title: Increased microorganisms DNA levels in peripheral blood monocytes from psoriatic patients using PCR with universal ribosomal RNA primers.
abstract: It has long been suspected that systemic and focal infections cause or exacerbate psoriatic lesions. We previously showed that peripheral blood monocytes in psoriatic patients are activated and overproduce inflammatory cytokines. In addition, it has been reported that macrophages activated by ingesting microorganisms release tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta. Therefore we hypothesized that the monocytes in psoriatic patients may be activated by ingesting microorganisms and overproduce inflammatory cytokines. We examined the detection of microorganism DNA in monocytes from 15 patients with psoriasis vulgaris and from 12 healthy controls. DNA was extracted from monocytes, and a polymerase chain reaction (PCR) assay was performed for the detection using universal primers from conserved regions of the bacterial 16S ribosomal RNA gene or the fungal 18S rRNA gene. At the same time, we calculated the psoriasis area and severity index (PASI) scores and analyzed their correlations with the microorganisms DNA levels. The results showed that bacterial 16S DNA levels in monocytes were significantly higher in psoriatic patients than in controls. The fungal 18S DNA levels were also higher in psoriatic patients than in controls, but the differences were not significant. Although the microorganisms DNA levels in monocytes of psoriatic patients were high, there was no correlation between the bacterial DNA levels in monocytes of the psoriatics and PASI scores. Our study suggests that monocytes in psoriatic patients engulf more bacteria than there in controls, causing an activation of monocytes and triggering the formation of new lesions in the initial stages of psoriasis.
authors.affiliation: Department of Dermatology, Tokyo Medical University, Japan.
authors.forename: Yukari
authors.initials: Y
authors.lastname: Okubo
authors.forename: Noriko
authors.initials: N
authors.lastname: Oki
authors.forename: Hidemi
authors.initials: H
authors.lastname: Takeda
authors.forename: Misato
authors.initials: M
authors.lastname: Amaya
authors.forename: Sonoko
authors.initials: S
authors.lastname: Ito
authors.forename: Masako
authors.initials: M
authors.lastname: Osada
authors.forename: Masako
authors.initials: M
authors.lastname: Utsumi
authors.forename: Michiyuki
authors.initials: M
authors.lastname: Koga
authors.forename: Hisashi
authors.initials: H
authors.lastname: Kawashima
mesh_terms: D000328:Adult; D000368:Aged; D001483:Base Sequence; D016022:Case-Control Studies; D002478:Cells, Cultured; D015331:Cohort Studies; D004269:DNA, Bacterial / Q000032:analysis*; D004271:DNA, Fungal / Q000032:analysis*; D005260:Female; D006801:Humans; D007375:Interleukin-1 / Q000032:analysis*; D007963:Leukocytes, Mononuclear / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D008969:Molecular Sequence Data; D016133:Polymerase Chain Reaction; D011336:Probability; D011446:Prospective Studies; D011565:Psoriasis / Q000097:blood* / Q000175:diagnosis / Q000382:microbiology*; D012313:RNA / Q000494:pharmacology*; D012016:Reference Values; D012680:Sensitivity and Specificity; D012720:Severity of Illness Index; D018709:Statistics, Nonparametric; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis*
chemical_list: D004269:DNA, Bacterial; D004271:DNA, Fungal; D007375:Interleukin-1; C034477:RNA primers; D014409:Tumor Necrosis Factor-alpha; D012313:RNA