Apmis

David, CHELLA S.

doi: 10.1111/j.1699-0463.1990.tb04974.xpmid: 1697756

Type II collagen induced arthritis (CIA) in mice is an animal model for polyarthritis. The susceptibility to the disease is linked to the class II genes of H‐2 gene complex (MHC). The susceptibility requires T cells expressing certain receptors coded by the Vβ genes. Further, the MIs gene products in combination with the class II molecules can up‐or down‐regulate the T cells involved in the disease. The disease is mediated by the presentation of an arthritogenic epitope on the collagen type II peptide by the MHC class II molecule, which is recognized by a T cell expressing certain Vβ receptors, triggering the autoimmune response. These studies point out possible mechanisms of rheumatoid arthritis in humans and suggest various methods of immune intervention to down‐regulate the disease.

Battelli, MARIA GIULIA; Barbieri, LUIGI; Stirpe, FIORENZO

doi: 10.1111/j.1699-0463.1990.tb04975.xpmid: 2397111

The toxicity of, and the lesions brought about by, several ribosome‐inactivating proteins (bryodin, gelonin, momordin, pokeweed antiviral protein from seeds, saporin 6, trichokirin and momorcochin‐S), either native, or conjugated to bovine IgG, or polymerized, were studied in the mouse. Severe necrotic liver damage was the main lesion present in animals receiving lethal doses of the proteins. The toxicity of ribosome‐inactivating proteins increased after conjugation to IgG or homopolymerization. The toxicity of conjugates to mouse was not predictable from the inhibitory activity on cell‐free protein synthesis.

Hviid, LARS; Theander, THOR G.; Jakobsen, PALLE H.; Abu‐Zeid, YOUSIF A.; Abdulhadi, NASRELDIN H.; Saeed, BAKRI O.; Jepsen, SØREN; Bayoumi, RIAD A. L.; Bendtzen, KLAUS; Jensen, JAMES B.

doi: 10.1111/j.1699-0463.1990.tb04976.xpmid:

Andreasen, A.; Hansen, E. S.; Fogh, K.; Kragballe, K.; Herlin, T.

doi: 10.1111/j.1699-0463.1990.tb04977.xpmid: 2168723

Synovial fluid cells obtained from a carragheenan‐induced chronic arthritis in the juvenile dog knee were allowed to adhere and proliferate in culture flasks. After twelve days secondary cultures were made and either 10−8M leukotriene B4 (LTB4), 25 μM 15‐hydroxy‐eicosatetraenoic acid (15‐HETE), or both, were added and the cells were cultured for another 6 days. LTB4 is generated via the 5‐lipoxygenase pathway of arachidonic acid metabolism and stimulates a number of phagocyte functions. Compared to control cells LTB4 increased proliferation in 9 out of 10 cell cultures (p > 0.05). The 15‐lipoxygenase product, 15‐HETE, is not proinflammatory and is an endogenous inhibitor of 5‐lipoxygenase. Addition of 15‐HETE decreased proliferation of cell cultures by 23% (p > 0.01). It is speculated that LTB4 in addition to its effect on phagocytes may play a role in synovial hyperproliferation observed in arthritis.

Elbagir, ADIL; Petterson, MARGARETA; Lindahl, MATS; Genc, MEHMET; FrÖMan, GUNNAR; MÅRdh, PER‐ANDERS

