Successful treatment by double-filtration plasmapheresis of a patient with bullous pemphigoid: effects in vivo on transcripts of several genes for chemokines and cytokines in peripheral blood mononuclear cells.
The involvement of various cytokines and chemokines has been reported in the pathogenesis of bullous pemphigoid (BP). Double-filtration plasmapheresis (DFPP) is an effective treatment for BP but the mechanism of action remains unclear. Using semiquantitative reverse transcription-polymerase chain reaction, we examined levels of transcripts for various cytokines and chemokines in freshly isolated peripheral blood mononuclear cells in a patient with BP before and after DFPP treatment. DFPP was performed four times. Relative levels of transcripts for interleukin (IL)-8, macrophage inflammatory protein (MIP)-1alpha and IL-5, and the ratio of relative levels of transcripts for IL-4 and interferon (IFN)-gamma, were higher, before treatment, than in healthy controls, and decreased when the extent of the lesions was reduced. Relative levels of transcripts for tumour necrosis factor (TNF)-alpha and IL-4 also decreased with regression of lesions, although they were similar to or lower than the corresponding levels in healthy individuals. When eruptions recurred, relative levels of transcripts for IL-8, MIP-1alpha, RANTES (regulated upon activation normal T cell expressed and secreted), IL-2, IFN-gamma and TNF-alpha were very much higher than those prior to the recurrence, while relative levels of mRNAs for IL-4 and IL-5 did not increase. Relative levels of transcripts for IL-8, MIP-1alpha, TNF-alpha and IL-2 were lower at the end of each individual DFPP and after the four treatments than at the beginning of treatment. Our observations suggest that cytokines and chemokines produced in mononuclear cells play important roles in the pathogenesis of BP and that regulation of their expression might be involved in the therapeutic effects of DFPP in BP.
Hatano
Y
Y
Department of Dermatology, Oita Medical University, 1-1 Idaigaoka, Hasama-machi, Oita-gun, Oita 879-5593, Japan. HATANO@oita-med.ac.jp
Katagiri
K
K
Arakawa
S
S
Umeki
T
T
Takayasu
S
S
Fujiwara
S
S
D018946:Chemokine CCL5 / Q000032:analysis / Q000235:genetics; D018925:Chemokines / Q000032:analysis / Q000235:genetics; D016207:Cytokines / Q000032:analysis / Q000235:genetics*; D005260:Female; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases / Q000032:analysis / Q000235:genetics; D006801:Humans; D007372:Interferons / Q000032:analysis / Q000235:genetics; D007378:Interleukins / Q000032:analysis / Q000235:genetics; D007963:Leukocytes, Mononuclear / Q000502:physiology; D019402:Macrophage Inflammatory Proteins / Q000032:analysis / Q000235:genetics; D008875:Middle Aged; D010391:Pemphigoid, Bullous / Q000235:genetics / Q000473:pathology / Q000628:therapy*; D010956:Plasmapheresis / Q000379:methods*; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000379:methods; D014158:Transcription, Genetic / Q000235:genetics; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics
D018946:Chemokine CCL5; D018925:Chemokines; D016207:Cytokines; D007378:Interleukins; D019402:Macrophage Inflammatory Proteins; D014409:Tumor Necrosis Factor-alpha; D007372:Interferons; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases