Biomedical subjects

A Brauner

Publications and source records attributed to A Brauner.

At least 19 recordsLinked to original sources

PubMed2005

Virulence characteristics of Escherichia coli strains causing acute cystitis in young adults in Iran.

BACKGROUND: Escherichia coli strains that cause cystitis posses virulence properties that facilitate their colonisation and persistence in the bladder. In Iran, despite the high number of the urinary tract infections, very few studies has been done to determine the role of these virulence properties in the pathogenesis of E. coli cyctitis. PATIENTS AND METHODS: Eighty-seven strains of E. coli, isolated from young adults with cystitis in Shiraz, Iran, were examined for the expression of type 1 and P-fimbriae, mannose resistant haemagglutination, haemolysin production, aerobactin-mediated iron uptake, O:K serotypes, biochemical phenotypes (BPTs) and their antibiotic susceptibility patterns. RESULTS: Seventy-six percent of the strains expressed multiple virulence properties. There was a significant correlation between the presence of aerobactin and the expression of type 1 fimbriae. All P-fimbriated strains produced aerobactin with 50% of them also coexpressing haemolysin. Of the 29 different O:K serotypes identified, 42% belonged to serotypes not commonly found among European serotypes associated with UTI. Strains of O groups 4 and 6 expressed more virulence factors than the others. A high resistance against ampicillin, trimethoprim and cotrimoxasol was observed among the isolates with 53% of the isolates showing multiresistance to these three antibiotics. Certain BPTs were also found among O:K serotypes with some containing strains of the same virulence profile. CONCLUSION: We conclude that certain colonal groups of E. coli are commonly associated with cystitis in young adults in Iran with strains possessing a combination of aerobactin and type 1 fimbriae being the dominant ones and belonging to serotypes not commonly found in Europe. We also conclude that the multiple antibiotic resistant E. coli strains causing cyctitis are highly prevalent in this part of the country.

Acute Disease↗

PubMed2003

Enhanced chemokine response in experimental acute Escherichia coli pyelonephritis in IL-1beta-deficient mice.

The aim of the present study was to investigate the effects of IL-1beta and Escherichia coli on the expression and secretion of MIP-2, the mouse equivalent to human IL-8, MCP-1 and RANTES in the kidneys of mice with acute pyelonephritis. Female Bki NMRI, as well as IL-1beta deficient mice and their wild-type littermates, were transurethrally infected with either E. coli CFT 073 or injected with NaCl 0.9% (w/v) and thereafter obstructed for 6 h. The Bki NMRI mice were killed at 0, 24, 48 h and 6 days and the IL-1beta-deficient mice at 48 h. Chemokine mRNA and protein levels peaked at 24 h for the tested chemokines with the mRNA expression localized in the tubular epithelial cells and for MIP-2 also in neutrophils. Obstruction per se, also induced a chemokine expression similar to E. coli infection although at a lower level. Interestingly, MIP-2 levels were higher in the IL-1beta deficient mice as compared with the wild-type littermates. Likewise, the inflammatory changes were more frequent and, when present, more widespread in the IL-1beta-deficient mice than in the wild-type mice. Stimulation of a human renal tubular epithelial cell line (HREC), A498 and of primary human mesangial cells (HMC) with the same bacterial antigen depicted gene expression of the same chemokines. A rapid release of IL-8 and MCP-1 was observed from both cell types. RANTES response was delayed both in the HREC and the HMC. We conclude that acute E. coli pyelonephritis induces a MIP-2/IL-8, MCP-1 and RANTES expression and secretion localized primarily to the epithelial cells and that this production is confirmed after in vitro stimulation with the same bacterial antigen of human epithelial and mesangial cells. Blockade of induction of chemokine response may thus be an attractive target for possible therapeutic intervention.

Acute Disease↗

PubMed2001

Antibodies against a truncated Staphylococcus aureus fibronectin-binding protein protect against dissemination of infection in the rat.

