To investigate the effect of 5-aminolevulinic acid photodynamic therapy (ALA-PDT) on () biofilm. biofilms were constructed on a cell slide and treated with ALA-PDT.According to different light doses,the biofilms were divided into six groups:ALA-PDT group [ALA-PDT1 (50 J/cm),ALA-PDT2 group (100 J/cm),ALA-PDT3 group (200 J/cm)],ALA-only group (ALA group),light-only group (LED),and a negative control group (ALA-PDT-group).The biofilm structure and the ratio of the dead bacteria/live bacteria were observed using a laser confocal microscope (CLSM).Biofilm viability was measured using the XTT assay. CLSM showed that the biofilm structures of ALA group and LED group were not significantly different from that of ALA-PDT-group,whereas the biofilm structure was more seriously damaged in ALA-PDT1 group,ALA-PDT2 group,and ALA-PDT3 group than in the ALA-PDT-group.The ratios of the dead/live bacteria in ALA-PDT-group,ALA group,LED group,ALA-PDT1 group,ALA-PDT2 group,and ALA-PDT3 group were 0.350±0.033, 0.305±0.046, 0.330±0.032, 1.525±0.439, 2.293±0.148 and 3.092±0.189,respectively.ALA group(=0.003, =1.000)and LED group(=-0.025, =1.000)did not significantly differ from the ALA-PDT-group.However,the ratio of dead/live bacteria in ALA-PDT-group was significantly lower than those in ALA-PDT1 group (=-0.162, <0.001),ALA-PDT2 group (=-0.254, <0.001),and ALA-PDT3 group (=-0.352, <0.001).The values of the XTT assay were were 0.462±0.028,0.465±0.044,0.437±0.047,0.301±0.040,0.207±0.001,and 0.110±0.007,respectively,in ALA-PDT-group,ALA group,LED group,ALA-PDT1 group,ALA-PDT2 group,and ALA-PDT3 group.Although the values of XTT assay in ALA(=-0.044, =1.000)and LED groups (=-0.020, =1.000)did not significantly differ from that in ALA-PDT-group,it was significantly higher in ALA-PDT-group than in ALA-PDT1 group (=1.175, <0.001),ALA-PDT2 group (=1.942, <0.001),and ALA-PDT3 group (=-0.352, =2.742, <0.001). ALA-PDT has an inhibitory effect on biofilm.ALA-PDT destroys biofilm structure and inhibits biofilm viability.
Aminolevulinic Acid ; Biofilms ; Photochemotherapy ; Photosensitizing Agents ; Propionibacterium acnes

Propionibacterium acnes is one of the commensals living on the human skin and glands, implicated mainly in acnes, but seldom in deep infection. Pleural empyema is rarely complicated with closed thoracostomy. We experienced 1 case of empyema caused by P. acnes after pleural biopsy and closed thoracostomy through a percutaneous pigtail catheter. A 79-year-old man was admitted for cough, purulent sputum and shortness of breath. Three weeks ago, closed thoracostomy and pleural biopsy were performed to confirm a diagnosis for his recurrent pleural effusion. He had increased amount of right pleural effusion. Through the pigtail catheter, pleural effusion was removed. Gram-positive rods were observed in Gram stain, but not cultured. By 16S rRNA analysis, P. acnes was confirmed as the pathogen. His empyema was repeatedly treated with antibiotics, fibrolysis and irrigation. Pleural decortication was recommended. We report the first case of empyema with P. acnes in Korea, possibly complicated with closed thoracostomy procedures.
Aged ; Anti-Bacterial Agents ; Biopsy ; Catheters ; Cough ; Diagnosis ; Dyspnea ; Empyema ; Empyema, Pleural* ; Gram-Positive Rods ; Humans ; Korea ; Pleural Effusion ; Propionibacterium acnes* ; Propionibacterium* ; Skin ; Sputum ; Thoracostomy ; Thoracotomy

To investigate the pathogenesis of acne vulgaris, and to provide new ideas for non-antibiotic therapy for acne vulgaris.
 Methods: Normal human epidermal keratinocyte (NHEK) was exposed to Propionibacterium acnes (P. acnes) [multiplicity of infection (MOI)=10, 20, 30] for 12, 24, or 36 hours. The enzyme-linked immunosorbent assay (ELISA) and real-time PCR were used to detect the protein and mRNA of IL-1β in NHEK. Three groups were set up as follows: A negative control group (no NHEK pretreatment), a positive control group (P. acnes was used to stimulate NHEK), and a siRNA group (pretreated NHEK with siRNA). ELISA, real-time PCR, and Western blotting were used to detect the protein, mRNA of IL-1β and nucleotide-binding oligomerization domain-like receptor containing pyrin domain 3 (NLRP3) in NHEK.
 Results: IL-1β of NHEK in the positive control group was significantly increased in a time and dose-dependent manner compared with the negative control group (P<0.05). After pretreating NHEK with siRNA, IL-1β level was decreased compared with the positive control group, but it was higher than that in the negative control group (P<0.05).
 Conclusion: P. ances can stimulate NHEK to secrete IL-1β, and the process is possibly involved in NLRP3. The inflammatory response induced by P. ances could be inhibited by suppressing the activity of NLRP3.
Acne Vulgaris ; Humans ; Inflammasomes ; Interleukin-1beta ; Keratinocytes ; NLR Family, Pyrin Domain-Containing 3 Protein ; Propionibacterium acnes

