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PubMed1987

Antibodies to P. acnes and P. acnes exocellular enzymes in the normal population at various ages and in patients with acne vulgaris.

Total serum IgM and IgG agglutinins to P. acnes and neutralizing antibodies to P. acnes lipase, hyaluronate lyase and acid phosphatase were measured in normal individuals of different age groups. Agglutinins to P. acnes were detected in infants at 4 months of age and were present at a high level throughout life. A switch from predominantly IgM agglutinins in children, to IgG agglutinins in adults, occurred during adolescence. Anti-P. acnes lipase antibodies were present in 20% of teenagers and 17-42% of adults. Anti-P. acnes hyaluronate lyase antibodies were found in adults only (4-17%). Antibodies to acid phosphatase were not detected. Agglutinins to P. acnes were measured in individuals with mild, moderate and severe acne, and in normal controls. Only patients with severe acne had significantly higher titres than the controls. IgM and IgG agglutinins were determined in 13-14-year-olds with mild, moderate and severe acne, and in normal controls. Thirty-three per cent, 60% and 100% of the acne patients, respectively, but none of the normal controls, had predominantly IgG agglutinins. No difference in the prevalence or titre of antibodies to P. acnes exocellular enzymes was observed when patients with severe acne were compared with normal controls. There was no evidence to suggest a role for antibodies to P. acnes exocellular enzymes in the initiation of inflammatory acne.

Acne Vulgaris↗
PubMed1990

Steroid sulfatase activity in epidermis of acne-prone and non-acne-prone skin of patients with acne vulgaris.

Abnormal keratinization of hair follicles appears to be intimately associated with acne vulgaris. Whether steroid metabolism in follicular wall keratinocytes of acne-prone skin plays a role in the development and maintenance of acne vulgaris is unknown at this time. The enzymatic hydrolysis of dehydroepiandrosterone sulfate to dehydroepiandrosterone and of estrone sulfate to estrone in cultured epidermal keratinocytes has been demonstrated. Thus, we sought to establish whether steroid sulfatase activity in freshly obtained epidermal tissue (greater than 90% keratinocytes) from acne-prone skin in patients with acne vulgaris was altered when compared with that in epidermal tissue from non-acne-prone skin in the same individuals. We found that there were no differences in the rates of enzymatic hydrolysis of steroid sulfates in epidermis of acne-prone and non-acne-prone skin; however, the rate of estrone sulfate hydrolysis was two to eight times greater than that of dehydroepiandrosterone sulfate in all of the tissues evaluated in this study.

Acne Vulgaris↗
PubMed1979

Intergeneric and intrageneric inhibition between strains of Propionibacterium acnes and micrococcaceae, particularly Staphylococcus epidermidis, isolated from normal skin and acne lesions.

Two hundred and forty-one strains or resident skin bacteria comprising 93 isolates of Propionob acterium acnes and 148 of Micrococcaceae derived from 36 acne patients and 8 control subjects were screened for their ability to inhibit 32 indicator strains, including 20 strains of P. acnes and 12 strains of Staphylococcus epidermidis derived from patients with all grades of acne and from normal skin. Fifty-three strains (22%) showed some activity against at least one indicator strain. Both broad- and narrow-spectrum inhibition was detected. Inhibitory isolates of P. acnes outnumbered inhibitory Micrococcaceae by four to one. There was a low frequency of inhibition of S. epidermidis by Micrococcaceae (2.7%) and by P. acnes (1.1%) and a higher frequency of inhibition of P. acnes by Micrococcaceae (9.5%) and by P. acnes (40.8%). Furthermore, 81.8% of the subjects sampled possessed strains inhibitory to P. acnes. The significance of this finding is, as yet, unknown. No difference in the prevalence of active strains in normal (20%) and acne (22.5%) skin was detected. These findings suggest that the possession of inhibitory strains and conversely the possession of sensitive strains does not predispose to acne.

Acne Vulgaris↗
PubMed1980

Polymorphonuclear leukocyte lysosomal release in response to Propionibacterium acnes in vitro and its enhancement by sera from inflammatory acne patients.

Propionibacterium acnes cells were tested for the ability to trigger lysosomal hydrolase release from human polymorphonuclear leukocytes. Representative strains of P. acnes serotype I and II failed to stimulate lysosomal release in the absence of serum. P. acnes growth culture supernatants failed to trigger release under any test condition. Addition of fresh or heat-inactivated human serum resulted in lysosomal hydrolase release directly proportional to the number of P. acnes/PMN. Pooled sera from acne patients, with a high anti-P. acnes titer stimulated release to P. acnes. Preabsorption of this reagent with P. acnes cells reduced the anti-P. acnes titer and produced 93.37 +/- 11.49% inhibition of lysosomal enzyme release compared to unabsorbed anti-serum. Electron microscopy indicated that P. acnes was readily phagocytosed by PMNs when fresh or heated serum was present.

