Understanding PRRSV Infection in Porcine Lung Based on Genome-Wide Transcriptome Response Identified by Deep Sequencing

Porcine reproductive and respiratory syndrome (PRRS) has been one of the most economically important diseases affecting swine industry worldwide and causes great economic losses each year. PRRS virus (PRRSV) replicates mainly in porcine alveolar macrophages (PAMs) and dendritic cells (DCs) and develops persistent infections, antibody-dependent enhancement (ADE), interstitial pneumonia and immunosuppression. But the molecular mechanisms of PRRSV infection still are poorly understood. Here we report on the first genome-wide host transcriptional responses to classical North American type PRRSV (N-PRRSV) strain CH 1a infection using Solexa/Illumina's digital gene expression (DGE) system, a tag-based high-throughput transcriptome sequencing method, and analyse systematically the relationship between pulmonary gene expression profiles after N-PRRSV infection and infection pathology. Our results suggest that N-PRRSV appeared to utilize multiple strategies for its replication and spread in infected pigs, including subverting host innate immune response, inducing an anti-apoptotic and anti-inflammatory state as well as developing ADE. Upregulation expression of virus-induced pro-inflammatory cytokines, chemokines, adhesion molecules and inflammatory enzymes and inflammatory cells, antibodies, complement activation were likely to result in the development of inflammatory responses during N-PRRSV infection processes. N-PRRSV-induced immunosuppression might be mediated by apoptosis of infected cells, which caused depletion of immune cells and induced an anti-inflammatory cytokine response in which they were unable to eradicate the primary infection. Our systems analysis will benefit for better understanding the molecular pathogenesis of N-PRRSV infection, developing novel antiviral therapies and identifying genetic components for swine resistance/susceptibility to PRRS

The Aging Hair Pigmentary Unit

NoAs a highly visual and social species we communicate significantly via our physical appearance. Thus, it is unsurprising that the phenotypic aspects (including color) of our skin and hair feature prominently in such communication. Perhaps, one of the more potent reminders of aging is the change in pigmentation from birth to puberty and through to young adulthood, middle age, and beyond. Indeed, the hair bulb melanocyte may be viewed as an exquisitely sensitive aging sensor. In this context, we can appreciate that the loss of pigmentation from the hair tends to be earlier and much more striking than the age-associated pigmentation changes that we see in the epidermis. This phenotypic difference between the hair follicle and the epidermis-melanocyte subpopulations is of considerable interest, not least as both subpopulations originate from the same embyrologic neural crest and that the melanoctye stem cells in the adult hair follicle can occupy vacant niches in the epidermis. A major source of the differential aging of melanocytes in the hair bulb vs. the epidermis is likely due to the former¿s stringent coupling to the hair growth cycle when compared with the latter¿s continuous and UV-sensitive melanogenesis. Also likely to be involved is the maintenance of permissive microenvironments in these different skin compartments including their differing redox environments and variable connectivity with neuroendocrine axis. Over the last few years, we and others have striven to develop advanced cell culture methodologies for isolated hair follicle melanocytes and for intact anagen hair follicle organ culture, which may provide research tools to elucidate the regulatory mechanisms of hair follicle pigmentation. Others have assessed the robustness of the hair follicle-melanocyte stem compartment with age and other functional stressors. In the long term, it may be feasible to develop strategies to modulate some of these aging-associated changes in the hair follicle that impinge particularly of the melanocyte populations