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S Lira

Publications and source records attributed to S Lira.

6 recordsLinked to original sources

Tachykinin NK3-receptor deficiency does not inhibit pulmonary eosinophilia in allergic mice.

Tachykinins are important in the development of pulmonary inflammation in mice but the tachykinin receptor subtype mediating this response has not been defined. To elucidate the role of tachykinin NK3-receptors on allergen-induced pulmonary inflammation, studies were performed on ovalbumin (OVA) sensitized and challenged mice with genetic disruption of the tachykinin NK3-receptor (NK3-/-). Aerosol OVA (0.5%) challenge produced eosinophil influx into the bronchoalveolar lavage fluid and lung tissue, goblet cell hyperplasia and damage to the airway epithelium of both NK3-/- mice and in wild type control mice (NK3+/+). There was no difference in the magnitude of these allergic inflammatory pulmonary responses between NK3-/- and NK3+/+ mice. These results find no role for tachykinin NK3-receptors on the pulmonary eosinophilia and lung damage after antigen challenge in mice.

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The role of chemokines in the immunopathology of the liver.

Chemokines are small protein inflammatory mediators that were classically known for their elicitation of inflammatory cells out of the vasculature. However, more contemporary studies show that these ubiquitous factors impinge on many facets of biology, including hematopoiesis, angiogenesis, and mitogeneis. The elucidation of mechanisms involved in the immunopathogenesis of liver disease has magnified the importance of chemokines in this organ. Accordingly, a number of in vitro and in vivo studies have highlighted the importance of chemokine biology in both acute and chronic liver disease, and a variety of liver diseases have been shown to involve chemokines and their receptors during the initiation and main tenance of liver pathology. A greater understanding of the role chemokines play during liver disease may permit the employment of therapies that target or enhance chemokines in the liver. This review will highlight the current clinical and experimental research in the immunopathogenesis of acute and chronic liver diseases.

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Expression of FosB during mouse development: normal development of FosB knockout mice.

FosB, one of the members of the Fos family, is rapidly induced in many cell types upon stimulation and has a stimulatory effect on the proliferation of cultured cells. To understand the tissue distribution of FosB, we have studied its expression pattern by immunohistochemistry in newborn and late embryonic stage mice. These results show that FosB is widely expressed with the highest levels of expression observed in both bony and cartilagenous regions of developing bone. FosB is also detected within whisker follicles, liver, and epidermal tissue. To study the role of FosB in mammalian development we generated embryonic stem (ES) cells, mice and mouse embryo fibroblasts (MEFs) that are deficient for FosB. FosB -/- mice are born at a normal frequency, are fertile and present no obvious phenotypic or histologic abnormalities. FosB-deficient ES cells and MEFs proliferate and enter the S phase normally and we do not find upregulation of other fos family genes to compensate for the lack of FosB. However, we do find that the induction of two AP-1 containing genes is reduced after stimulation of FosB-deficient cells, demonstrating that FosB does indeed play a functional role in transcriptional regulation.

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Lessons from gene modified mice.

Chemokines have been implicated in leukocyte trafficking, angiogenesis, immunoregulation and development. Understanding these and other chemokine functions in vivo is an enormously complex task, but one that is being facilitated by the application of powerful genetic techniques. Here I will summarise the results of a variety of genetic studies in mice and discuss how they have helped us to understand the biological role of chemokines and their receptors.

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