Staphylococcus aureus bacteraemia (SAB) originating from local infections can lead to severe secondary infections such as endocarditis. The protective effect of antibodies against secondary infections was studied in a rat model, where a local joint infection leads to bacteraemia and endocarditis on damaged aortic valves. In this study, immunizations with a truncated D2-domain of the S. aureus fibronectin-binding protein displayed on a cow-pea mosaic virus (CPMV-D) carrier induced protection against endocarditis (P < 0.05). Opsonization of S. aureus with antibodies raised against CPMV-D stimulated both neutrophil activity and macrophage phagocytosis in vitro. Furthermore, intravenous administration of these antibodies protected mice from weight loss due to SAB.

Adhesins, Bacterial↗

PubMed2001

Increased expression of CD25 and HLA-DR on lymphocytes recruited into the peritoneal cavity in non-infected CAPD patients.

The impact of uremia per se, peritoneal dialysis (PD) and hemodialysis (HD) treatment was evaluated on characteristics of lymphocytes. CD4, CD8, CD25 and HLA-DR were analyzed, with flow cytometry, in lymphocytes prepared from peripheral blood of uremic (n = 10) and hemodialysis patients (n = 10). Peritoneal dialysate was also obtained from patients on CAPD (n = 12). A decreased relative and absolute lymphocyte count was observed in peripheral blood from uremic, HD and CAPD patients compared to healthy controls (p < 0.03, p < 0.03 and p < 0.02, respectively). On the other hand, the relative distribution of lymphocytes was significantly higher in peritoneal dialysate compared to peripheral blood of CAPD patients (p < 0.02). Likewise, the absolute CD4 positive lymphocyte count was lower in the peripheral blood from uremic. HD and CAPD patients as compared to healthy controls (p < 0.001, respectively). In CAPD patients the relative distribution of CD4 positive cells (p < 0.001) was lower, while quantitative CD25 level (p < 0.01) and the relative count of HLA-DR (p < 0.0001) was increased in the peritoneal dialysate compared to blood. Taken together a selective activation of lymphocytes in peritoneal dialysate as compared to peripheral blood from uremic, HD and CAPD patients was observed. The altered biological function of the inflammatory cells may therefore explain the increased susceptibility to infectious diseases.

Adult↗

PubMed2001

Escherichia coli-induced expression of IL-1 alpha, IL-1 beta, IL-6 and IL-8 in normal human renal tubular epithelial cells.

The aim of the present study was to investigate whether the IL-1 family cytokines, in addition to IL-6 and IL-8, could be induced in normal human cortical epithelial cells in response to bacterial stimuli. Human renal tissue was obtained from 9 patients undergoing elective tumour nephrectomy. Renal cortical epithelial cells of tubular origin were prepared from the unaffected tissue. The proximal tubular cells were stimulated for 2, 6 and 24 h with a heat-inactivated pyelonephritogenic Escherichia coli strain DS-17. Cultured unstimulated tubular cells served as controls. IL-1 alpha, IL-1 beta, IL-1 receptor antagonist, IL-6, IL-8, IL-10, TNF-alpha, G-CSF and GM-CSF were analysed using immunohistochemistry at the single cell level. The nonstimulated cells were found to express low levels of IL-6 and IL-8 (mean value < 3% of total cells). In contrast, E. coli exposure resulted in significantly increased incidences of IL-6 and IL-8 expressing cells (mean values approximately 18% of total cells) peaking within two hours of stimulation (P < 0.008 and P < 0.02 versus non-stimulated cells, respectively). A gradual decrease was thereafter observed at 6 and 24 h, respectively, although persistently higher compared to controls. A different kinetic response was found for IL-1 alpha, IL-1 beta and IL-1 receptor antagonist-expressing cells, which peaked 24 h after E. coli stimulation (mean values 3--10%) (P < 0.008, P < 0.02, P < 0.02 versus non-stimulated cells, respectively). Low levels of TNF-alpha and GM-CSF were found in 3 of the 9 donated epithelial cells, peaking at 2 h, and IL-10 and G-CSF producing cells in 1 patient each. In conclusion we found that heat-inactivated pyelonephritic E. coli induced a proinflammatory cytokine response in the normal human proximal tubular cells including the IL-1 family, IL-6 and IL-8.

