Common anti-bacterial preps used in the operating room may not provide sufficient efficacy for skin eradication compared to other common skin flora [ 7 ]. Inflammatory makers including CRP, ESR, white blood cell count, and even IL-6 have all shown poor sensitivity and specificity for the detection of infection [ 27 , 30 , 32 ].
A low index of suspicion for P. It is crucial that institutional microbiology labs are notified to hold aspiration and operative cultures for an extended period of time as it may take up to 21 days for a culture to become positive with P. Traditionally, the penicillin family of antibiotics have been utilized to assist in infection eradication [ 42 ]; however, some advocate coverage with two differing agents to help prevent resistance in addition to covering polymicrobial infection [ 31 ].
There is a paucity in the literature regarding long-term functional outcomes and success of the eradication of P. More research is needed to elucidate optimal antibiotic coverage and duration, one vs.
This article does not contain any studies with human or animal subjects performed by any of the authors. David Saper, Email: moc.
Nina Capiro, Email: moc. Richard Ma, Email: moc. Xinning Li, Phone: , Email: moc. National Center for Biotechnology Information , U. Curr Rev Musculoskelet Med.
Published online Jan Author information Copyright and License information Disclaimer. Corresponding author. This article has been cited by other articles in PMC. Abstract Propionibacterium acnes P. Introduction Shoulder pain and associated pathologies are among the most common complaints presenting to an orthopedic office [ 1 ]. Organism and structure P. Open in a separate window. Table 1 Studies that show percentage of positive P.
Study Type of surgery No. Diagnosis of P. Management of P. Outcomes of P. Conclusion P. Human and Animal Rights and Informed Consent This article does not contain any studies with human or animal subjects performed by any of the authors. Contributor Information David Saper, Email: moc. American Academy of Orthopaedic Surgeons. Increasing incidence of shoulder arthroplasty in the united states. J Bone Joint Surg Am. Prevalence and projections of total shoulder and elbow arthroplasty in the United States to J Should Elbow Surg.
Deep infection after rotator cuff repair. Revision shoulder arthroplasty with positive intraoperative cultures: the value of preoperative studies and intraoperative histology. Propionibacterium acnes colonization of the human shoulder. Efficacy of surgical preparation solutions in shoulder surgery. The taxonomic position of Corynebacterium acnes. J Bacteriol. The skin microbiome. Nat Rev Microbiol. Studies on the cytotoxic effects of Propionibacterium acnes strains isolated from cornea.
Microb Pathog. Susceptibility of Propionibacterium acnes to killing and degradation by human neutrophils and monocytes in vitro. Infect Immun. Bruggemann H. Insights in the pathogenic potential of Propionibacterium acnes from its complete genome.
Semin Cutan Med Surg. Perry A, Lambert P. Propionibacterium acnes: infection beyond the skin. Expert Rev Anti Infect Ther. Incidence of acute postoperative infections requiring reoperation after arthroscopic shoulder surgery.
Am J Sports Med. Periprosthetic infections after total shoulder arthroplasty: a year perspective. Periprosthetic infections after shoulder hemiarthroplasty. Reverse total shoulder arthroplasty: a review of results according to etiology. Infection after shoulder arthroplasty. Clin Orthop Relat Res. Prognostic factors for bacterial cultures positive for Propionibacterium acnes and other organisms in a large series of revision shoulder arthroplasties performed for stiffness, pain, or loosening.
Management of early deep infection after rotator cuff repair surgery. Sensitivity of frozen section histology for identifying Propionibacterium acnes infections in revision shoulder arthroplasty. The management of infection in arthroplasty of the shoulder. J Bone Joint Surg Br ; 86 1 —9. Infection after mini-open rotator cuff repair.
Propionibacterium acnes postoperative shoulder arthritis: an emerging clinical entity. Clin Infect Dis. Positive culture rate in revision shoulder arthroplasty. Management of deep postoperative shoulder infections: is there a role for open biopsy during staged treatment? J Shoulder Elbow Surg. Management of chronic deep infection following rotator cuff repair.
