0
We're unable to sign you in at this time. Please try again in a few minutes.
Retry
We were able to sign you in, but your subscription(s) could not be found. Please try again in a few minutes.
Retry
There may be a problem with your account. Please contact the AMA Service Center to resolve this issue.
Contact the AMA Service Center:
Telephone: 1 (800) 262-2350 or 1 (312) 670-7827  *   Email: subscriptions@jamanetwork.com
Error Message ......
Research Letter |

Identification of Bacterial DNA in the Peripheral Blood of Patients With Active Psoriasis FREE

Ana Ramírez-Boscá, MD1,2; Vicente Navarro-López, MD2,3; Asunción Martínez-Andrés, MD1,2; José Such, MD4,5,6; Rubén Francés, PhD4,5; José Horga de la Parte, MD7; Manuel Asín-Llorca, MD1
[+] Author Affiliations
1Department of Dermatology, Centro Dermatológico Estético, Alicante, Spain
2Clinical Research Unit, Centro Dermatológico Estético, Alicante, Spain
3Infectious Diseases Unit, Centro Dermatológico Estético, Alicante, Spain
4Department of Clinical Medicine, Miguel Hernández University, Elche, Alicante, Spain
5Centro de Investigación Biomédica en Red, Enfermedades Hepáticas y Digestivas, Instituto de Salud Carlos III, Madrid, Spain
6Digestive Disease Institute, Cleveland Clinic Abu Dhabi, Abu Dhabi, United Arab Emirates
7Department of Pharmacology, Pediatrics and Organic Chemistry, Miguel Hernández University, Elche, Alicante, Spain
JAMA Dermatol. 2015;151(6):670-671. doi:10.1001/jamadermatol.2014.5585.
Text Size: A A A
Published online

Psoriasis is a systemic autoimmune inflammatory disease that shares some immunological aspects with other inflammatory-based diseases, such as Crohn disease.1 Bacterial DNA (bactDNA) fragments have been shown to induce a systemic immunological response in Crohn disease and other settings.2,3 Although the results of most blood bacterial cultures are negative in patients with psoriasis, we hypothesized that the presence of bactDNA in the blood might act as a molecular trigger in disease outbreaks and induce a systemic inflammatory response in these patients.

This study included a consecutive series of patients whose psoriasis had previously cleared or was being controlled exclusively with topical medications who had a new flare of psoriasis and a group of sex- and age-matched control participants without psoriasis. The study protocol was approved by the Research Ethics Committee of the Hospital General Universitario de Alicante and all patients gave written informed consent. Exclusion criteria were the use of systemic corticosteroids, methotrexate sodium, cyclosporine, or anti–tumor necrosis factor drugs in the previous 3 months, antibiotic use in the previous 2 weeks, and the concomitant diagnosis of cirrhosis, intestinal bowel disease, and signs of bacterial infection. At the time of inclusion, patients were classified into severe, severe to moderate, moderate, or slight psoriasis, according to the international Psoriasis Area Severity Index.

A peripheral blood sample was collected from all participants and analyzed for routine biochemical laboratory values as well as interleukin (IL) 1B, IL-6, IL-12, tumor necrosis factor, and interferon γ levels. An aliquot of blood was inoculated under aseptic conditions in sterile, rubber-sealed Vacutainer SST II tubes (BD Diagnostics) to detect and identify bactDNA in the blood, as described previously.4 Statistical analyses were performed using SPSS, version 22 (IBM). The odds ratio and 95% CIs were determined as a measure of effect size. P < .05 was considered significant.

Fifty-four patients with psoriasis and 27 controls were included in the study. The baseline characteristics of these participants are shown in Table 1. Blood bactDNA was present in 16 patients with psoriasis, all of whom showed the phenotype of plaque psoriasis (16 of 45 [35.5%]), whereas 6 patients with guttate psoriasis, 3 with inverse psoriasis, and all 27 controls did not have bactDNA in the blood. Species identification corresponded to Escherichia coli (n = 9), Klebsiella pneumoniae (n = 2), Enterococcus faecalis (n = 2), Proteus mirabilis (n = 1), Streptococus pyogenes (n = 1), and Shigella fresneli (n = 1).

Table Graphic Jump LocationTable 1.  Baseline Clinical and Analytical Characteristics of Patients With Psoriasis and Controls

A higher proportion of findings of bactDNA in the blood was observed in patients with plaque psoriasis compared with patients with other psoriasis phenotypes (35.5% vs 0%; P < .05). The patient’s age at diagnosis of psoriasis and years since the first episode of psoriasis showed statistically significant differences in patients with and without bactDNA in the blood. The systemic inflammatory response was significantly higher in patients with bactDNA compared with other patients and controls (Table 2).

Table Graphic Jump LocationTable 2.  Baseline Clinical, Serum, and Analytical Characteristics of Patients by the Absence or Presence of BactDNA in Serum

In the patients with psoriasis in this study, bactDNA was associated with increased levels of IL-1β, IL-6, IL-12, tumor necrosis factor, and interferon γ. BactDNA induces a potent immune response by joining toll-like receptor 9 in immune cells.4 The levels of cytokines in patients with psoriasis and bactDNA in the blood were significantly higher than those of patients with psoriasis without evidence of bactDNA. Moreover, the presence of bactDNA was evident in patients with longer duration of the disease and in those whose disease was evident at a younger age (Table 2). It may be that the presence of bactDNA identifies a subset of patients with a more aggressive course of psoriasis.

Nucleotide sequencing revealed that E coli was the most prevalent source of bactDNA (9 of 16 isolates). The rest of the bacterial species’origin of the detected genomic fragments also corresponded to the type of flora commonly found in the intestinal lumen. Therefore, the bactDNA detected in our patients with psoriasis may have their origin in the intestinal lumen.5 Supporting this hypothesis is the fact that intestinal permeability has already been reported to be increased in patients with psoriasis.6 Taken together, these data suggest a role for bactDNA translocation in active plaque psoriasis.

