Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001486 (Adenovirus)
 3,125 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adenoviral vectors are highly efficient for transferring genes to islets. However, the inflammatory and immune responses stimulated by adenovirus may be detrimental to islet survival. Given the role of chemokines and their receptors in inflammation, we analyzed their expression in isolated murine islets, in a murine beta cell line and in syngeneic islet grafts after adenovirus transduction (AdRSVLacZ). AdRSVLacZ transduction enhanced and induced the expression of a variety of chemokines. Transduced syngeneic transplanted islets showed significantly enhanced expression of multiple chemokines and receptors, including monocyte chemoattractant protein-1 (MCP-1), CC chemokine receptor 2 (CCR2) and regulated upon activation, normal T cell expressed and secreted (RANTES), compared with untransduced islet grafts. AdRSVLacZ-transduced islet grafts had significant mononuclear infiltrates, and in situ hybridization demonstrated intragraft expression of MCP-1, CCR2 and RANTES. Although adenovirus transduction did not impair in vitro insulin secretion, diabetes was reversed in only one of six recipients of a marginal mass of AdRSVLacZ-transduced islets, compared with six of six control recipients. In conclusion, multiple chemokines and chemokine receptors are expressed by murine islets constitutively and in response to adenovirus transduction. Adenovirus transduction impairs engraftment of marginal mass of transplanted islets. This is not because of direct vector toxicity of islet secretory capacity, but may be related to host innate immunity in response to adenovirus vector.
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PMID:Adenovirus transduction induces expression of multiple chemokines and chemokine receptors in murine beta cells and pancreatic islets. 1451 Jun 96

In order to broaden our knowledge of the primary immune responses to respiratory syncytial virus (RSV) and adenovirus infections, we compared the concentrations of interleukin (IL)-6, IL-8, and regulated on activation, normal T cell expressed and secreted (RANTES) produced in vitro during RSV and adenovirus infections of bronchial epithelial cells. We infected BEAS-2B cells-a human bronchial epithelial cell line-with RSV, adenovirus serotype 3, or serotype 7 and measured the concentrations of IL-6, IL-8, and RANTES in the cell culture supernatants. When the multiplicity of infection (MOI) was 1, RSV induced the production of markedly higher concentrations of IL-6, IL-8, and RANTES than the adenovirus. When the MOI of the adenovirus was increased to 100, the production of IL-6 and IL-8 increased. However, the amounts produced were still lower than those produced by RSV with the MOI of 1. There was no statistically significant increase in the production of RANTES in spite of the MOI of the adenovirus was increased to 100. Adenovirus serotype 7 induced the production of considerably more IL-6 and IL-8 than serotype 3 in the MOI of 100. However, neither adenovirus serotype triggered an increase in the production of RANTES in spite of the MOI of 100. This demonstrates that RSV could have a superior capacity to stimulate the production of IL-6, IL-8, and RANTES in the bronchial epithelial cells. This study may help to explain the differences in the clinical outcomes of RSV and adenovirus infections.
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PMID:Cytokine induction by respiratory syncytial virus and adenovirus in bronchial epithelial cells. 1724 36