Biofilm formation by Propionibacterium acnes is a characteristic of invasive isolates. Clin Microbiol Infect. Cyanoacrylate microbial sealant may reduce the prevalence of positive cultures in revision shoulder arthroplasty. Propionibacterium acnes infection after shoulder arthroplasty: a diagnostic challenge.
Arthroplastic and osteosynthetic infections due to Propionibacterium acnes: a retrospective study of 52 cases, — C-reactive protein, erythrocyte sedimentation rate and orthopedic implant infection. In a submitted their work to the issue. Dekio et al. McDowell, S. Patrick, and L. Albert, J. Sorensen, B. Christensen, and C. Zappe, S. Graf, P. Ochsner, W. Zimmerli, and P. Sendi, Journal, vol.
Clayton, W. Baig, G. Reynolds, and J. Arnell, K. Cesarini, A. Lagerqvist-Widh, T. Wester, and J. Perry and P. Levy, S. Lyer, E. Atoun et al. Valanne, G. Ramage et al. McDowell, A. Perry, P. Lambert, and S. Lomholt and M. McDowell, E. Barnard, I. Nagy et al. Fitz-Gibbon, S. Furthermore, a parallel proposal that the genus Propionibacterium should now be divided into four genera based on whole genome analysis and consideration of isolation source has also been made, with the cutaneous propionibacteria being reclassified within the new genus Cutibacterium [ 25 ].
This proposal has, however, proved controversial for a number of reasons [ 33 ], and also did not accommodate the subspecies proposals due to the overlapping timeline of the publications; very recently, the latter issue has been corrected [ 34 ].
For the purposes of this current review, and to prevent any confusion, we have decided to still use Propionibacterium which it is still valid to do [ 33 ] until the new genus name is broadly adopted by the wider medical microbiology community. The disease has a multifactorial aetiology and is triggered initially during adrenarche in susceptible individuals, and can be mild to very severe with respect to symptoms [ 36 ]. Furthermore, for a growing number of individuals, particularly females, the condition can continue, or occur for the first time, in adulthood [ 37 ].
Although not life-threatening, acne can have profound social and psychological effects, which are frequently more significant when symptoms are severe and scarring occurs. In relation to acne pathogenesis, the perceived wisdom has always been that the condition develops within a follicle as a result of four main events: 1 androgen-induced hyperseborrhoea, 2 follicular hypercornification, 3 colonisation and proliferation of P. These changes then cause a normal follicle or pore to evolve into an invisible subclinical precursor lesion known as a microcomedo, which then progresses to a non-inflammatory open and closed comedones and inflammatory lesion papule, pustule or nodule.
While comodogenesis was once thought to precede the inflammatory phase of lesion development, this view has now changed with evidence that inflammation may play a fundamental role in the development of microcomedone lesions, even before keratinocyte proliferation [ 39 ].
Evidence for a role in the pathogenesis of inflammatory acne is therefore circumstantial, and primarily based on the observation that antimicrobial treatments are efficacious for the resolution of symptoms Figure 3. Furthermore, non-response to antibiotic treatment is commonly associated with the presence of antibiotic-resistant strains, thus negating the argument that the effects of antibiotics are solely due to their anti-inflammatory activity [ 40 ].
In addition, it has been shown that patients with severe forms of acne have higher antibody titres to the bacterium compared to healthy controls [ 41 ]. A year-old adolescent boy who presented with moderate inflammatory and non-inflammatory acne lesions A. Despite these observations, our understanding of how P. In particular, skin surface concentrations of Propionibacterium do not differ between individuals with and without acne, and within follicles there does not appear to be any correlation between levels of the bacterium and the degree of inflammation [ 43 ].
Furthermore, some lesions are inflamed, yet show no evidence of viable bacterial colonization highlighting the importance of other factors in the initiation of the condition, such as altered sebum composition; notably, not all patients with acne display hyperseborrhoea [ 36 ]. In contrast, direct visualisation of P. Furthermore, highly complex P. A further example of the changing views on the pathophysiology of acne can be seen with the recent suggestion that little evidence actually exists for follicular keratinocyte hyperproliferation in acne lesions versus autologous healthy hair follicles, and that alternate mechanisms may exist for infundibular hyperkeratinisation [ 45 ].