Acne Vulgaris↗
PubMed1995

Induction of proinflammatory cytokines by a soluble factor of Propionibacterium acnes: implications for chronic inflammatory acne.

Although many cytokines have been implicated in the development and persistence of inflammatory immune responses, it is unknown if any of these are important in inflammatory acne. This study investigated the production of the proinflammatory cytokines interleukin-8 (IL-8), IL-1 beta, and tumor necrosis factor alpha (TNF-alpha) by human monocytic cell lines, ThP-1 and U937, and by freshly isolated peripheral blood mononuclear cells from acne patients. Both Propionibacterium acnes and supernatants obtained from 72-h P. acnes cultures could induce significant concentrations of IL-1 beta, TNF-alpha, and IL-8 by both cell lines and by peripheral blood mononuclear cells as determined by enzyme-linked immunosorbent assay. There was no significant difference between acne and non-acne subjects. Endotoxin quantification and addition of polymyxin B to assays indicated no lipopolysaccharide (LPS) contamination. P. acnes supernatant was fractionated into components with molecular weights of < 3,000, < 10,000, and < 30,000 and assayed for the ability to induce IL-8 and TNF production in ThP-1 cells. Nearly 90% of the original activity was found in the < 30,000-molecular-weight fraction, 50% was in the < 10,000-molecular-weight fraction, and only 15% remained in the < 3,000-molecular-weight fraction. The effluent from the < 3,000-molecular-weight fraction contained about 70% activity, indicating that the inducing factor was not retained in the membrane. Incubation of P. acnes supernatant with various concentrations of mutanolysin or lysozyme resulted in a loss of 60% of the original activity. The addition of jimson lectin, which binds peptidoglycan, resulted in a loss of 70% of the activity in a dose-response manner, whereas peanut lectin had little or no effect on the activity. Heating of the P. acnes supernatant to 65 degrees C also had no effect on the activity. Blocking of CD14, a receptor for both LPS and peptidoglycan, reduced cytokine production by > 50%, suggesting that the soluble stimulating factor may be a secreted form of peptidoglycan-polysaccharide.

Acne Vulgaris↗
PubMed1985

Antibody titers to Propionibacterium acnes cell wall carbohydrate in nodulocystic acne patients.

In order to determine which structures in Propionibacterium acnes are most antigenic to severe acne patients, we studied the specificity of anti-P. acnes antibodies in serum from 15 nodulocystic acne patients and 5 normals. Complement fixation titers to P. acnes cell wall fractions were determined using guinea pig serum as a complement source. The mean titers of patients and normals to whole cells were 39.6 and 3 (p less than 0.1); to crude cell wall, 138 and 8 (p less than 0.01); and to protein and nucleic acid-free cell wall, 225 and 9.33 (p less than 0.001), respectively. The mean precipitin titer to P. acnes cytosol was 12.7 for patients and 0 for normals. Immunoelectrophoresis of cytosol from 8 P. acnes strains were developed with each of the 15 patient sera. A single broadly migrating anionic antigen was detected. The antigen was also present in P. acnes culture supernatants. Sephadex G-100 chromatography of cytosol revealed a single peak of antigenic reactivity at Mr = 100,000. Three patients' sera revealed a second weakly reacting antigen in the cytosol preparation. Twentyfold concentration of immunoglobulin from patient sera failed to reveal any other antigenic reactivities. The antigen was found to be resistant to nuclease, pronase, and lysozyme treatment; was precipitable with 70% ethanol; and was destroyed by sodium m-periodate--findings that are consistent with a carbohydrate structure.

Acne Vulgaris↗
PubMed1986

Pituitary function and DHEA-S in male acne and DHEA-S, prolactin and cortisol before and after oral contraceptive treatment in female acne.

Pituitary function (TRH-LHRH stimulation test) was investigated in male acne patients and serum levels of dehydroepiandrosterone sulphate (DHEA-S), sex hormone binding globulin (SHBG) and other biochemical parameters were investigated in male acne patients and in female acne patients before and after treatment with an oral contraceptive. The TRH-LHRH stimulation test was performed with 15 male patients suffering from severe cystic acne and 7 healthy volunteers. Basal and stimulated prolactin, LH and FSH levels were statistically similar in the patients and control groups. However, the stimulated LH levels of the patients were 60% higher than those in controls. SHBG levels were significantly) higher in the patient group compared to those in the control group. Thirty-three female acne patients were randomly divided into two groups and treated for six months with an oral contraceptive containing 0.030 mg ethinylestradiol (EE) plus 0.150 mg levonorgestrel or 0.150 mg levonorgestrel. After six months' treatment a 30% decrease in DHEA-S levels were observed in the desogestrel/EE group and a 15% decrease in the levonorgestrel/EE group; the difference was not statistically significant. At the same time serum total cortisol increased by 75-100% and free testosterone fell by 30-40% in both groups, whereas SHBG elevated 250% in the desogestrel/EE group and 30% in the levonorgestrel/EE group. Acne improved significantly in both groups, desogestrel/EE showing greater improvement. A decrease in SHBG and increase in DHEA-S levels appear to be the most common hormonal changes in acne. Oral contraceptive treatment induces an increase in SHBG and decrease in DHEA-S and also improves acne.

