Comparison of cytokine profiles induced by nonlethal and lethal doses of influenza A virus in mice.
influenza virus is most commonly Human and the pathogen responsible for causing seasonal extensive morbidity and mortality. To investigate the immunological factors associated with severe influenza infection, the immune response in infected mice with nonlethal (LD0) doses of A / PR / 8/34 (H1N1) influenza virus compared with those of mice infected with a dose of off (LD100) of the virus. Virus titers and activation of the retinoic acid-induced gene (RIG) -I-like receptor signaling pathways similar in mice infected with LD0 and LD100 at 2 days post-infection;
However, mice infected with LD100 exhibited a greater abundance of cytokines and cytokine profile that is more diverse. LD100 infection induced the expression of the following factors: Interleukin ( IL s), IL -4, IL -7, IL -10, IL – 11 , IL -12p40, IL -13 and IL < / em> -15; inflammatory chemokines, C-C motif chemokine ligand (CCL) 2, CCL3 / 4, CCL12, CCL17, CCL19; and lung injury associated cytokines, leptin, leukemia inhibitory factor, macrophage colony stimulating factor, pentraxin (PTX) 2 and PTX3, WNT1-induced-signaling pathway protein 1, matrix metallopeptidase (MMP) -2, MMP-3, proprotein convertase Subtilisin / Kexin type of 9 and T cell immunoglobulin and mucin domain.
Switching in polarization of M1 to M2 macrophages was evidenced by an increase in markers M2, including arginase-1 (arg1) and early growth response protein 2 (Egr2), in the lungs of mice infected with the LD100. Since the IL -12 and interferon-γ is the main T helper (Th) 1 cytokine, increased expression of interferon regulatory factor 4, IL -4, IL -10 and IL -13 promoted the differentiation of naive CD4transcriptomic characterization of related cultural change in murine and precision-cut slices of human tissue.
Active Interleukin 20 (IL20)
Our knowledge of the pathological mechanisms underlying complex organ fibrosis mainly derived from animal studies. However, the relevance of animal models for Human disease is limited; Therefore, ex vivo model of Human tissue slices precision-cut (PCT) may become an indispensable tool in the study of fibrosis and the development of medicine by bridging of animals Human translational gap. This study, presented as a two-part, providing a comprehensive characterization of the dynamic changes in the PCT during transcription by RNA sequencing culture. Part I investigate the differences in the cultural response induced in murine and Human PCT comes from a healthy liver, kidneys and intestines.
Part II depicts the molecular processes in cultured Human PCT generated from the diseased liver, kidney and ileum. We show that culture is associated with extensive transcriptional changes and PCT universal influence on organ and two species with triggers an inflammatory response and fibrosis associated extracellular matrix (ECM) remodeling. All PCT together with mRNA upregulation of IL – 11 and ECM-degrading enzyme matrix metalloproteinase-3 and MMP10.
slice preparation and active cultures various channels in all PCT, especially those involved in inflammation ( IL -6, IL -8 and signaling HMGB1) and tissue remodeling (osteoarthritis pathways and integrin signaling). Although the effect of converging cultures, PCT featuring species -, – organ and specific pathological differences in the regulation of gene and the canonical pathway. The underlying pathology in the Human PCT ever sick and influence biological processes such as the release of cytokines.