Collectively, such results serve to highlight the complicated and multifactorial nature of the disease process underlying acne and the challenges facing researchers, including fully elucidating the role played by P. While the role of inflammation in the later stages of acne has been well accepted, it has become increasingly clear that the inflammatory process occurs much earlier in the evolution of the acne lesion and is not a secondary event [ 46 ].
The observation of inflamed lesions in the absence of bacteria would suggest that while P. The strong immunostimulatory nature of P. The bacterium also produces lipases which facilitate breakdown of sebum carbon source , a complex of different lipid types, into free short chain fatty acids SCFAs which are pro-inflammatory [ 52 ]. The capacity to elicit an inflammatory response from the host is mediated via pattern recognition receptors on antigen presenting cells, such as Toll-like receptors TLR 2 and 4 [ 53 ], and nucleotide oligomerization domain NOD -like receptors [ 54 ], as well as damage-associated molecular patterns [ 55 ].
Of particular note is the observation that P. In addition, P. Over the last decade, the development of various molecular typing methods for P. Such studies have breathed new life into acne research and proved important in helping to address the issue of why P. Furthermore, identification of specific lineages associated with a disease state also ensures that the correct strains are utilised when trying to determine mechanisms of pathogenicity, especially in relation to host interactions.
One issue that has complicated epidemiological investigations has been the use of various skin sampling techniques swab, scrape, tape stripping, cyanoacrylate gel biopsy which target different microbial populations e. Also, analysis of only a single isolate, while potentially identifying a dominant clonal lineage within a sample, may also miss other phylogroups present. Yet, despite these methodological issues, several independent culture-based studies have found that acne is strongly associated with strains from the type IA 1 and IC clades, while those from the type IA 2 , IB, II and III phylogroups are much more frequently associated with skin health and other types of opportunistic infections and conditions [ 10 , 11 , 21 , 22 , 27 , 62 ].
Analysis of the P. Association of P. Data was analysed from the current MLST 8 isolate database. One other interesting observation from the MLST 8 isolate database is that type III strains are the only phylogroup that have never been cultivated from acneic regions of the skin, at least to date, but have been found on normal skin primarily the back Figure 5 and more recently have been linked to the skin condition PMH [ 10 , 11 ], thus suggesting they may not be true commensal bacteria.
While isolates from other phylogroups have been recovered from acneic skin IA 2 , IB, II the rates of recovery are low; these phylogroups may, however, still prove clinically relevant to the condition in some instances thereby challenging the view of highly distinct acne- and non-acne-associated phylogroup lineages [ 63 , 64 ].
As we have proposed previously, the apparent loss of phylogroup diversity in acne and the dominance of type IA 1 strains may reflect a dysbiotic shift within a follicle as microenvironmental changes lead to lesion formation [ 27 ]; alternatively, it could mean that certain individuals already lack P.
Principal component analysis PCA plot of P. Data is from the MLST 8 isolate database. Using the presence or absence of an allele at each specific gene locus as a separate coordinate, each ST is represented here as a point in a dimensional space. Note: phylogroup III has never been associated with acne.
Within these CCs, the founding genotypes ST1, ST3 and ST4 appear particularly dominant lineages associated with acne Figure 6 B , but are also part of the normal skin microbiota as well as globally disseminated. Data was analysed from the MLST 8 isolate database. This study again highlighted that the clonal composition of surface skin may not always reflect the composition of the sebaceous follicle.
A 16s rDNA-based metagenomics approach for the study of P. Such an approach offers distinct advantages to traditional culture-based methods that may be unintentionally biased towards the isolation of specific strain types. This study largely focused on sampling the pre-lesional follicular microbiome on the nose of subjects where lesions are normally not present , so as to minimise any variation due to skin site differences. Amplification and cloning of 16s rDNA from the pilosebaceous units of 49 patients with acne, and 52 normal controls, followed by Sanger sequencing of nearly full length sequences, revealed P.