Acne Vulgaris↗
PubMed1995

Increased chemiluminescence of whole blood and normal T-lymphocyte subsets in severe nodular acne and acne fulminans.

To investigate the inflammatory and immunological aspects of severe acne, we examined the luminol-enhanced chemiluminescence of whole blood, T-cell subsets and natural killer cell functions in 11 patients with severe nodular acne and 4 patients with acne fulminans. In patients with severe nodular acne, the active phase of the disease, compared to the values in remission (means 47 mV, SD 24.8 and 32 mV, SD 8.3, p < 0.05). The patients with acne fulminans also showed high values in the active phase of the disease (mean mV 68.3, SD3.5) compared to remission (mean 30.5 mV, SD 15.3). No marked alterations were seen in the percentages of T-helper cells, T-suppressor cells or DR-positive lymphocytes or in the levels of soluble interleukin 2 receptor. The percentages and activities of natural killer cells did not show any significant changes either. Five patients (4 with severe nodular acne and one with acne fulminans, accounting for 33% of all patients) carried HLA Cw6 antigen, which is a significantly increased frequency compared to health controls (pc = 0.015). The present chemiluminescence results suggest that peripheral blood neutrophils are activated in patients with severe acne.

Acne Vulgaris↗
PubMed1978

[Sociologic studies in acne vulgaris. 1. Disease significance of acne vulgaris].

A questionnaire was presented to 2009 18--19 year old military recruitment candidates which enabled assessment of antipathy towards patients with severe acne vulgaris, the occupational handicap associated with severe acne and subjective inhibitions in acne patients. In addition, these persons were examined clinically with regard to presence of acne vulgaris. Finally, the level of education of the persons questioned was determined. The investigations show that severe acne has an appreciable disease rating. This results from antipathy of other people, the occupational inpediment and the psychological inhibitions of the acne patient. This disease rating appears to be objectively greater the lower the level of education of the acne patient. The disease rating does not appear to be entirely clear to the acne patient with a low level of education.

Acne Vulgaris↗
PubMed1983

Propionibacterium acnes resistance to antibiotics in acne patients.

The minimal inhibitory concentration (MIC) of Propionibacterium acnes in seventy-five acne patients receiving long-term antibiotic therapy demonstrated the emergence of resistant strains. The mean MIC in thirty-three patients receiving long-term tetracycline was four to five times higher than that found in control groups of acne patients not receiving antibiotic therapy and controls free of acne. The average MIC for erythromycin was more than 100 times higher in those receiving long-term antibiotic therapy. In a second group of sixty-two patients, the clinical course and number of P. acnes were correlated with the presence of "resistant strains" defined as P. acnes with a tenfold increase in MIC to tetracycline or erythromycin. Patients with resistant strains had higher counts of P. acnes and clinically were not doing as well as those with sensitive strains.

Acne Vulgaris↗
PubMed1984

Intradermal injection of Propionibacterium acnes: a model of inflammation relevant to acne.

The intradermal injection of 140 micrograms of Propionibacterium acnes (CN 6134) into the ears of female Sprague-Dawley rats produced a chronic inflammation with formation of acneiform lesions. Inflammation was characterized by more than a doubling of ear thickness at 24 h and a peak of 3-4 times control levels at day 21. At 42 days post injection ears were still 3 times normal thickness. Histologically there was early polymorph accumulation giving way to macrophages and lymphocytes by day 7. Pilosebaceous follicles overlying the inflamed area lost their sebaceous glands and became hyperplastic cords of cells that grew down and encapsulated inflammatory loci. By day 9 many of these follicles had become secondary comedones. Three isolates of P. acnes from inflammatory acne lesions and 4 of 5 isolates from non-acne patients produced results similar to that of the strain CN 6134. In these cases the number of histologically evident secondary comedones was correlated with ear thickness. In contrast, samples of Streptococcus lactis, Escherichia coli B, and Staphylococcus epidermidis failed to produce this combination of chronic inflammation and high lesion count. Benzoyl peroxide, tetracycline, erythromycin, phenidone, naproxen, and cis and trans retinoic acid were inactive as inhibitors of P. acnes CN 6134-induced ear thickening. The corticosteroid fluocinolone acetonide produced dramatic suppression of inflammation, but upon cessation of treatment the ears returned to inflamed levels. The specificity for P. acnes, the formation of acneiform lesions, and the recalcitrance of the inflammation suggest our model is indeed relevant to acne.

