The effect of substance P on peripheral blood mononuclear cells in patients with atopic dermatitis.
BACKGROUND
There is increasing evidence that neuropeptides, especially substance P (SP), may be involved in the pathogenesis of atopic dermatitis (AD).


OBJECTIVE
We performed this study to determine more precisely the role of SP in AD.


METHODS
We separated peripheral blood mononuclear cells (PBMCs) from AD patients and normal controls, and measured proliferation response and cytokine release after adding SP (10(-11), 10(-10) and 10(-9) M). We also compared substance P receptor expression by semi-quantitative RT-PCR.


RESULTS
PBMCs from AD patients proliferated at significantly higher rates (ca. by 30%). Semi-quantitative RT-PCR showed that the level of expression of SP receptor increased in AD patients versus normal controls. IL-4 release from PBMCs was significantly higher in AD patients, while IFN-gamma release from PBMCs was significantly lower in AD patients. Different concentrations of SP did not cause any difference in IL-4 and IFN-gamma secretions. However, TNF-alpha release from PBMCs in AD patients increased significantly at 10(-10) and 10(-9) M of SP compared to SP (-) control. IL-10 release from PBMCs increased significantly in AD patients with 10(-9) M of SP compared to SP (-) control.


CONCLUSIONS
SP might aggravate AD by increasing the production of TNF-alpha and IL-10 rather than by affecting IL-4 and IFN-gamma. This different immune response is considered to be the result of upregulated SP receptor in AD.
Kim
Kyu Han
KH
Department of Dermatology, Seoul National University College of Medicine, Clinical Research Institute, Seoul National University Hospital, 28 Yongon-Dong, Chongno-Gu, 110-744, Seoul, South Korea. kyuhkim@snu.ac.kr
Park
Kyoung Chan
KC
Chung
Jin Ho
JH
Choi
Hae Ryung
HR
D000328:Adult; D002455:Cell Division / Q000187:drug effects; D002478:Cells, Cultured; D016207:Cytokines / Q000378:metabolism*; D003876:Dermatitis, Atopic / Q000097:blood / Q000378:metabolism*; D005260:Female; D006801:Humans; D007371:Interferon-gamma / Q000378:metabolism; D016753:Interleukin-10 / Q000378:metabolism; D008297:Male; D009000:Monocytes / Q000378:metabolism* / Q000473:pathology*; D018040:Receptors, Neurokinin-1 / Q000378:metabolism; D013373:Substance P / Q000494:pharmacology*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D016207:Cytokines; D018040:Receptors, Neurokinin-1; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D013373:Substance P; D007371:Interferon-gamma