Acne vulgaris is a very common condition affecting up of about 80% to 90% of adolescents. The patients with acne have been shown to be adversely impacted by the effect of acne on their quality of life. Four factors are believed to play a key role in the development of acne lesions: excess sebum production, disturbed keratinization within the follicle, colonization of the pilosebaceous duct by Propionibacterium acnes, and the release of inflammatory mediators into the skin. Consequently, the target for acne therapy is these well-known pathogenic factors responsible for this disease state. Topical retinoids correct abnormal keratinization, but it should be applied cautiously because of irritation. Benzoyl peroxide is an effective bactericidal agent against P. acnes. Main topical antibiotics are erythromycin and clindamycin. Fixed combination topical products with retinoids, benzoyl peroxide and antibiotics have been introduced. Use of systemic antibiotics, including tetracyclines and macrolides rapidly improves inflammatory acne lesions. Oral isotretinoin is effective against all of the main pathogenic features of acne but is contraindicated in pregnant women and has been associated with cheilitis and dry skin. Hormonal therapy has been found to improve acne in some selective patients and should be considered for appropriate candidates. This review will present the general aspects of the pharmacological treatments for acne.
Acne Vulgaris ; Adolescent ; Anti-Bacterial Agents ; Benzoyl Peroxide ; Cheilitis ; Clindamycin ; Colon ; Drug Therapy ; Erythromycin ; Female ; Humans ; Isotretinoin ; Macrolides ; Pregnant Women ; Propionibacterium acnes ; Quality of Life ; Retinoids ; Sebum ; Skin ; Tetracyclines

BACKGROUND: Acne vulgaris is a disease of the pilosebaceous unit characterized by increased sebum production, hyperkeratinization, and immune responses to Propionibacterium acnes (PA). Here, we explore a possible mechanism by which a lipid receptor, G2A, regulates immune responses to a commensal bacterium. OBJECTIVE: To elucidate the inflammatory properties of G2A in monocytes in response to PA stimulation. Furthermore, our study sought to investigate pathways by which lipids modulate immune responses in response to PA. METHODS: Our studies focused on monocytes collected from human peripheral blood mononuclear cells, the monocytic cell line THP-1, and a lab strain of PA. Our studies involved the use of enzyme-linked immunosorbent, Western blot, reverse transcription polymerase chain reaction, small interfering RNA (siRNA), and microarray analysis of human acne lesions in the measurements of inflammatory markers. RESULTS: G2A gene expression is higher in acne lesions compared to normal skin and is inducible by the acne therapeutic, 13-cis-retinoic acid. In vitro, PA induces both the Toll-like receptor 2-dependent expression of G2A as well as the production of the G2A ligand, 9-hydroxyoctadecadienoic acid, from human monocytes. G2A gene knockdown through siRNA enhances PA stimulation of interleukin (IL)-6, IL-8, and IL-1β possibly through increased activation of the ERK1/2 MAP kinase and nuclear factor kappa B p65 pathways. CONCLUSION: G2A may play a role in quelling inflammatory cytokine response to PA, revealing G2A as a potential attenuator of inflammatory response in a disease associated with a commensal bacterium.
Acne Vulgaris ; Blotting, Western ; Cell Line ; Cytokines* ; Gene Expression ; Gene Knockdown Techniques ; Humans* ; In Vitro Techniques ; Interleukin-8 ; Interleukins ; Isotretinoin ; Microarray Analysis ; Monocytes* ; NF-kappa B ; Phosphotransferases ; Polymerase Chain Reaction ; Propionibacterium acnes* ; Propionibacterium* ; Reverse Transcription ; RNA, Small Interfering ; Sebum ; Skin ; Toll-Like Receptors

The aim of this study was to identify the non-Aggregatibacter actinomycetemcomitans bacteria grown on the tryptic soy-serum-bacitracin-vancomycin (TSBV) medium, an A. actinomycetemcomitans selective medium. A total of 82 unidentified bacterial isolates from the oral cavities of a Korean population were kindly provide by the Korean Collection for Oral Microbiology. All the clinical isolates were grown on TSBV medium and bacterial DNA purified from each isolate was subjected to PCR with universal primers specific for bacterial 16S rRNA genes (16S rDNAs) sequence. The each bacterial 16S rDNA was amplified by PCR and the nucleotide sequences of it was determined by the dideoxynucleotide chain termination method. They were identified by 16S rDNA sequence comparison method at the specie-level. The data showed that Neisseria spp. (42 strains), Fusobacterium spp. (10 strains), Capnocytophaga spp. (8 strains), Propionibacterium acnes (5 strains), Aggregatibacter aprophilus (4 strains), Campylobacter spp. (5 strains), Veillonella dispar (3 strains), Streptococcus sp. (1 strain), Haemophilus parainfluenzae (1 strain), Leptotrichia wadei (1 strain), Morococcus sp./Neisseria sp. (1 strain), and Staphylococcus sp. (1 strain) were identified. These results could be used to develop a new A. actinomycetemcomitans-selective medium which is more effective than the TSBV medium in future studies.
Aggregatibacter ; Bacteria* ; Base Sequence ; Campylobacter ; Capnocytophaga ; DNA, Bacterial ; DNA, Ribosomal ; Fusobacterium ; Genes, rRNA ; Haemophilus parainfluenzae ; Leptotrichia ; Methods ; Neisseria ; Polymerase Chain Reaction ; Propionibacterium acnes ; Staphylococcus ; Streptococcus ; Veillonella