doi: 10.1111/j.1699-0463.1990.tb04978.xpmid: 2397112

A study of the effect of human breast milk, and components thereof, on the capacity of Chlamydia trachomatis to form inclusions in cycloheximide‐treated McCoy cells, was undertaken. Pooled whole milk collected during the first week of breast feeding caused a concentration‐dependent inhibition of the chlamydial inclusion‐formation. The activity resided in the fat and fat globule membrane (FGM) components of the milk. The active principle in the FGM fraction is heat‐stable and pronase‐sensitive, but resistant to both neuraminidase and periodate. Immunoglobulins was not responsible for the inhibition. Whey and casein fractions of milk increased the chlamydial inclusion‐formation. The activity of the whey was heat‐stable, dose‐related, and had a mol.wt. of 12,000. The casein fraction was still active after heat treatment. Whey samples collected up to 28 days after delivery varied slightly in their stimulatory activity, with an optimum between the 7th and 14th days. The present study demonstrated a multieffect of breast milk on chlamydial inclusion‐formation: an inhibitory activity due to a protein compound as well as another factor in the fat fraction and an enhancing effect due to a heat‐stable factor(s).

Christensen, LISE

doi: 10.1111/j.1699-0463.1990.tb04979.xpmid: 2397113

The connective tissue glycoprotein, fibronectin (FN) is known to be increased in the stromal desmoplastic response associated with invasive breast carcinoma (IBC). In a previous study of 77 IBCs we found that all tumours, irrespective of desmoplasia, displayed an intense stromal immunoreactivity for FN, although those with a high metastatic potential tended to lack this in foci along their infiltrating border (Chrislensen et al. 1988). In order to test the diagnostic value of this observation, FN immunoreactivity was estimated semiquantitatively in 131 small primary IBCs, 23 in situ carcinomas, 20 borderline lesions, 142 benign proliferative breast lesions and 35 samples of normal breast tissue. All IBCs, including those without apparent desmoplasia, were accompanied by an intense stromal staining for FN forming a diffuse or pericellular pattern around the tumour cells (FN positive reaction). This was not seen in the benign lesions (FN negative reaction) with the exception of an FN positive, linear staining around some cysts and ectatic ducts and a diffuse staining of the connective tissue core of some intraductal papillomas. Intraductal carcinomas, multiple papillomas and radial scars could display a substantial staining for FN, sometimes enclosing small islands or tubules of epithelial cells. However, the fact that all IBCs of this study produced an overall reliable and consistent FN positive stromal reaction, which was only interrupted in minute foci along the infiltrating border in a few of the largest tumours (11/131), makes immunohistochemical staining for FN an excellent adjunct to morphology in tracing small, primary IBCs.

Juul‐Madsen, H. R.; Olsson, L.

doi: 10.1111/j.1699-0463.1990.tb04980.xpmid: 1697757

Major histocompatibility complex class I transcriptional products and cell surface expression of their corresponding proteins were measured in tumorigenic Lewis lung carcinoma cells with either high metastatic activity (G4 cells) or with no metastatic activity (G2 cells). The transcriptional products were measured by hybridization to gene‐specific oligonucleotide probes for H‐2Kb and H‐2Db respectively. The cell surface density of the corresponding H‐2 glycoproteins was determined by FACS cell sorter analysis and by radioimmunoassay using anti‐H‐2Kb and anti‐H‐2Db specific monoclonal antibodies. The analyses revealed that the cell surface density of both Kb and Db was reduced 4–9 fold in G4 cells compared to G2 cells. However, this reduction of G4 cell surface expression of MHC class I molecules was not reflected at the mRNA level since both subclones had similar low levels of detectable Kb and Db specific mRNA. β2‐microglobulin was analysed at the mRNA and protein level and found not to be the rate‐limiting factor in the MHC class I expression of the metastatic G4 cells. Thus, the cell surface expression of H‐2Kb and H‐2Db by the two Lewis lung carcinoma subclones did not correlate with the amount of specific mRNA. Other regulatory mechanisms of gene expression acting at the levels between transcription and the appearance of the gene product at the cell surface must therefore account for the observed difference in the cell surface expression of MHC class I molecules of the two Lewis lung carcinoma cells. The potential importance of MHC class I expression in the metastatic capacity of the tumor cells is discussed.

