Substance P potentiates TGFbeta-1 production in lung epithelial cell lines.
ABSTRACT Transforming growth factor-beta (TGF-beta) is one of the most important cytokines implicated in growth, differentiation, repair and also the pathogenesis of the lung fibrosis by its stimulatory effect on extracellular matrix deposition. Pulmonary epithelial cells are considered as a source of TGF-beta in lung. Substance P (SP), as a neuroimmunomodulator has elevated levels in inflamed airways and although it has significant role in the pathogenesis of the lung fibrosis, but its effect on transforming growth factor -beta (TGF-beta) production of the lung epithelial cells (and so its regulatory potential) remains unclear. In this study TGFbeta-1 levels in supernatants of the normal (BEAS-2B) and cancerous (A549) lung epithelial cell line cultures at the presence of various concentrations of SP were examined and MTT assay was performed to evaluate cells viability. We have observed that SP (without any other stimulator) significantly augments TGF-beta production of both BEAS and A54 cells and this effect is inhibited by NK1-receptor antagonist (CP-96345). We have also observed that the viability of cells did not significantly affect at the presence of SP. It can be concluded that SP can directly modulate the release of TGF-beta from human bronchial epithelial cell line and thereby participates in various lung functions or pathologic conditions.
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ABSTRACT: Take home message 1. Appropriate loading and adaptation increases cross-sectional area and tensile strength of the tendons, while immobilization and inappropriate adaptation leads to tendon degeneration and tendinopathy. 2. External forces like mechanical loading to the tendon, can be transduced by the peripheral nervous system and its messengers to produce tissue adaptive changes – either physiological or pathological. 3. Mechano-neuro-biological pathways may establish new markers for “tendon health”, and most interestingly open for new strategies for pharmacological and physical promotion of tendon repair.01/2010; DJO Publications.
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ABSTRACT: As global resistance to conventional antibiotics rises we need to develop new strategies to develop future novel therapeutics. In our quest to design novel anti-infectives and antimicrobials it is of interest to investigate host-pathogen interactions and learn from the complexity of host defense strategies that have evolved over millennia. A myriad of host defense molecules are now known to play a role in protection against human infection. However, the interaction between host and pathogen is recognized to be a multifaceted one, involving countless host proteins, including several families of peptides. The regulation of infection and inflammation by multiple peptide families may represent an evolutionary failsafe in terms of functional degeneracy and emphasizes the significance of host defense in survival. One such family is the neuropeptides (NPs), which are conventionally defined as peptide neurotransmitters but have recently been shown to be pleiotropic molecules that are integral components of the nervous and immune systems. In this review we address the antimicrobial and anti-infective effects of NPs both in vitro and in vivo and discuss their potential therapeutic usefulness in overcoming infectious diseases. With improved understanding of the efficacy of NPs, these molecules could become an important part of our arsenal of weapons in the treatment of infection and inflammation. It is envisaged that targeted therapy approaches that selectively exploit the anti-infective, antimicrobial and immunomodulatory properties of NPs could become useful adjuncts to our current therapeutic modalities.Current Protein and Peptide Science 12/2012; · 2.33 Impact Factor