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Biomedical subjects

W E Peetermans

Publications and source records attributed to W E Peetermans.

At least 73 records · Page 4Linked to original sources
PubMed1995

Mucosal expression by B7-positive cells of the 60-kilodalton heat-shock protein in inflammatory bowel disease.

BACKGROUND/AIMS: Heat-shock protein (Hsp) 60 is an immunodominant antigen of mycobacteria and other microorganisms that is highly homologous to its human counterpart. Hsp60 may provide a link between immunity to invading microorganisms and autoimmune diseases. METHODS: Expression of Hsp60 was studied by immunohistochemistry in gut resection specimens of patients with Crohn's disease (n = 14), ulcerative colitis (n = 7), acute self-limited colitis (infective type) (n = 5), and controls (n = 9) using the monoclonal antibodies LK1 and LK2. RESULTS: A strong staining positivity for Hsp60 was observed in numerous mononuclear cells of the mucosa and submucosa in ileum and colon tissue biopsy specimens of patients with Crohn's disease from inflamed and healthy areas. In ulcerative colitis, Hsp60 expression was limited to the mucosa. In biopsy specimens from patients with acute self-limited colitis and controls, Hsp60-positive cells were absent or only present in low numbers and staining intensity was weak. Differentiation between mammalian and bacterial Hsp60 showed expression of the human homologue. Double staining for B7 and Hsp60 showed that Hsp60 was expressed by B7-positive cells. CONCLUSIONS: Human Hsp60 is strongly expressed by B7-positive antigen-presenting mononuclear cells in the mucosa of patients with inflammatory bowel disease and might play a role in the initiation or maintenance of the inflammatory process.

Acute Disease↗
PubMed1995

Streptococcus pyogenes bacteremia: a retrospective study in a Belgian university hospital.

We retrospectively studied 29 cases of S.pyogenes bacteremia, treated from September 1985 through September 1993, in order to define the clinical pattern, predisposing factors and the outcome of S.pyogenes bacteremia in our region. The number of infections, the clinical picture and mortality rate of S.pyogenes bacteremia did not change during the study period and only 2 of 29 cases presented with a fulminant clinical course, meeting the criteria of streptococcal toxic shock syndrome. In many patients, predisposing factors such as skin abnormalities (n = 14) and airway diseases (n = 10) could be identified. Patients with underlying skin disease were mostly characterized by a clinically benign bacteremia with good prognosis. We suspect that the recently reported so-called rising incidence of severe S.pyogenes infections might be due to epidemiologic clustering and selection bias in certain regions.

Adolescent↗
PubMed1995

Mycobacterial 65-kilodalton heat shock protein induces tumor necrosis factor alpha and interleukin 6, reactive nitrogen intermediates, and toxoplasmastatic activity in murine peritoneal macrophages.

The 65-kDa heat shock protein (Hsp65) is supposed to play a role in host defense against infections with various microbial pathogens and in autoimmune inflammatory disorders. These effects are thought to result mainly from an Hsp65-specific T-lymphocyte-mediated immune response that recognizes conserved epitopes. The aim of the present study was to assess whether mycobacterial Hsp65 has a direct effect on resident murine peritoneal macrophages, independent of Hsp65-sensitized T lymphocytes. Exposure of peritoneal macrophages from naive C57BL/6 mice to the mycobacterial Hsp65 in vitro induced an enhanced release of tumor necrosis factor alpha (TNF-alpha) and interleukin 6. These cells also produced large amounts of reactive nitrogen intermediates (RNI) and inhibited the intracellular proliferation of Toxoplasma gondii. Small amounts of gamma interferon acted synergistically with Hsp65. Thus, exposure of murine macrophages to Hsp65 results in activation of these cells. The acquisition of these characteristics by peritoneal macrophages occurred in the absence of sensitized T lymphocytes. Addition of anti-TNF-alpha antiserum resulted in an attenuation of the Hsp65-induced release of RNI and toxoplasmastatic activity, indicating that endogenous TNF-alpha is involved in the Hsp65-induced macrophage activation. The conclusion of this study is that in vitro exposure of peritoneal macrophages to the mycobacterial Hsp65 induces the release of proinflammatory cytokines and RNI and results in inhibition of the intracellular proliferation of T. gondii. These effects on murine macrophages occur independently of Hsp65-specific T lymphocytes. The proinflammatory effect of Hsp65 demonstrated in this study suggests that this heat shock protein may play a role in the initiation of inflammation that adds to a non-species-specific resistance in the early stages of infections.

