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Biomedical subjects

G Lapucci

Publications and source records attributed to G Lapucci.

2 recordsLinked to original sources

Nerve growth factor and asthma.

An increasing body of evidence shows that nerve growth factor (NGF) exerts biological activity not only on the central and peripheral nervous system, but also on the immune system thereby influencing allergic diseases and asthma. (1) NGF circulating levels are increased in patients with allergic diseases and asthma, and are related to the severity of the inflammatory process and disease. In vernal keratoconjunctivitis, NGF plasma levels correlate with the number of mast cells infiltrating the conjunctiva, and NGF mRNA is increased in nasal mucosal scrapings of patients with allergic rhinitis who have high levels of NGF in serum and nasal fluids; NGF is further increased in nasal fluids after specific allergen challenge. (2) NGF is produced and released by several modulatory and effector cells of allergic inflammation and asthma, for example T-helper 2 lymphocytes, mast cells and eosinophils. (3) NGF receptors are expressed on the conjunctival epithelium of patients with allergic conjunctivitis and the number of NGF-receptor positive cells is increased in the conjunctiva of these patients. Indeed, local administration of NGF induces fibroblast activation and healing processes of human corneal ulcers, which suggests that NGF plays a role in tissue remodelling processes occurring in asthma. (4) NGF increases airway hyperreactivity to histamine in an animal model of asthma, while anti-NGF treatment reduces airway hyperreactivity induced by ovalbumin topical challenge in the sensitized mouse.

Animals↗

Human lung fibroblast response to NGF, IL-1beta, and dexamethsone.

It has been shown that lung mast cells, eosinophils, and fibroblasts are receptive to the action of nerve growth factor (NGF) and that NGF is released in to the bloodstream of subjects affected by allergic inflammatory response. The role of NGF in lung inflammatory disorders is unclear because there is evidence suggesting that NGF can be involved in both proinflammatory and anti-inflammatory responses. Lung fibroblasts play a marked role in inflammation. In this study we investigated the effect of NGF, interleukin 1beta (II-1beta), and dexamethasone (DEX) on human lung fibroblasts in vitro. We found that II-1beta, but not NGF, promotes fibroblasts' survival and that NGF stimulates trkA receptor expression, down regulates TFG-alpha, and has no effect on TNF-beta immunoreactivity. Moreover, DEX exerts different effects on NGF release by fibroblasts pre-exposed to II-1gamma. Our findings suggest that the NGF released by lung fibroblast during inflammation is not associated with the increase of proinflammatory factors such as TNF-alpha and II-1beta.

Animals↗