While no statistically significant difference was found in the relative abundance of P. Skin strain differences between acne and healthy subjects based on the study and data of Fitz-Gibbon et al. Furthermore, a subset of type II ribotypes RT6 revealed a statistically significantly enrichment in healthy skin Table 1. Despite differences in sampling approaches and methodology used, and problems with detailed comparison of the results obtained from ribotyping and MLST due to a lack of equivalency in resolving power the 16S locus is very highly conserved with only a small number of type-specific SNPs [ 27 , 67 ], the data from the 16S rDNA metagenome generally matches those from culture-based MLST investigations with respect to the association of specific type IA 1 CCs with acne Table 1 [ 21 , 22 , 27 ].
One explanation for this discrepancy may reflect the fact that RT1 is also representative of CC5 strains type IB which are not acne-associated but common on normal skin, potentially skewing the results for the control population. Strains from the type IA 2 lineage, not found to be acne-associated by culture-based MLST analyses [ 21 , 22 , 27 ], were also not associated with the condition based on 16S rDNA metagenomics and were more frequent on normal skin, although this did not quite meet statistical significance Table 1 [ 66 ].
An interesting observation that arose from this metagenome study was the association of the type II genotype RT6 with healthy skin; this ribotype corresponds to CC6. Apart from the ST26 lineage, however, STs from this CC have also been cultivated from clinical samples, including prostate tumours, prosthetic joint infections, corneal scrape and blood samples [ 27 ].
Furthermore, type II STs from CC72, which were previously described only in association with healthy skin based on MLST analysis [ 22 ], have now also been isolated from clinical specimens, although their exact relevance is unknown in these contexts. These associations would tentatively suggest a potential role for type IIs in skin health, but also a capacity to cause opportunistic infection under the correct circumstances; such potential causal effects will, however, require further studies for confirmation.
It was also very interesting to note that type II RT2 strains, although not statistically associated with acne, were approximately equal in abundance on the skin of acne patients versus controls based on the percentage of clones , but yet appear infrequently isolated from acneic skin based on earlier culture-based studies [ 21 , 22 , 27 ]. This could potentially reflect ethnic differences in the populations sampled and the grade or severity of the condition [ 65 ].
Also, IFM analysis of skin biopsy samples with monoclonal antibodies MAbs has shown the presence of both type IA and type II within the sebaceous follicles of both acne and control subjects, with evidence that type II is more predominant upon semi-quantitative analysis of selected samples [ 44 ]. In a follow-up study from the same group, Barnard et al. From a population genetic perspective, RT4, RT5 and RT8 were again found to be more abundant and prevalent in acne patients, while RT6 was more prevalent in healthy individuals.
Some new observations from this study were the increased levels of P. A positive correlation between P. Of most interest was data demonstrating that the population genetic composition of P. The widespread use of oral and topical antibiotics to treat acne, and other chronic skin conditions like rosacea where P. This resistance is primarily mediated via mutations within the rRNA operon; P. Other mechanisms of resistance include the presence of the erm X gene which is located on a mobile genetic element [ 71 ].
Early attempts to understand the relationship between antibiotic resistance and specific P. This provided evidence that different resistance genotypes were distributed throughout Europe among patients with acne and other infection types. Furthermore, a clonal distribution was observed for strains carrying the 16S rRNA SNP associated with tetracycline resistance, while no correlation was found between genotype and 23s RNA SNPs conferring resistance to clindamycin and erythromycin.
In particular, the ST3 lineage RT4 appears overrepresented in many of these studies, being associated with high level resistance to tetracycline, erythromycin and clindamycin. Furthermore, resistant forms of this genotype have been found worldwide Figure 7 B and can also be found on the skin of healthy individuals who have not been treated with antibiotics, indicating its circulation within the human population [ 22 ].