Animals↗
PubMed1995

[Dental care and prevention of infectious endocarditis].

Infective endocarditis causes substantial morbidity and mortality despite adequate antimicrobial, medical and surgical treatment. The rationale for antibiotic prophylaxis against endocarditis is derived from the etiology and pathogenesis of the disease. Endocarditis usually follows bacteremia with certain endocarditis-prone bacteria in a patient with a predisposing heart condition. Protection by antibiotic prophylaxis is estimated to reach only 50% for a lot of reasons (transient bacteremia without dental or surgical intervention, predisposing heart disease not diagnosed previously, etc). Most authorities in the field of infective endocarditis strongly advocate the use of antibiotic prophylaxis for patients at risk. Clear guidelines are published by various highly qualified scientific committees. Recent schemes allow orally administered antibiotic prophylaxis because of a better doctor and patient compliance.

Administration, Oral↗
PubMed1994

Mycobacterial heat-shock protein 65 induces proinflammatory cytokines but does not activate human mononuclear phagocytes.

The 65 kDa heat-shock protein (Hsp65), a well-conserved and immunodominant antigen which elicits a cellular and humoral immune response, may play a role in host defence against invading microorganisms and autoimmune disorders. The aim of the present study was to assess the effects of Hsp65 on the functional activities of human mononuclear phagocytes in the absence of lymphocytes. Incubation with Hsp65 resulted in an enhanced release of TNF-alpha and IL-1 beta by human monocytes and monocyte-derived macrophages (MDM). The amount of cytokines released by these cells in response to Hsp65 was similar to that released in response to IFN-gamma together with LPS. Incubation with ovalbumin did not stimulate the release of these cytokines. In vitro stimulation of monocytes with Hsp65 enhanced the membrane expression of complement receptor III but did not influence either the expression of Fc gamma-receptor I and HLA class-II antigens or the release of reactive oxygen intermediates. Therefore, Hsp65-stimulated monocytes cannot be considered to be activated according to classical criteria. The release of the proinflammatory cytokines TNF-alpha and IL-1 beta by human mononuclear phagocytes in response to Hsp65 indicates that this protein can contribute to both host defence and tissue damage in inflammatory lesions characterized by an abundant expression of Hsp65.

Antigens, Surface↗
PubMed1993

Murine peritoneal macrophages activated by the mycobacterial 65-kilodalton heat shock protein express enhanced microbicidal activity in vitro.

After an intraperitoneal (i.p.) injection of purified protein derivative, peritoneal macrophages from mice infected with Mycobacterium bovis bacillus Calmette-Guérin (BCG) show an enhanced respiratory burst, inhibit the intracellular proliferation of Toxoplasma gondii, and kill Listeria monocytogenes more efficiently than peritoneal macrophages from normal mice. One of the immunodominant antigens of Mycobacterium spp. is the 65-kDa heat shock protein (Hsp 65), and in the present study, we determined whether injection of this protein into mice leads to activation of their peritoneal macrophages. After an i.p. injection of Hsp 65, peritoneal macrophages from BCG-infected CBA/J mice also released more H2O2, inhibited the proliferation of T. gondii, and killed L. monocytogenes faster than peritoneal macrophages from normal mice, although Hsp 65 was less effective than purified protein derivative. When normal mice were injected with Hsp 65 suspended in saline after a booster injection with Hsp 65, their macrophages did not display enhanced antimicrobial activity, indicating that an adjuvant was required for a cellular immune response against Hsp 65. In the present study, the adjuvant dimethyl dioctadecylammonium bromide (DDA) was preferred because it contains no endotoxin or mycobacterial antigens and because it has been reported that DDA does not induce the production of gamma interferon. Peritoneal macrophages from C57BL/6 and CBA/J mice that had received a subcutaneous injection of Hsp 65 suspended in DDA followed by an i.p. booster injection of Hsp 65 suspended in saline were activated, as indicated by the enhanced production of H2O2, inhibition of the intracellular proliferation of T. gondii, and increased rate of intracellular killing of L. monocytogenes in vitro relative to that by resident peritoneal macrophages and peritoneal macrophages obtained from mice that had received ovalbumin instead of Hsp 65. The rate of phagocytosis of L. monocytogenes was not affected by Hsp 65 treatment. Despite the in vitro expression of enhanced microbicidal activity of peritoneal macrophages, no difference in the growth of L. monocytogenes in the liver and spleen between Hsp 65-treated and control mice was found.