Adult↗

PubMed2001

Tetanus antibody levels of female volunteers after injection with solvent/detergent-treated human tetanus immunoglobulin (Tetabulin S/D).

BACKGROUND AND OBJECTIVES: The aim of this study was to analyse the increase of antitetanus titre in volunteers following injection with human tetanus immunoglobulin (HTI). MATERIALS AND METHODS: Twelve females with tetanus antibody titres of < or = 0.05 international units (IU)/ml were injected with 500 IU of human tetanus immunoglobulin (Tetabulin S/D). The tetanus antibody titres were determined before injection, and after 30 h, 48 h and 4 days. RESULTS: A fast and sustained increase of protective tetanus antibody levels was observed in 10 of 12 volunteers. No adverse events related to the study drug were reported. CONCLUSIONS: HTI confers rapid and effective immunity to tetanus.

Aged↗

PubMed2001

Inhibition of macrophage proinflammatory cytokine expression by steroids and recombinant IL-10.

Chronic lung disease (CLD) of prematurity is a prolonged respiratory failure in very-low-birth-weight neonates. Proinflammatory cytokines have been implicated in the development of CLD. Steroids have been shown to produce some improvement in neonates with this disease. The purpose of this study was to evaluate the downregulation of these proinflammatory cytokines by dexamethasone, budesonide and recombinant IL-10 (rIL-10) in order to elucidate the mechanism of the clinical benefit of steroids in babies. Our results showed that dexamethasone, budesonide and rIL-10 significantly inhibited both IL-6 and TNF-alpha production in the THP-1 cell line stimulated by lipopolysaccharide and Ureaplasma urealyticum antigen. Similar effects were found in macrophages from tracheobronchial aspirate fluid from newborn infants. In the rat alveolar macrophage cell line, steroids inhibited IL-6 and TNF-alpha production, while rat rIL-10 did not significantly decrease production. In conclusion, steroids and human rIL-10 were able to downregulate proinflammatory cytokine production, which may explain the beneficial effect of steroids and suggests that rIL-10 could be tried as an anti-inflammatory agent in neonates with a high risk of CLD.

Animals↗

PubMed2001

Meconium induces expression of inducible NO synthase and activation of NF-kappaB in rat alveolar macrophages.

Meconium aspiration causes intensive inflammatory reactions in the lungs, and may lead to neonatal respiratory disorder. Infiltrated inflammatory cells, particularly macrophages, play an important role in such an inflammation. A rat alveolar macrophage cell line (ATCC8383) was exposed to meconium alone or in combination with dexamethasone, budesonide, or interferon-gamma. Nitric oxide (NO) accumulation in the supernatant of the cell culture was detected by Griess reaction, and mRNA of inducible NO synthase (iNOS) expression was detected by reverse transcriptase-PCR. Nuclear factor-kappa B was analyzed by electrophoretic mobility shift assay, and iNOS location and nuclear factor-kappa B transactivation were determined by immunostaining. Our results showed that meconium was capable of inducing production of NO and expression of iNOS in alveolar macrophages in a dose- (1-25 mg/mL, p < 0.05) and time- (4-48 h, p < 0.05) dependent manner. This capability of meconium could be further enhanced in the presence of interferon-gamma (100 IU/mL, p < 0.05). Budesonide (10(-4)-10(-10) M) or dexamethasone (10(-4)-10(-6) M) effectively inhibited the meconium-induced NO production (p < 0.05). Using the protein synthesis inhibitor cycloheximide, we demonstrated that meconium directly induced iNOS in macrophages. Furthermore, meconium also triggered nuclear factor-kappa B activation, a mechanism possibly responsible for the iNOS expression. Our findings suggest that meconium is a potent inflammatory stimulus, resulting in iNOS expression, leading to overproduction of NO from the macrophages, which may be of pathogenic importance in meconium aspiration syndrome. In vitro steroids down-regulated the iNOS expression, thus suggesting a potential to down-regulate NO-mediated inflammation in neonates with meconium aspiration syndrome.