Another interesting observation from these molecular epidemiology studies has been the association of antibiotic resistance with the type IC clade [ 22 ]. While only a small number of these strains have been described, they have so far all contained SNPs in both the 16S and 23S rRNA genes associated with tetracycline and MLS antibiotic resistance [ 22 ].
Further studies will, however, be required to determine whether antibiotic resistance is a defining characteristic of this phylogroup. While originally isolated from patients with acne, this clade has now also been recovered from normal skin [ 75 ]. Resistance has also been identified in strains from the type IA 2 , IB and II phylogroups, but at much smaller rates [ 22 , 63 , 64 , 74 ]. Association of antibiotic resistance with P. Countries to date in which inter-continental spread of multi-resistant forms of the ST3 lineage CC3 of P.
The first P. Since then, over complete and draft genome sequences are now available for the bacterium. The average genome size is 2. Circular map of the KPA genome. Initial analysis of the KPA genome sequence revealed the pathogenic potential of the organism, with many features that help to explain its lifestyle adaptions and capacity to induce inflammation and tissue damage [ 76 ]. These contiguous stretches, which are generated via slipped strand mispairing, are signatures of antigenic or phase variation thus modulating interaction of the bacterium with the host.
WGS analysis has provided important insights into the pathogenic potential of P. The historic view that P. With the growing number of multiple whole genome sequences of P.
The P. Analysis of 82 genome sequences has shown the total length of noncore regions to be approximately 0. Most importantly, the island-like regions which contribute to this flexible gene pool encode a range of putative virulence determinants and fitness factors [ 80 ].
Of particular interest are a small number of genetic elements, designated genomic loci 1, 2, 3 and 4, that are present in specific acne-associated lineages and, therefore, may prove to be important in acne pathogenesis [ 66 , 68 , 79 , 80 ] Figure 9.
Clustering of noncore genomic regions present in 82 P. Rows represent genomes, and columns represent noncore regions that are longer than bp. The presence of a noncore region is coloured in yellow, and the absence is coloured in blue. Taken from Tomida et al. Briefly, genomic locus 1 contains prophage-related genes, while genomic locus 2 CC3; RT4 and RT5 spans over 20 kb and encodes 23 ORFs, including a cluster of Streptolysin S-associated genes sag which are involved in the biosynthesis and transport of a bacteriocin.
Other genes present in this locus include those with putative roles in virulence, cell viability and self-immunity. Locus 3 CC1, CC2, CC3, CC is present on a 55 kb linear plasmid that encodes a tight adhesion TAD locus with homology to the tight adherence genes of Aggregatibacter actinomycetemcomitans , and which may be important for host colonization. Subsequent metagenomic studies have confirmed a higher relative abundance and prevalence of all three loci in acne patients versus healthy controls; indeed, locus 2 appears rarely found in the microbiome of healthy skin [ 68 ].
This locus encodes a series of nonribosomal peptide synthetases that may enhance pathogenicity, as well as genes involved in the synthesis of a cyclic lipopeptide. Genomic analysis of a small number of CC1 isolates from acneic and healthy follicles has also shown no differences in group-specific genes, plasmid content or sequences that may affect gene expression promoters and homopolymeric tracts [ 65 ]; this therefore highlights the importance of the host response as a contributing factor in the development of acne.
In relation to other phylogroups, type IA 2 strains RT3 and RT16 appear to have fewer non-core regions which may reflect a lack of rearrangement hot spot family proteins which function in genomic rearrangements [ 67 ].
The type IB phylogroup, which is a tight phylogenetic cluster, also contains a genomic region that appears to be a cryptic prophage [ 78 ]. This island has been inserted into a gene for a type II restriction enzyme, with the resulting gene fragments flanking the region. Type IB strains, and the aberrant type IA strain SK, also contain an island with a region encoding a thiopeptide antibiotic, which targets Gram-positive bacteria [ 78 ].
The large type II phylogroup also displays several genomic differences when compared to type I strains, including the deletion of genes involved in iron uptake which may impact on survival under low iron conditions; this region is also missing from type IC strains [ 77 ]. Inspection of genome sequences for type II strains has also identified insertions and deletions in putative lipase genes compared to type I strains, which may help to explain previous reports of reduced lipase activity within this group and their lack of association with acne [ 67 ].
