Characterization of Propionibacterium acnes isolates from sarcoid and non-sarcoid tissues with special reference to cell invasiveness, serotype, and trigger factor gene polymorphism

Furukawa, Asuka; Uchida, Keiji; Ishige, Yuki; Ishige, Ikuo; Kobayashi, Ichiro; Takemura, Tamiko; Yokoyama, Tetsuji; Iwai, Kazuo; Watanabe, Kunitomo; Shimizu, Shinichiro; Ishida, Noriko; Suzuki, Yoshimi; Suzuki, Takashige; Yamada, Tetsuo; Ito, Takashi; Eishi, Yoshinobu

doi:10.1016/j.micpath.2008.10.013

Cited by 52 publications

(43 citation statements)

References 27 publications

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“…A clinical isolate of P. acnes was cultured from a patient with sarcoidosis lymph node as reported previously (15). P. acnes was grown anaerobically in Schaedler broth (Sigma, St. Louis, MO) at 37 8 C and frozen at 280 8 C in 1:10 Glycerol (Fisher, Waltham, MA) in phosphatebuffered saline (Gibco, Carlsbad, CA) until administration.…”

Section: P Acnes Culturementioning

confidence: 99%

Induction of Pulmonary Granuloma Formation byPropionibacterium acnesIs Regulated by MyD88 and Nox2

Werner

Escolero

Hewlett

et al. 2017

Am J Respir Cell Mol Biol

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Sarcoidosis is characterized by noncaseating granulomas with an unknown cause that present primarily in the lung. Propionibacterium acnes, an immunogenic commensal skin bacterium involved in acne vulgaris, has been implicated as a possible causative agent of sarcoidosis. Here, we demonstrate that a viable strain of P. acnes isolated from a patient with sarcoidosis and instilled intratracheally into wild-type mice can generate pulmonary granulomas similar to those observed in patients with sarcoidosis. The formation of these granulomas is dependent on the administration of viable P. acnes. We also found that mice deficient in the innate immunity adapter protein MyD88 had a greater number and a larger area of granuloma lesions compared with wild-type mice administered P. acnes. Early after P. acnes administration, wild-type mice produced proinflammatory mediators and recruited neutrophils into the lung, a response that is dependent on MyD88. In addition, there was an increase in granuloma number and size after instillation with P. acnes in mice deficient in CybB, a critical component of nicotinamide adenine dinucleotide phosphate oxidase required for the production of reactive oxygen species in the phagosome. Myd882/2 or Cybb 2/2 mice both had increased persistence of P. acnes in the lung, together with enhanced granuloma formation. In conclusion, we have generated a mouse model of early granuloma formation induced by a clinically relevant strain of P. acnes isolated from a patient with sarcoidosis, and, using this model, we have shown that a deficiency in MyD88 or CybB is associated with impaired bacterial clearance and increased granuloma formation in the lung.

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Section: P Acnes Culturementioning

confidence: 99%

Induction of Pulmonary Granuloma Formation byPropionibacterium acnesIs Regulated by MyD88 and Nox2

Werner

Escolero

Hewlett

et al. 2017

Am J Respir Cell Mol Biol

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“…Cell viability was measured using the MTT (3 [4,5] dimethylthiazol-2, 5-diphenyltetrazolium bromide) assay as described previously (22).…”

Section: Cell Viabilitymentioning

confidence: 99%

“…Several investigators have isolated bacteria such as Propionibacterium acnes and Mycobacterium tuberculosis from the tissues of these patients. Although the role of these microbes in disease pathogenesis remains unclear (4)(5)(6), its similarities to infectious granulomatous diseases and its association with major histocompatibility (MHC) loci suggest a major role for inciting microbial triggers. Nonetheless, how specific antigen signaling might lead to such an immune response and sustained inflammation is still largely unknown.…”

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confidence: 99%

Dysregulation of p38 and MKP-1 in Response to NOD1/TLR4 Stimulation in Sarcoid Bronchoalveolar Cells

Rastogi¹,

Du²,

Ju³

et al. 2011

Am J Respir Crit Care Med

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Rationale: Sarcoidosis is a systemic inflammatory disorder characterized by distinct up-regulation of Th1 cytokines, such as tumor necrosis factor (TNF)-a and IL-12. The mechanism underlying this up-regulation remains unclear. Recognition of microbial moieties through Toll-like or Nod-like receptors evokes sequential activation of mitogen-activated protein kinases (MAPKs), which plays a role in Th1-immune response. Objectives: To test the hypothesis that dysregulation in MAPK signaling in response to microbial stimulation is important in mediating Th1 response in sarcoidosis. Methods: Ex vivo cultured bronchoalveolar lavage (BAL) cells isolated from patients with sarcoidosis and control subjects were stimulated with low-dose Toll-like receptor 4 (TLR4) and nucleotide-binding oligomerization domain 1 (NOD1) ligands as a model of microbial stimulation, and MAPK signaling and inflammatory response were analyzed. Measurements and Main Results: BAL cells from patients with sarcoidosis exhibited higher basal p38 activity, greater p38 phosphorylation, and more robust production of TNF-a and IL-12/IL-23p40 on stimulation with NOD1 and TLR4 agonists than cells isolated from control subjects. In contrast, control BAL cells had greater basal extracellular signal-regulated kinase (ERK) activity and NOD1 and TLR4 agonists preferentially activated the ERK pathway. Inhibition of p38, but not ERK, attenuated production of both IL12/IL23p40 and TNF-a. Interestingly, stimulation of cells from patients with sarcoidosis with either NOD1 or TLR4 ligand failed to induce MAPK phosphatase 1 (MKP-1). Adenovirus-mediated overexpression of MKP-1 attenuated p38 activation and decreased the production of IL12/IL23p40 and TNF-a in sarcoid BAL cells. Conclusions: Our results suggest that enhanced p38 signaling in response to microbial products is caused by abnormal regulation of MKP-1 and contributes to heightened inflammation in sarcoidosis.