Animals↗
PubMed1991

Isolation of vancomycin-resistant enterococci in haematologic patients.

After the occurrence of septicaemia with a vancomycin-resistant Enterococcus faecalis strain in a patient, it was decided to determine the number of carriers of vancomycin-resistant cocci among haematologic patients. During a period of six months 135 stool samples from 25 children, and 400 samples from 70 adults were studied. All samples from the children were negative for vancomycin-resistant cocci. Nine of the adult patients had cultures positive for cocci, all identified as enterococci, which were highly resistant to vancomycin (MIC greater than 250 micrograms/ml), sensitive to amoxicillin, moderately resistant to gentamicin, slightly resistant to teicoplanin, and sensitive to daptomycin. None of these patients had been given vancomycin prior to the isolation of the vancomycin-resistant enterococci.

Adult↗
PubMed1991

Sciatic neuritis as initial symptom of spontaneous clostridial myonecrosis.

A 21-year-old woman is reported with aplastic anaemia, who presented with pain in the leg. Rapid loss of sciatic nerve function followed. MRI showed irregular streaks of low intensity in the muscles of the pelvic region. A diagnosis of sciatic neuritis as initial symptom of clostridial myonecrosis was made.

Adult↗
PubMed1991

Vancomycin-resistant Enterococcus faecalis in a bone-marrow transplant recipient.

Since 1988 a number of reports on the emergence of vancomycin-resistant enterococci have been published. We describe an additional case of colonization of and subsequent infection with a vancomycin-resistant Enterococcus faecalis in a bone-marrow transplant recipient, who had never before received vancomycin therapy. The strain was resistant to most antibiotics tested, including low-level resistance to gentamicin and cross-resistance to teicoplanin. It was sensitive to amoxicillin and the lipopeptide antibiotic daptomycin. The origin, the mode of acquisition and the incidence of vancomycin-resistant enterococci are still unknown. The clinical and bacteriological features of the cases reported thus far and the genetic and biochemical basis of vancomycin resistance are discussed.

Adult↗
PubMed1990

Antistaphylococcal activities of teicoplanin and vancomycin in vitro and in an experimental infection.

The efficacies of vancomycin and teicoplanin in an experimental Staphylococcus aureus infection in granulocytopenic mice were related to their activities in vitro and their pharmacokinetic profiles. In vitro teicoplanin had a higher intrinsic activity than vancomycin did; and it also had a more favorable pharmacokinetic profile, resulting in higher peak concentrations in plasma, a longer elimination half-life, and a larger area under the concentration-time curve than those of vancomycin. To predict the antibacterial efficacies of the drugs in vivo on the basis of their activities in vitro and pharmacokinetics, a mathematical model was applied. In the model the in vitro effect was expressed as the difference in growth rate between control cultures and those in the presence of the antibiotic (ER), and the in vivo effect was expressed as the difference between numbers of CFU in control and antibiotic-treated animals (EN). The integral of ER against time, ERt, was calculated by using the concentrations found in vivo. A significant linear relationship was found between EN and ERt for different dosages at the same times (4 h) after drug administration as well as for the same doses at consecutive times, although at the lowest doses of teicoplanin the observed effect was less than the predicted effect.

Animals↗
PubMed1989

Ankylosing spondylitis. An unusual manifestation of familial Mediterranean fever. Report of a case complicated by amyloidosis and polyneuropathy.

We report a case of familial Mediterranean fever (FMF) with typical clinical and roentgenological findings of ankylosing spondylitis. The spinal involvement in FMF is discussed. A second unusual feature of this case is the occurrence of polyneuropathy which could possibly be ascribed to the slowly evolving amyloidosis during continuous colchicine treatment.

Amyloidosis↗