As type III strains have never been recovered from acneic skin, comparative analysis of their noncore regions to acne-associated strains could prove valuable to filter and identify genes and genetic elements that may be relevant to acne virulence and skin health. Analysis of four publicly available type III genomes has shown the presence of eight noncore regions specific to this phylogroup, and a further two regions which are present in three of the four genomes [ 10 ].
These regions contain ORFs with putative functions in transcriptional regulation and transport, metabolism, phage proteins and hypotheticals. One interesting observation was the presence of a region containing putative type III secretion system T2SS genes in close proximity to a putative tight adherence Tad locus, although unrelated to the plasmid Tad locus described in type IA 1 strains associated with acne [ 66 ].
For more detailed analysis of indels within P. Within type I and III phylogroups, however, only remnants or fragments of the system exist due to partial deletion events [ 80 , 81 ]. Interestingly, sequence analysis of CRISPR spacers among multiple type II strains has revealed previous challenges with genomic loci 2 and 3, present in a subset of type I strains, as well as P.
The results from this analysis are consistent with phylogenetic relationships based on whole genome SNP clustering [ 67 ]. The presence of HPTs in P. Using 90 genomes spanning the known diversity of P. A correlation between repeat variation and different clades was observed, indicating HPT changes are uncommon and relatively stable, thus accumulating over a long time frame.
HPT variation effected gene expression, highlighting how these sequences could influence the functional activity of the different phylogroups, and the expression of genes associated with putative virulence factors.
These may prove important in the context of acne. While inspection of the genome provides some insight into potential functional differences between phylogroups in the context of health and disease, it provides no information regarding variation at the transcriptional and translational levels.
To address this issue, several studies have also compared differences between the major genetic divisions of P. Differences at the transcriptome level between strain types representing acne- and non-acne associated phylogroups has been described by Brzuskiewicz et al. After growth in brain heart infusion broth BHI , comparison of the KPA transcriptome with the type IA 1 strain pleuropulmonary infection; ST20, CC1 revealed differential expression of common genes during mid-log phase.
A putative haemolysin PPA and the immunoreactive iron acquisition protein htaA PPA were also found to be upregulated in ; in the latter case this may be important for survival and growth in iron limited conditions. Other expression differences which were observed between these distinct lineages related to energy metabolism and protein biosynthesis with strain possessing an extended anaerobic metabolic versatility for fermentative pathways that utilise amino acids.
Differential and global RNA-seq analysis has also revealed pervasive transcription within KPA, with an extensive array of riboswitches, leaderless mRNAs, small non-protein-coding RNAs and vegetative promoters in gene regulation, although how these differ between phylogroups in relation to expression profiles associated with disease is currently not clear [ 83 ].
Whole cell proteomic profiling of P. Using a type IB strain that could grow under different oxygen tensions, or in its absence, this study also showed that protein expression under anaerobic or microaerophilic conditions was similar, but distinct from that produced during aerobic growth.
More generally, this study highlighted clear differences between the major genetic divisions in terms of their proteome. Proteomic comparison of the secretome mid-exponential phase from P. A set of 20 proteins was found to be produced by the majority of the strains tested, and eight proteins by all the strains. These differences, especially in relation to differential production of GehA, DsA1 and DsA2 proteins, may be particularly relevant in the context of acne pathogenesis.
Furthermore, some cells derived from a clonal strain did not show any reactivity tentatively indicating within strain phase variation in expression. We can speculate that the potential for type IAs to modulate their interaction with the host immune system via the DsA immunogenic proteins may be important in the recurring nature of acne.
Interestingly, all phylogroups tested in the study by Holland et al. Of particular note was the observation that CAMP factor 1 protein production was not detected, even though previous Western blotting experiments with anti-CAMP factor sera revealed that this protein is produced in abundance by type IB and type II strains after anaerobic growth on blood agar [ 30 ]; interestingly, significant expression levels of the CAMP factor 1 gene have also been observed in KPA during exponential phase growth [ 78 ].
