AI Article Synopsis
- The neuropeptide substance P (SP) enhances the migration and cytotoxicity of natural killer (NK) cells, potentially linking innate immunity with neurogenic inflammation, such as asthma.
- SP's effect on NK cell migration is dose-dependent, reaching its peak at 10(-8) M, and operates through the neurokinin-1 receptor, which is present in NK cells.
- Additionally, SP may increase NK cell cytotoxicity against certain target cells through a mechanism that doesn't rely on receptors, highlighting its role in connecting neural activity and immune function.
Article Abstract
The neuropeptide substance P (SP) can modulate a number of immunological functions in vitro and in vivo. Here, we investigated if SP boosts migration and cytotoxicity of natural killer cells, thus providing a further link between "innate immunity" and neurogenic inflammatory processes like asthma bronchiale. We demonstrate a dose-dependent effect of SP on natural killer cell migration with a maximal response at 10(-8) M SP. SP was shown to stimulate unstimulated as well as interleukin-2 (IL-2)-activated natural killer cells. Stimulation of natural killer cell migration was neurokinin-1 receptor dependent. Furthermore, mRNA encoding the neurokinin-1 receptor was demonstrated as being present in natural killer cells using RT-PCR while mRNA of the neurokinin-2 receptor was not detectable. Additionally, SP seems to influence specific cytotoxicity against Raji and K567 effector cells by a receptor-independent mechanism. In conclusion, our data indicate that functionally active neurokinin-1 receptors can be expressed by human natural killer cells. Substance P might therefore be a novel link between neural structures and innate immunity.
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| http://dx.doi.org/10.1016/s0167-0115(03)00193-9 | DOI Listing |
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