Animals↗

PubMed2000

Renal cytokine responses in acute Escherichia coli pyelonephritis in IL-6-deficient mice.

The aim of this study was to investigate the influence of IL-6 on mortality, bacterial growth and cytokine expression in experimental acute pyelonephritis. Female IL-6-deficient mice and their wild-type counterparts, 8-10 weeks old, were infected with Escherichia coli CFT 073 or injected with NaCl 0.9% (w/v) via the urethra and thereafter obstructed for 6 h. Animals were killed at 48 h, 6 days or 8 weeks and cytokine and bacterial renal levels were assessed at each time point. We found that IL-6-deficient mice had increased mortality and extensive renal bacterial growth on day 6, compared with wild-type mice (P < 0.05) and the histopathological changes were generally more severe and widespread in the IL-6-deficient mice. Peak mRNA expression of IL-1beta, IL-4, IL-10, IL-12 and interferon-gamma (IFN-gamma) occurred 48 h after infection in both IL-6 knock out and wild-type mice. Transforming growth factor-beta (TGF-beta) levels also peaked at 48 h in E. coli-infected wild-type mice, while in the IL-6-deficient strain both TGF-beta mRNA and protein levels were significantly lower at 48 h than wild-type levels (P < 0.0008 and P < 0.03, respectively) and remained stationary throughout the study period. Animals injected with NaCl 0.9% (w/v) displayed a similar decrease in TGF-beta expression (P < 0.02). When splenocytes from the IL-6-deficient mice were incubated with murine recombinant IL-6, TGF-beta levels increased to those of wild-type mice. No increase was observed when splenocytes from wild-type mice were incubated with the same doses of rIL-6. We therefore conclude that IL-6 plays an important role in bacterial clearance and directly influences the TGF-beta levels in experimental acute pyelonephritis. We also demonstrate that urethral obstruction per se induces an increase in TGF-beta the magnitude of which is decreased in IL-6-deficient mice.

Animals↗

PubMed2000

Downregulatory cytokines in tracheobronchial aspirate fluid from infants with chronic lung disease of prematurity.

UNLABELLED: Chronic lung disease of prematurity (CLD) is associated with an inflammatory response in the preterm lung and increased levels of proinflammatory cytokines in tracheobronchial aspirate fluid (TAF). We investigated TAF levels of transforming growth factor-beta1 (TGF-beta1), interleukin-10 (IL-10), interleukin-4 (IL-4) and interleukin-12 (IL-12) cytokines possibly important in downregulating the proinflammatory response and/or inducing lung fibrosis in infants with developing and established CLD. Infants with CLD (n = 24) were compared with preterm infants with RDS that resolved (n = 22) and postoperative infants without lung disease (n = 23). TAF levels of TGF-beta1, IL-10, IL-4 and IL-12 were studied by quantitative enzyme immunoassay. Levels of TGF-beta1 were significantly higher during the first week of life in infants who developed CLD, remained high at 2 wk and past 4 wk of age. TAF levels of TGF-beta1 did not decrease significantly in six infants with CLD after treatment with steroids. TAF IL-10 was detected in 12/46 (26%) preterm infants. Infants with CLD or RDS were more likely to have measurable TAF levels of IL-10, compared with the postoperative infants without lung disease (p < 0.02 and 0.04, respectively). TAF levels of IL-4 or IL-12 were below the detection limits in all samples. CONCLUSIONS: We have demonstrated a sustained increase of TGF-beta1 levels in TAF from preterm infants who develop CLD, suggesting an important role for TGF-beta1 in the fibrotic response in the CLD lung. The elevated TGF-beta1 levels, combined with an absent or irregular secretion of IL-4, IL-10 and IL-12, can have importance for the increased tendency for the development of CLD in preterm infants.