Jepsen, HANS HENRIK; Rasmussen, JENS MØLLER; Teisner, BØRGE; SchrØDer, LISE; Holmskov, UFFE; JarlbæK, LENE; Isager, HENRIK; Svehag, SVEN‐ERIK

doi: 10.1111/j.1699-0463.1990.tb04981.xpmid: 2144431

Erythrocytes (E) from a cross‐sectional group of 22 outpatients with systemic lupus erythematosus (SLE) and/or mixed connective tissue disease (MCTD), the majority without active disease (n = 14), were analyzed for CR1 antigen expression and capacity to bind complement opsonized, radiolabeled immune complexes (IC). Furthermore, E‐bound C3 fragments and the plasma C3d concentration were determined. E‐bound C3b/iC3b fragments were not elevated in patients with SLE, whereas E from 11 out of 22 SLE patients had increased C3d levels which correlated with the plasma C3d concentration (Rs 0.73, p < 0.001). E‐fixed C3d fragments did not affect the binding of Mab or preopsonized IC to E‐CR1 and were not correlated with disease activity or medical treatment. Antigen expression of E‐CR1 measured by ELISA or agglutination showed positive correlation with the IC binding capacity of E‐CR1 (Rs 0.92 and 0.72 respectively, p < 001). The IC binding capacity of E‐CR1 from SLE patients was significantly reduced (p > 0.005), whereas the antigen expression of CR1 (ELISA) on E from the patients did not differ from that of E from healthy donors (p > 0.1). E‐CR1 antigen was measured by Mab reacting with an epitope outside the IC‐binding site of E‐CR1. E‐CR1 antigen expression or IC binding showed no correlation either with disease activity or prednisolone treatment. However, 4 og 5 patients with MCTD and 4 of 5 patients receiving Imurel® were found to have low E‐CR1 expression and capacity to bind IC. Thus, measurement of antigenic E‐CR1 in a cross‐sectional group of SLE outpatients by use of Mab reacting with an epitope outside the ligand‐binding region of CR1 did not reveal a significantly reduced CR1 expression. However, an assay for CR 1 ‐mediated IC binding showed a clearly reduced E‐CR1 function.

Nir, M.; Prag, J.; Jensen, J.; Arpi, M.

doi: 10.1111/j.1699-0463.1990.tb04982.xpmid: 2397114

The detection power of the automated blood culture system Bactec NR 660®, based on infrared detection of carbon dioxide in an agitated aerobic medium and a non‐agitated anaerobic medium, was compared with that of our conventional 12‐tube blood culture system. Of 1685 paired blood cultures, 258 (15.3%) were positive in one or both systems. Clinically relevant isolates were found in 11.5%. The dominating species were Escherichia coli (41%), followed by Staphylococcus aureus (14%) and Klebsiella spp. (8%). The Bactec® system detected 178 (10.6%) and the 12‐tube system 157 (9.3%) clinically relevant microorganisms after seven days' incubation. Significantly more clinically relevant isolates were detected by the Bactec® system alone as compared with the conventional system alone (40 versus 19, p < 0.01). The detection time was significantly shorter in the Bactec® system for all isolates and for E. coli and S. aureus separately (p < 0.01). 1.8% of the isolates in the Bactec® system and 2.1% in the 12‐tube system were considered clinically non‐relevant contaminants.

Jung, K.; Aronsson, B.

doi: 10.1111/j.1699-0463.1990.tb04983.xpmid: 2397115

A rapid latex agglutination test, Culturette Brand CDT from Marion Laboratories, was evaluated and compared to a tissue culture assay (TCA) and isolation of Clostridium difficile in 380 faecal specimens from 226 patients with clinically suspected Clostridium difficile‐associated diarrhoea. The sensitivity and specificity of the latex test compared with the TCA were 83% and 80% respectively, and the positive and negative predictive values were 55% and 94% respectively. In patients with repeated sampling the sensitivity increased to 95%. The latex test may be useful as a screening test for negative specimens in laboratories where TCA is not available, but positive specimens have to be confirmed by TCA.