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“…A number of genes have been associated with the virulence of P. acnes (20,35), including two invasion-associated proteins (PAmce and Pap60) and four predominant immunoreactive surface proteins (PA-25957, PA-5541, PA-21293 and PA-4687), the first two of which have homology with M-like protein of Streptococcus equi and have dermatan sulfate-binding activity, while the other proteins are similar to the product of the Corynebacterium diphtheriae htaA gene, which codes for an ironregulated hemin binding protein. We used the previously reported primers to amplify and sequence internal fragments of PAmce and Pap60 (35) and designed primers to amplify and sequence fragments of each gene of these putative virulence determinants from a selection of P. acnes strains isolated in this study.…”

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confidence: 99%

Propionibacterium acnes and Staphylococcus epidermidis Isolated from Refractory Endodontic Lesions Are Opportunistic Pathogens

Niazi

Clarke

et al. 2010

J Clin Microbiol

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The predominant cultivable microbiota from 20 refractory endodontic lesions (9 with abscesses and 11 without abscesses) were determined, and Propionibacterium acnes and Staphylococcus epidermidis were among the most predominant organisms. The number of species identified from lesions with abscesses (14.1 ؎ 2.6) was significantly greater (P < 0.001) than the number from lesions without abscesses (7.4 ؎ 5.9). Comparison of perioral isolates using repetitive extragenic palindromic PCR of the same species from the same subjects demonstrated that the endodontic and skin populations were significantly different. The P. acnes isolates were typed on the basis of recA gene sequence comparison, and only three types (types I, II, and III) were identified among 125 isolates examined. However, we found that type I (type IA and IB) isolates were primarily isolated from the skin, while types II and III were significantly more likely to be isolated from the endodontic lesions (P < 10 ؊10 ). We found that the robustness of the recA phylotypes was not strong by comparing the partial gene sequences of six putative virulence determinants, PAmce, PAp60, PA-25957, PA-5541, PA-21293, and PA-4687. The resulting neighbor-joining trees were incongruent, and significant (phi test; P ‫؍‬ 2.2 ؋ 10 ؊7 ) evidence of recombination was demonstrated, with significant phylogenetic heterogeneity being apparent within the clusters. P. acnes and S. epidermidis isolated from refractory endodontic infections, with or without periapical abscesses, are likely to be nosocomial infections.Propionibacterium acnes and coagulase-negative staphylococci, including Staphylococcus epidermidis, have been identified among the microflora of endodontic infections (8,12,40,50,52,55,56,63,64), but their importance as endodontic pathogens has largely been ignored due to their nearly universal presence on the skin and the consequent likelihood of sample contamination. However, there is now considerable evidence that these organisms are increasingly isolated from human infections, and so their association with endodontic infections requires clarification. P. acnes, a non-spore-forming, Gram-positive anaerobic or aerotolerant rod, is a member of the resident microflora of the large intestine, conjunctiva, and external ear canal (10, 15) and accounts for approximately half of the total skin microbiota (59), predominating over other pilosebaceous flora (16,39). Although traditionally considered to be relatively nonpathogenic, an increasing number of studies have implicated P. acnes as an opportunistic pathogen responsible for a wide range of infections and inflammatory conditions. In addition to its well-established role in the pathogenesis of acnes vulgaris (16, 34), it has also been linked to synovitis-acnes-pustulosis-hyperostosis-osteitis syndrome (44, 54), sarcoidosis (17), and prostate cancer (14). Recent studies have revealed trauma and surgery as the predisposing factors associated with numerous P. acnes infections, which include brain abscesses (36), osteomyelitis ...

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Characterization of Propionibacterium acnes isolates from sarcoid and non-sarcoid tissues with special reference to cell invasiveness, serotype, and trigger factor gene polymorphism

Cited by 52 publications

References 27 publications

Induction of Pulmonary Granuloma Formation byPropionibacterium acnesIs Regulated by MyD88 and Nox2

Induction of Pulmonary Granuloma Formation byPropionibacterium acnesIs Regulated by MyD88 and Nox2

Dysregulation of p38 and MKP-1 in Response to NOD1/TLR4 Stimulation in Sarcoid Bronchoalveolar Cells

Propionibacterium acnes and Staphylococcus epidermidis Isolated from Refractory Endodontic Lesions Are Opportunistic Pathogens

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