Age Factors↗

PubMed2000

Expression of and cytokine activation by Escherichia coli curli fibers in human sepsis.

Curli organelles are expressed by commensal Escherichia coli K12 and by Salmonella typhimurium at temperatures <37 degrees C, which bind serum proteins and activate the contact-phase system in vitro. This study demonstrates, by means of an anti-CsgA (curli major subunit) antibody, that a significant fraction of E. coli isolates (24 of 46) from human blood cultures produce curli at 37 degrees C in vitro. Serum samples from 12 convalescent patients with sepsis, but not serum from healthy controls, contained antibodies against CsgA (n=12). This study further demonstrates that a curli-expressing E. coli strain and a noncurliated mutant secreting soluble CsgA induce significantly (P<.05) higher levels of proinflammatory cytokines (tumor necrosis factor-alpha, interleukin [IL]-6, and IL-8) in human macrophages differentiated from THP-1 cells. These data, therefore, provide direct evidence that curli are expressed in vivo in human sepsis and suggest a possible role for curli and CsgA in the induction of proinflammatory cytokines during E. coli sepsis.

Adult↗

PubMed2000

Human cervical ripening, an inflammatory process mediated by cytokines.

An extensive remodelling process, referred to as cervical ripening, takes place in the cervical tissue during pregnancy and labour. It is recognized as softening and dilation of the cervical canal, and starts as a slow process during pregnancy, becoming rapid close to partum. In this study we focus on cytokines as possible mediators of this final remodelling. mRNA levels for interleukin (IL)-8, IL-6 and granulocyte colony-stimulating factor (G-CSF) were upregulated in the ripe postpartum cervical tissue (n = 8) compared to the unripe state (n = 9). Likewise, released cytokine concentrations increased from non-pregnant (n = 11) to the term-pregnant group (n = 13) with a further increase at partum (n = 16). IL-8 concentrations increased 4-fold from non-pregnant to term-pregnant (P<0.01), and a further 10-fold to postpartum state (P<0.0001). Concentrations of IL-6 and G-CSF were similarly increased. Specific IL-8 immunostaining was identified in the epithelia of pregnant cervical tissue (n = 7) and was most pronounced in the epithelia and stroma of postpartum tissue (n = 4). In conclusion, IL-8, IL-6 and G-CSF increase in the human cervix during the ripening process, indicating their important role in the cervical remodelling. These data demonstrate that cervical ripening is similar to an inflammatory process.

Adult↗

PubMed2000

Activation of nuclear factor kappaB and induction of inducible nitric oxide synthase by Ureaplasma urealyticum in macrophages.

Chronic lung disease (CLD) of prematurity is an inflammatory disease with a multifactorial etiology. The importance of Ureaplasma urealyticum in the development of CLD is debated, and steroids produce some improvement in neonates with this disease. In the present study, the capability of U. urealyticum to stimulate rat alveolar macrophages to produce nitric oxide (NO), express inducible nitric oxide synthase (iNOS), and activate nuclear factor kappaB (NF-kappaB) in vitro was characterized. The effect of NO on the growth of U. urealyticum was also investigated. In addition, the impact of dexamethasone and budesonide on these processes was examined. We found that U. urealyticum antigen (> or =4 x 10(7) color-changing units/ml) stimulated alveolar macrophages to produce NO in a dose- and time-dependent manner (P<0.05). This effect was further enhanced by gamma interferon (100 IU/ml; P<0.05) but was attenuated by budesonide and dexamethasone (10(-4) to 10(-6) M) (P<0.05). The mRNA and protein levels of iNOS were also induced in response to U. urealyticum and inhibited by steroids. U. urealyticum antigen triggered NF-kappaB activation, a possible mechanism for the induced iNOS expression, which also was inhibited by steroids. NO induced by U. urealyticum caused a sixfold reduction of its own growth after infection for 10 h. Our findings imply that U. urealyticum may be an important factor in the development of CLD. The host defense response against U. urealyticum infection may also be influenced by NO. The down-regulatory effect of steroids on NF-kappaB activation, iNOS expression, and NO production might partly explain the beneficial effect of steroids in neonates with CLD.