Acne Vulgaris↗
PubMed1980

Delayed skin test reactivity to Propionibacterium acnes correlates with severity of inflammation in acne vulgaris.

Propionibacterium acnes is the bacterial species most consistently isolated from acne lesions. Intradermal injection of a heat-killed suspension of P. acnes induced a delayed erythematous and often popular inflammatory reaction which was maximal after 24-48 h. This response was dose related and was probably mediated at least partly by immune mechanisms. In eighty-one subjects with acne of varying severity of the acne. These findings indicate that the host response to P. acnes is an important variable in determining the severity of inflammatory acne.

Acne Vulgaris↗
PubMed1978

Complement activation in acne vulgaris: in vitro studies with Propionibacterium acnes and Propionibacterium granulosum.

To better define the role of bacteria in inflammatory acne vulgaris, we have investigated the ability of four strains of Propionibacterium acnes and three strains of Propionibacterium granulosum to activate complement. Complement activation was assayed by incubating normal human serum with varying concentrations of each strain and measuring residual total hemolytic complement activity. When serum was tested unaltered, P. acnes strains were approximately threefold more potent than an equal weight of P. granulosum in consuming complement, which could reflect classical and/or alternative pathway activation. All strains also consumed complement in serum chelated with ethyleneglycol-bis (beta-aminoethyl ether)-N,N'-tetraacetic acid, which selectively assays alternative pathway activation. Incubation of unaltered serum with both P. acnes and P. granulosum resulted in immunoelectrophoretic conversion of C4, C3, and factor B of the alternative pathway. Incubation of chelated serum resulted in conversion of C3 and factor B. These data taken together suggest that both species can activate complement through either pathway. Serum incubated with P. acnes was chemotactic for polymorphonuclear leukocytes, and this chemotactic activity was largely C5 dependent as shown by antibody inhibition. It is suggested that complement activation may occur in vivo in acne, and the inflammatory response may be contributed to by the generation of C5-dependent chemotactic factors.

Acne Vulgaris↗
PubMed1990

Androgen excess in women with acne alone compared with women with acne and/or hirsutism.

Acne is known to be one of the features of hyperandrogenism. The aim of the present work was to study women with persistent acne and without other evidence of hyperandrogenism, such as hirsutism, alopecia, or irregular menses. Among 87 female patients with acne and/or hirsutism, we defined three groups: group 1 (n = 29), patients having treatment-resistant acne without menstrual disturbance, alopecia, or hirsutism; group 2 (n = 27), patients with acne and hirsutism; and group 3 (n = 31), patients with hirsutism alone. Clinical chemistry criteria for hyperandrogenism were based on elevated values of one or more of the following parameters: plasma testosterone, delta-4-androstenedione, dehydroepiandrosterone, urinary 5 alpha-androstane 3 alpha-17 beta-diol, and 17-ketosteroids (with chromatography). Plasma and urine samples were drawn between the 18th and 25th days of the cycle. Among group 1 patients, we found 25 subjects (86%) with hyperandrogenism, according to these laboratory criteria. The etiologies were: polycystic ovary syndrome (36%), adrenal hypersecretion (40%, of which 12% showed secondary polycystic ovaries), isolated increase in 5 alpha-androstane 3 alpha-17 beta-diol (20%), and hyperandrogenism without diagnosis (4%). The parameters were found to be more elevated in these patients than in a control group of 30 normal volunteer women. In groups 2 and 3, the findings were essentially the same as in group 1, except for increased levels of testosterone and the testosterone/SHBG ratio. Furthermore, it was evident that persistent acne may be an isolated sign of hyperandrogenism.

Acne Vulgaris↗
PubMed1977

Acne vulgaris: an investigation into the number of anaerobic diphtheroids and members of the Micrococcaceae in normal and acne skin.

A quantitative study was made of the microflora of 174 acne and 68 non-acne subjects. Two groups of organisms were investigated, the anaerobic diphtheroids and members of the Micrococcaceae. The results showed high numbers of both groups of bacteria in skin bearing blackheads, papules or pustules and in non-acne adolescent skin. There were significantly lower numbers of bacteria in the pilosebaceous ducts of normal looking skin in acne areas and in pre-adolescent skin when compared with non-acne adolescent skin. It is suggested that increased numbers of bacteria alone do not predispose to acne, but that their interaction with the skin, which is a function of the localized skin environment, may be important.

Acne Vulgaris↗