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E Helin

Publications and source records attributed to E Helin.

6 recordsLinked to original sources

Measles virus enhances the expression of cellular immediate-early genes and DNA-binding of transcription factor AP-1 in lung epithelial A549 cells.

In this work we investigated the effect of measles virus (MV) infection on the expression of immediate-early genes junB, c-jun and c-fos mRNA as well as AP-1 DNA-binding activity in the lung epithelial-like adenocarcinoma cell line A549. The transcription factor AP-1, which is a group of dimeric complexes of the Fos and Jun family proteins, is an important regulator in many cellular responses to different extracellular stimuli. Membrane cofactor protein CD46, which acts as a receptor for laboratory-adapted and vaccine strains of MV, has been reported to associate with beta1 integrin molecules, which are known to trigger signaling events and activate immediate-early genes. The expression of junB and c-jun mRNA was rapidly induced by MV. It was observed already at 1 h postinfection and detected again at the later phase of infection. Moreover, the expression of c-fos mRNA seemed to be weak and transient. The early induction was apparently associated with MV binding and CD46 clustering, whereas the later induction coincided with virus replication. MV infection also enhanced the activation of AP-1 DNA-binding. Our results suggest that changes in the expression of immediate-early genes and in the activation of AP-1 DNA-binding may have an important role in many cellular events detected in MV-infected cells.

Antigens, CD↗

Measles virus activates NF-kappa B and STAT transcription factors and production of IFN-alpha/beta and IL-6 in the human lung epithelial cell line A549.

Epithelial cells of the respiratory tract are the primary targets of measles virus (MV) infection. In this work we have studied the effect of MV infection on the activation of transcription factors nuclear factor (NF)-kappa B and signal transducer and activator of transcription (STAT) and the production of cytokines in the lung epithelial A549 cell line. NF-kappa B and STAT activation were induced by MV in A549 cells as analyzed by electrophoretic mobility shift assay. NF-kappa B activation was rapid and it was not inhibited by the protein synthesis inhibitor cycloheximide, suggesting that MV directly activates NF-kappa B. In contrast, Stat1, Stat3, and interferon-stimulated gene factor 3 (ISGF3) DNA binding was induced by MV infection with delayed kinetics compared to NF-kappa B activation. MV infection also resulted in an efficient interferon (IFN)-alpha/beta and interleukin-6 production. Cycloheximide and neutralizing anti-IFN-alpha/beta antibodies inhibited MV-induced activation of Stat1, Stat3, and ISGF3 DNA binding in A549 cells. In conclusion, the results suggest that MV infection activates transcription factors involved in the initiation of innate immune responses in epithelial cells by two different mechanisms: directly by leading to NF-kappa B activation and indirectly via IFN-alpha/beta leading to STAT activation.

Animals↗

A reduced estimate of the number of kilometre-sized near-Earth asteroids.

Near-Earth asteroids are small (diameters < 10 km), rocky bodies with orbits that approach that of the Earth (they come within 1.3 AU of the Sun). Most have a chance of approximately 0.5% of colliding with the Earth in the next million years. The total number of such bodies with diameters > 1 km has been estimated to be in the range 1,000-2,000, which translates to an approximately 1% chance of a catastrophic collision with the Earth in the next millennium. These numbers are, however, poorly constrained because of the limitations of previous searches using photographic plates. (One kilometre is below the size of a body whose impact on the Earth would produce global effects.) Here we report an analysis of our survey for near-Earth asteroids that uses improved detection technologies. We find that the total number of asteroids with diameters > 1 km is about half the earlier estimates. At the current rate of discovery of near-Earth asteroids, 90% will probably have been detected within the next 20 years.

Earth, Planet↗

Measles virus replication in cells of myelomonocytic lineage is dependent on cellular differentiation stage.

Measles virus (MV)-infected monocytes may have a central role in virus-induced immunosuppression. Our understanding of MV replication in monocytic cells is, however, incomplete. In this work we have investigated MV replication in cells of human myelomonocytic lineage with different maturation stages in order to study the effect of cellular maturation on virus infection. MV was able to infect human bone marrow myeloid granulocyte-macrophage colony-forming cells (CFC-GM) as well as monocytes and macrophages, but the replication cycle seemed to be regulated by the maturation stage of the cells. Virus infection in CFC-GM was productive, unlike in monocytes and macrophages, where an extensive viral RNA synthesis occurred and high amounts of proteins were synthesised without a remarkable release of infectious virus. Efficiency of viral macromolecular synthesis in macrophages was comparable to that of promonocytic cell line U-937 and human epithelial cell line A549, but in contrast to macrophages the cell lines highly supported productive infection. On the other hand, chemically induced maturation of the human promyelocytic and promonocytic cell lines HL-60, THP-1, and U-937 to more mature macrophage-like forms did not markedly alter the replication cycle of MV in these cell lines. Our results showed that MV replication in myelomonocytic cells varied depending on the maturation stage of the cells. The immature myelomonocytic cells supported productive virus infection, but the maturation process lead to cellular changes that caused a restriction of MV replication cycle partly at posttranscriptional and partly at posttranslational level. The metabolic milieu of monocytes and macrophages as such was sufficient to support extensive viral macromolecular synthesis.

Blotting, Western↗

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Belgium↗

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Child Welfare↗