Animals↗

PubMed2000

Ureaplasma urealyticum-induced production of proinflammatory cytokines by macrophages.

Ureaplasma urealyticum is relatively common in the respiratory tract of very low birth weight infants and has been hypothesized to be involved in the development of chronic lung disease. The purpose of this study was to investigate whether U. urealyticum could stimulate macrophages to produce proinflammatory cytokines in vitro, which are early pathologic changes in the lung during the development of chronic lung disease. A human monocytic cell line (THP-1) differentiated to macrophages, a rat alveolar macrophage cell line (Nr8383), and human lung macrophages from tracheobronchial aspirate fluid in preterm infants were exposed to U. urealyticum antigen for 24 h. The protein levels of human IL-6, tumor necrosis factor-alpha (TNF-alpha), and rat TNF-alpha were measured with ELISA. Rat IL-6 was analyzed with a specific bioassay. The mRNA levels of these cytokines were detected by reverse transcriptase-PCR. The production of TNF-alpha and IL-6 increased after stimulation with U. urealyticum in both the human and rat macrophage cell lines. In tracheobronchial aspirate fluid macrophages, U. urealyticum increased the production of TNF-alpha from 14 to 84% and IL-6 from 46 to 268% above control levels. U. urealyticum also induced gene expression of TNF-alpha and IL-6. In conclusion, U. urealyticum could be an important factor in the development of chronic lung disease because of its ability to induce alveolar macrophage proinflammatory cytokine production.

Animals↗

PubMed2000

Angiotensin II type 1 receptor antagonist (losartan) down-regulates transforming growth factor-beta in experimental acute pyelonephritis.

PURPOSE: To study the effect of an angiotensin II type 1 receptor antagonist, losartan, on cytokine expression, kidney growth and renal scarring in experimental acute pyelonephritis. MATERIALS AND METHODS: Female Bki NMRI mice, 8 weeks old were infected with E. coli CFT 073 via the urethra. Mice were divided into four groups; either left untreated; or treated with NaCl 0.9%; or an angiotensin II type 1 receptor antagonist, losartan, in doses of 1 mg. or 40 mg. /kg. body weight. The treatment was given daily i.p. for 48 hours, 3 weeks or 8 weeks respectively. Kidneys were weighed and sectioned for histo-pathology and in situ hybridization for mRNA of IL-1beta, TNF-alpha, IL-4, IL-6, IL-10, IL-12, TGF-beta and IFN-gamma. Homogenized kidneys were used for EIA of TGF-beta and bacterial growth. RESULTS: The mRNA expression of the studied cytokines generally peaked at 48 hours in all four groups. In animals treated with losartan, kidney TGF-beta, IFN-gamma and IL-6 decreased significantly at 3 and 8 weeks as compared with controls, untreated or those treated with NaCl, (p <0.005 respectively). Infection was associated with a declining kidney weight, also in the presence of losartan. A 50% reduction of the spread of renal scarring was observed in the losartan treated group, but this did however not reach significance. The proportion of kidneys showing bacterial growth was not influenced by losartan although in these kidneys the mean bacterial counts at 3 weeks were significantly higher in the losartan treated mice (p <0.006). CONCLUSIONS: Losartan is associated with downregulation of TGF-beta, IFN-gamma and IL-6 and may, in combination with antimicrobial therapy, reduce the risk of cortical renal scarring in recurrent acute pyelonephritis in infants.

Acute Disease↗

PubMed1999

Soluble interleukin-1 receptor type II levels are elevated in cerebrospinal fluid in Alzheimer's disease patients.