BACKGROUND: Laser/light-based devices may provide an alternative to conventional acne therapeutics in some patients with nonresponsive acne. OBJECTIVE: We investigated the efficacy of red or infrared light-emitting diode (LED) devices in a mouse model of Propionibacterium acnes-induced inflammation through clinical examination and histopathological and immunohistochemical studies. METHODS: A human-derived Propionibacterium acnes suspension (10(9) colony-forming units /µl) was injected into the back of an HR-1 mouse. Then, a 28.9 J/cm2 650-nm red LED or 9.3 J/cm2 830-nm infrared LED was applied to the mouse with P. acnes-induced inflammation once daily for 2 weeks. Two weeks after treatment, histological findings with hematoxylin and eosin staining and expression levels of inflammatory biomarkers (integrin α6, neutrophils, interleukin [IL]-1β, and matrix metalloproteinase [MMP]-2/9) were evaluated in tissue specimens using immunohistochemical staining. RESULTS: Mice treated with red and infrared LED showed clinical improvement in inflammatory nodules compared to mice in the control group. Red LED was much more effective than infrared LED. Epidermal hyperplasia, comedone-like cysts, and integrin α6 expression improved to a similar extent in the red and infrared LED treatment groups and control group. Neutrophil, IL-1β, MMP-2, and MMP-9 expression after treatment with red and infrared LED decreased considerably compared to expression in the control group. CONCLUSION: In a mouse model of P. acnes-induced inflammatory nodules, red and infrared LED devices may be an alternative to conventional acne therapies. In addition, a mouse model of P. acnes-induced inflammatory nodules is helpful for laboratory research of acne.
Acne Vulgaris ; Animals ; Biomarkers ; Eosine Yellowish-(YS) ; Hematoxylin ; Humans ; Hyperplasia ; Inflammation* ; Interleukins ; Mice* ; Neutrophils ; Propionibacterium acnes ; Propionibacterium* ; Stem Cells

Propionibacterium acnes, a gram-positive, anaerobic, and aerotolerant bacterium that is found frequently in the skin as part of the human microbiome causes inflammatory acne, shoulder infection, and the contamination of medical devices. The study goals were the antibiotic resistant and molecular epidemiological characterization of the P. acnes isolates in Korea. A total of 22 P. acnes isolates originated from diverse patients were obtained from three National Culture Collections for Pathogens in South Korea. The hemolytic properties and minimum inhibitory concentrations (MIC) of five antibiotics (tetracycline, doxycycline, clindamycin, erythromycin, and minocycline) were determined. Only one isolate showed high MIC values and resistance to all five antibiotics. Genotypic characterization was achieved by multilocus sequence typing (MLST) for eight loci (aroE, guaA, tly, camp2, atpD, gmk, lepA, and sodA) and repetitive-sequence-based PCR (rep-PCR) analysis using the DiversiLab kit. MLST revealed four phylogroups that were type IA₁ (27.3%), type IA₂ (18.2%), type IB (13.6%), and type II (40.9%). Rep-PCR results demonstrated three clusters that were cluster I (39.1%), cluster II (45.5%), and cluster III (13.6%). The isolates of cluster I were part of phylogroup type IA (both IA₁ and IA₂), and the isolates of cluster II belonged to phylogroup type II. All isolates of phylogroup type IB were hemolytic and belonged to cluster III. The results of rep-PCR clustering analysis showed a good correlation with those of MLST phylogroups, suggesting that rep-PCR could be an alternative method to track P. acnes subtype lineages.
Acne Vulgaris ; Anti-Bacterial Agents ; Clindamycin ; Doxycycline ; Erythromycin ; Humans ; Korea ; Methods ; Microbial Sensitivity Tests ; Microbiota ; Multilocus Sequence Typing* ; Polymerase Chain Reaction* ; Propionibacterium acnes* ; Propionibacterium* ; Shoulder ; Skin

No abstract available.
Biomarkers* ; Magnesium* ; Propionibacterium acnes* ; Propionibacterium*

No abstract available.
Biomarkers* ; Propionibacterium acnes* ; Propionibacterium* ; Vitamin D* ; Vitamins*