In this task, you're given a paragraph from the research paper and your task is to generate a suitable title for the research paper based on the given paper. Under 100 words is a good title length.

[Q]: The bone marrow contains heterogeneous population of cells that are involved in the regeneration and repair of diseased organs, including the lungs. In this study, we isolated and characterized progenitor epithelial cells from the bone marrow of 4-to 5-week old germ-free pigs. Microscopically, the cultured cells showed epithelial-like morphology. Phenotypically, these cells expressed the stem cell markers octamer-binding transcription factor (Oct4) and stage-specific embryonic antigen-1 (SSEA-1), the alveolar stem cell marker Clara cell secretory protein (Ccsp), and the epithelial cell markers pan-cytokeratin (Pan-K), cytokeratin-18 (K-18), and occludin. When cultured in epithelial cell growth medium, the progenitor epithelial cells expressed type I and type II pneumocyte markers. Next, we examined the susceptibility of these cells to influenza virus. Progenitor epithelial cells expressed sialic acid receptors utilized by avian and mammalian influenza viruses and were targets for influenza virus replication. Additionally, differentiated type II but not type I pneumocytes supported the replication of influenza virus. Our data indicate that we have identified a unique population of progenitor epithelial cells in the bone marrow that might have airway reconstitution potential and may be a useful model for cell-based therapies for infectious and non-infectious lung diseases.
[A]: Epithelial Cells Derived from Swine Bone Marrow Express Stem Cell Markers and Support Influenza Virus Replication In Vitro


[Q]: Currently available diagnostic assays for leptospirosis cannot differentiate vaccine from infection serum antibody. Several leptospiral proteins that are upregulated during infection have been described, but their utility as a diagnostic marker is still unclear. In this study, we undertook a lipidomics approach to determine if there are any differences in the serum lipid profiles of horses naturally infected with pathogenic Leptospira spp. and horses vaccinated against a commercially available bacterin. Utilizing a high-resolution mass spectrometry serum lipidomics analytical platform, we demonstrate that cyclic phosphatidic acids, diacylglycerols, and hydroperoxide oxidation products of choline plasmalogens are elevated in the serum of naturally infected as well as vaccinated horses. Other lipids of interest were triacylglycerols that were only elevated in the serum of infected horses and sphingomyelins that were increased only in the serum of vaccinated horses. This is the first report looking at the equine serum lipidome during leptospiral infection and vaccination.
[A]: Lipidomic analysis of immune activation in equine leptospirosis and Leptospira- vaccinated horses


[Q]: Introduction. Cytosolic pattern recognition receptors (PRR) have been shown to detect nucleic acids from RNA and DNA viruses in order to launch a type I interferon mediated antiviral state [1]. Here we show that RNA of the facultative intracellular bacterium Salmonella typhimurium is a ligand for RIG-I, triggers production of type-I interferons and contributes to pathogenicity in vivo. Methods. We use RIG-IÀ/À MEFs [2] or human epithelial cells depleted of RIG-I by lentiviral shRNA transduction for transfection and infection experiments. IFNbeta production was measured by 293T IFNbeta-reporter cells or qPCR. Intracellular bacterial titers were determined by gentamycin protection assay. In vivo infection experiments were performed as described [3] using SL1344 or SL1344 aroA deficient Salmonella strains in RIG-I+/+ and RIG-IÀ/À mice [4]. Results. Infection of fibroblasts and epithelial cells with S. typhimurium, but not with non-invasive E. coli, triggers IFNbeta transcription, suggesting that intracellular replication is required. RIG-I dependent recognition of bacterial RNA is dominant in non-phagocytic cells, as shown in RIG-I knockout and knockdown model cells. Despite presence of other pathogen-associated patterns (PAMP), like LPS or flagellin, no IFNbeta was produced in fibroblasts and epithelial cells lacking RIG-I upon S. typhimurium infection. In contrast, in macrophages TLR dependent recognition of bacterial PAMPs through TRIF/Myd88 overcomes RIG-I deficiency and leads to robust induction of type I interferon. We observed higher bacterial titers at early time points after infection in the cecum of S. typhimurium infected RIG-IÀ/À mice, when compared to wild type animals. However, at later stages of infection, S. typhimurium overcomes the innate response leading to similar weight loss and mortality in wildtype and RIG-IÀ/À mice. Conclusion. In summary, our data implicate a role of RIG-I mediated innate immune recognition of bacterial RNA in early control of bacterial replication, most likely mediated by non-phagocytic intestinal epithelial cells targeted by S. typhimurium. Disclosure of interest: None declared. Combined action of type I and type III IFN restricts initial replication of SARScoronavirus in the lung but fails to inhibit systemic virus spread
[A]:
P133 RIG-I mediates recognition of Salmonella RNA in non-phagocytic cells and con- tributes to early bacterial replication in vivo P135 Defining the intracellular innate immune synapse