Intriguingly, although produced in large amounts by types IB and II, which are not considered to be important in acne pathogenesis, the CAMP factor 1 protein was observed in sebaceous follicles of both acne and healthy controls, although its significance here is not yet known [ 44 ]. Furthermore, a recent study has also demonstrated that CAMP factor 1 recognises TLR-2 and stimulates IL-8 production which indicates it may play a role in the inflammatory response to the bacterium [ 87 ] see Section 3.
Differences between studies in regard to CAMP factor production may reflect variation in the growth conditions used broth vs solid media. While it is not clear what exact role, if any, the CAMP factor family play in acne, the differential production of the proteins between phylogroups warrants further studies to better understand their importance.
In a follow-up transcriptomic and biochemical investigation of this observation, Nazipi et al. In the context of disease, the HLY of type IB and II strains may be important for degradation of glycoaminoglycans within dermal and epidermal extracellular matrix, facilitating tissue spread and bacterial dissemination.
Type IB and II strains appear more frequently associated with soft and deep tissue infections, although their clinical relevance in such circumstances is not always clear [ 27 ]. In contrast, in acne the incomplete degradation of HA by type IA 1 strains may result in the production of pro-inflammatory LMW fragments after comedone rupture and exposure of the underlying dermis [ 88 ]. These fragments could activate macrophages and dendritic cells via Toll-like receptor 2 and 4 signalling [ 89 , 90 ].
Further proteomic studies by Yu et al. Organisms were grown in reinforced clostridial media before mass spectrometry analysis. Secreted and cell wall protein concentration data is taken from the study of Yu et al. Consistent with previous studies, DsA1 and DsA2 were found to be produced by type IA strains only, although variability in secreted and cell wall production between type IA 1 CCs was observed Figure CAMP factor 2 was secreted by all phylogroup strains examined, especially type III, although some also appeared cell wall-associated Figure CAMP factor 1 was produced in much greater amounts both secreted and cell wall-associated by type II compared to CC1, consistent with that described by Valanne et al.
Although not described in previous proteomic and transcriptomic studies, biochemical analysis has also found that P. On the basis of data from Lomholt and Kilian [ 21 ], this activity appears confined to organisms from the type IA phylogroup only type IC not described , but data from Niazi et al.
These enzymes could function as putative virulence factors, and may also use the cleaved sialic acid as a carbon source. The production of porphyrins is also enhanced with vitamin B 12 supplementation [see Section 3.
Porphyrin levels are higher in acneic versus healthy skin, but are reduced in patients who positively respond to treatment [ 94 ]. At the intraspecies level, differences between acne- and non-acne-associated ribotypes in the production of porphyrins have recently been described [ 95 ]. Furthermore, a repressor gene of porphyrin biosynthesis deoR was identified, and was found to be present in all RT2 and RT6 strains but not in acne-associated RT4 and RT5.
While the latter is consistent with types IB and III not being associated with acne, it suggests that acne-associated type IC strains may also not produce these metabolites. A summary of the key virulence determinants that collectively may help to explain the association of type IA 1 strains with acne is highlighted in Figure Summary of key virulence determinants expressed by type IA 1 strains that, collectively, may help to explain, alongside host response, their dominant association with acne versus other phylogroups.
Data is compiled from genomic, proteomic, transcriptomic and biochemical studies. A key aspect of acne research has been understanding how P. While it is well known that P. One of the first studies to investigate the effect of different phylogroups types IA 1 , IB, II on the innate immune response of human epidermal keratinocytes was carried out by Nagy et al.
The type IA 1 strain also appeared capable of enhancing keratinocyte growth in vitro. In a follow-up study, the effect of these strains on immortalised sebocytes SZ95 was also investigated [ 29 ]. While these studies clearly illustrate the capacity of different P. These explants were treated with membrane-fraction lysate and the results compared to an LPS-treated control.
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