates pneumococcal replication; not viral suppression of the immune system or epithelial damage. This study provide the first evidence that HA induced inflammation drives pneumococcal replication in the middle ear cavity, which has important consequences to the treatment of pneumococcal OM. Five-day old C57BL/6 mice were colonised intranasally (i.n.) with 2×103 colony forming units (CFU) of S. pneumoniae EF3030Lux in 3 µLs of PBS. Alternatively, mice were mock-infected with an equivalent volume of phosphate buffered saline (PBS). At 14-days of age, infant mice were infected i.n. with 20 plaque forming units (PFU) (PR8/34, Cambridge/34 and WSN/33) or 102.5 PFU (all other virus strains) of egg-grown IAV in 3 µLs of PBS. Viral doses were selected to ensure a reproducible infection with minimum morbidity and no mortality. Six days post-IAV infection, mice were euthanised and organs were collected for analysis. Six independent biological replicates (where both ears from one mouse were pooled to create one sample) were used for each condition and analyzed using the NimbleGen platform (12×135K Mouse Gene Expression Arrays, Roche Nimblegen, USA). Indirect labeling, hybridization and washing was performed according to the manufacturer’s instructions. Array images were acquired with a NimbleGen MS200 scanner, and images were processed with NimbleScan software using the RMA algorithm. Data was processed using Arraystar (DNASTAR, USA) with default settings as described in the manual. Differential expression tests were performed with a moderated T-test implemented in Arraystar, followed by FDR correction of the P values (Q-values) according to the method of Storey and Tibshirani