Evidence from epidemiological, clinical and experimental studies favour the hypothesis that inflammatory events are part of the neuropathology in Alzheimer's disease. Proinflammatory cytokines such as interleukin-1 (IL-1), interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-alpha) have been found in activated microglia in the vicinity of amyloid plaques in Alzheimer's disease brain. In the present study, the levels of soluble IL-1 receptor type II (sIL-1R type II), IL-1 receptor antagonist (IL-1ra), IL-1beta, IL-6 and TNF-alpha were analyzed in cerebrospinal fluid (CSF) samples from Alzheimer's disease patients and control subjects. The levels of sIL-1R type II were significantly higher in CSF from Alzheimer's disease patients than in CSF samples from control subjects (38.5+/-8 pg/ml (mean+/-S.E.M.) vs. 7.9+/-4 pg/ml, p<0.05). Measurements of the proinflammatory cytokines IL-6 and TNF-alpha showed no significant difference between the two groups, and the levels of IL-1beta and IL-1ra in the present material were too low to permit detection. The increased levels of sIL-1R type II may reflect a compensatory mechanism to balance an increased release of IL-1 receptor agonists in the Alzheimer's disease brain.

Aged↗

PubMed1999

Increased levels of transforming growth factor beta 1 and basic fibroblast growth factor in patients on CAPD: a study during non-infected steady state and peritonitis.

Long-term influence of continuous ambulatory peritoneal dialysis (CAPD) on concentrations of transforming growth factor beta1 (TGF-beta1) and basic fibroblast growth factor (bFGF) in the peritoneal effluent, and the effect of peritonitis on these cytokines were investigated. TGF-beta1 and bFGF were assayed in effluent samples from dialysate bags collected during the initial week of treatment with CAPD and at 5 months. To determine the effect of peritonitis, dialysate bags were collected on admission to the hospital and on days 3 and 10 and also during non-infected steady state. Serum was drawn prior to infection and on days 1 and 10. TGF-beta1 increased more than threefold during the longitudinal follow-up period, median concentrations of 35 pg/ml to 106 pg/ml (P<0.05). No change in bFGF was seen during this initial 5 months. TGF-beta1 was increased on the first day of peritonitis (median concentration 169 pg/ml) and reached its maximum on day 3 of infection, (median concentration 216 pg/ml) (P<0.05 vs non-infected state, median concentration 39 pg/ml). Basic FGF reached a maximum on day three of infection (median concentration 7.7 pg/ml; P=0.01 vs non-infected state) and then slowly declined. In conclusion, TGF-beta1 is influenced by CAPD treatment per se, and together with bFGF is increased during peritonitis, indicating its importance in the peritoneum and its potential involvement in the development of tissue fibrosis and eventually ultrafiltration failure.

Adult↗

PubMed1998

Granulocyte stimulating factor in patients on peritoneal dialysis and LPS stimulated peripheral blood mononuclear cells.

Dialysate and serum levels of granulocyte-colony stimulating factor (G-CSF), granulocyte macrophage colony stimulating factor (GM-CSF) and leukemia inhibitory factor (LIF) were analyzed in patients with continuous ambulatory peritoneal dialysis (CAPD). Samples from the peritoneal effluent and from serum were obtained during the first months of dialysis and during peritonitis from the first three dialysate bags drained on the day of admittance and form nightbags on days three and ten. Serum samples were drawn on days one and ten. On the first day of infection G-CSF was detected in twelve out of fifteen samples in the dialysate and reached its peak median level, 443 pg/ml, in the first drained bag and thereafter decreased significantly. Also in serum a peak, 190 pg/ml, was observed on the first day. LIF was found in six of ten analyzed dialysate samples, with a peak median level of 77 pg/ml on day one, while only four of ten patients had detectable GM-CSF. Peripheral blood mononuclear cells from non-infected CAPD patients were stimulated with lipopolysaccharide and G-CSF levels in the supernatants increased significantly (P < 0.05) after 6 h stimulation. We conclude that G-CSF is produced locally in the dialysate during the acute stage of peritonitis and to a lesser extent also systemically. These findings are in line with G-CSF production after LPS stimulation of peripheral blood mononuclear cells.

Acute Disease↗