Accepted for Publication: December 11, 2014.

Corresponding Author: Vicente Navarro-López, MD, Unidad de Investigación Clínica, Centro Dermatológico Estético de Alicante, Calle Alonso Cano, 51, 03014 Alicante, Spain (vnavarro@centrodermatologicoestetico.com).

Published Online: March 11, 2015. doi:10.1001/jamadermatol.2014.5585.

Author Contributions: Drs Navarro-López and Ramírez-Boscá had full access to all the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis.

Study concept and design: Ramírez-Boscá, Navarro-López, Such.

Acquisition, analysis, or interpretation of data: All authors.

Drafting of the manuscript: Navarro-López, Such.

Critical revision of the manuscript for important intellectual content: All authors.

Statistical analysis: Navarro-López.

Administrative, technical, or material support: Martínez-Andrés, Francés, Asín-Llorca.

Study supervision: All authors.

Conflict of Interest Disclosures: None reported.

Additional Contributions: Encarna Espejo-Luna, BSN, Centro Dermatologico Estetico de Alicante, Spain, provided clinical contributions and effort into this work. She was not financially compensated.

Moran  CP, Shanahan  F.  Gut microbiota and obesity. Best Pract Res Clin Gastroenterol. 2014;28(4):585-597.
PubMed   |  Link to Article
de Vlam  K, Gottlieb  AB, Mease  PJ.  Current concepts in psoriatic arthritis: pathogenesis and management. Acta Derm Venereol. 2014;94(6):627-634.
PubMed   |  Link to Article
De Hertogh  G, Aerssens  J, Geboes  KP, Geboes  K.  Evidence for the involvement of infectious agents in the pathogenesis of Crohn’s disease. World J Gastroenterol. 2008;14(6):845-852.
PubMed   |  Link to Article
Such  J, Francés  R, Muñoz  C,  et al.  Detection and identification of bacterial DNA in patients with cirrhosis and culture-negative, nonneutrocytic ascites. Hepatology. 2002;36(1):135-141.
PubMed   |  Link to Article
Baker  PI, Love  DR, Ferguson  LR.  Role of gut microbiota in Crohn’s disease. Expert Rev Gastroenterol Hepatol. 2009;3(5):535-546.
PubMed   |  Link to Article
Humbert  P, Bidet  A, Treffel  P, Drobacheff  C, Agache  P.  Intestinal permeability in patients with psoriasis. J Dermatol Sci. 1991;2(4):324-326.
PubMed   |  Link to Article

Figures

Tables

Table Graphic Jump LocationTable 1.  Baseline Clinical and Analytical Characteristics of Patients With Psoriasis and Controls
Table Graphic Jump LocationTable 2.  Baseline Clinical, Serum, and Analytical Characteristics of Patients by the Absence or Presence of BactDNA in Serum

References

Moran  CP, Shanahan  F.  Gut microbiota and obesity. Best Pract Res Clin Gastroenterol. 2014;28(4):585-597.
PubMed   |  Link to Article
de Vlam  K, Gottlieb  AB, Mease  PJ.  Current concepts in psoriatic arthritis: pathogenesis and management. Acta Derm Venereol. 2014;94(6):627-634.
PubMed   |  Link to Article
De Hertogh  G, Aerssens  J, Geboes  KP, Geboes  K.  Evidence for the involvement of infectious agents in the pathogenesis of Crohn’s disease. World J Gastroenterol. 2008;14(6):845-852.
PubMed   |  Link to Article
Such  J, Francés  R, Muñoz  C,  et al.  Detection and identification of bacterial DNA in patients with cirrhosis and culture-negative, nonneutrocytic ascites. Hepatology. 2002;36(1):135-141.
PubMed   |  Link to Article
Baker  PI, Love  DR, Ferguson  LR.  Role of gut microbiota in Crohn’s disease. Expert Rev Gastroenterol Hepatol. 2009;3(5):535-546.
PubMed   |  Link to Article
Humbert  P, Bidet  A, Treffel  P, Drobacheff  C, Agache  P.  Intestinal permeability in patients with psoriasis. J Dermatol Sci. 1991;2(4):324-326.
PubMed   |  Link to Article

Correspondence

CME
Also Meets CME requirements for:
Browse CME for all U.S. States
Accreditation Information
The American Medical Association is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians. The AMA designates this journal-based CME activity for a maximum of 1 AMA PRA Category 1 CreditTM per course. Physicians should claim only the credit commensurate with the extent of their participation in the activity. Physicians who complete the CME course and score at least 80% correct on the quiz are eligible for AMA PRA Category 1 CreditTM.
Note: You must get at least of the answers correct to pass this quiz.
Please click the checkbox indicating that you have read the full article in order to submit your answers.
Your answers have been saved for later.
You have not filled in all the answers to complete this quiz
The following questions were not answered:
Sorry, you have unsuccessfully completed this CME quiz with a score of
The following questions were not answered correctly:
Commitment to Change (optional):
Indicate what change(s) you will implement in your practice, if any, based on this CME course.
Your quiz results:
The filled radio buttons indicate your responses. The preferred responses are highlighted
For CME Course: A Proposed Model for Initial Assessment and Management of Acute Heart Failure Syndromes
Indicate what changes(s) you will implement in your practice, if any, based on this CME course.

Multimedia

Some tools below are only available to our subscribers or users with an online account.

750 Views
0 Citations
×

Related Content

Customize your page view by dragging & repositioning the boxes below.

Articles Related By Topic
Related Collections
Jobs