Cytokine Genes are Down-Regulated When Attachment of Entamoeba histolytica to HT-29 Colon Epithelial Cells is Prevented

Entamoeba histolytica can cause invasive disease by disruption of the intestinal barriers and subsequent lysis of the intestinal cells. Adherence to and contact dependent killing of host cells requires the galactose inhibitable lectin. To elucidate the mechanism whereby E. histolytica influences host defence, the authors assessed the change of proinflammatory cytokine genes expressed by colon epithelial cells in response to co-culture with E. histolytica trophozoites and carbohydrates, including galactose, N -acetyl-galactosamine or N -acetyl-lactosamine, which prevented E. histolytica from attaching to epithelial cells. After HT-29 human colon epithelial cells were co-cultured with E. histolytica trophozoites in the presence or absence of carbohydrates (0.1–100 m m ), RNA was extracted from the epithelial cells by an acid guanidinium thiocyanate–phenol–chloroform method. Cytokine gene expression was assessed by quantitative RT-PCR using a synthetic internal standard, and proteins were determined by ELISA. IL-8 mRNA expressed by HT-29 cells in response to E. histolytica trophozoites was downregulated in the presence of galactose, N -acetyl-galactosamine or N -acetyl-lactosamine (0.1–100 m m ), and this was paralleled by decreased IL-8 protein secretion. GM-CSF and IL-1α/β mRNAs were also downregulated in those cells in the presence of these agents. These results suggest that the expression of proinflammatory cytokine genes could be inhibited by preventing E. histolytica from attaching to the host's colon epithelial cells.     

Hereditary spastic paraplegia and Evans's syndrome

Two brothers with hereditary spastic paraplegia and Evans's syndrome are recorded. Rapid deterioration of functional motor ability followed the development of Evans's syndrome.     

Secondary T-cell lymphoma presenting as a giant ulcer

Secondary cutaneous T-cell lymphoma may present with various types of skin lesions, but rarely produces ulceration in contrast to primary cutaneous T-cell lymphoma. We report a case of malignant lymphoma of the tonsil that recurred as a giant cutaneous ulcer on the back of a 45-year-old man. Biopsy of the ulcer revealed a malignant lymphoma of diffuse, mixed-cell type. Surface marker analysis of the tumour cells showed suppressor/cytotoxic T-cell characteristics. The skin lesions were treated by electron beam therapy.     

Anti-idiotypic antibodies specific for a pathologic anti-Pr2 cold agglutinin

The heterogeneity of human red cell (RBC) autoantibodies may be assessed by using anti-idiotypic antibodies. In this study, mouse monoclonal anti-idiotypic antibodies were produced against a pathologic RBC autoantibody with anti-Pr2 specificity. Epstein-Barr virus-transformed B-cell clones were established from a patient who had splenic lymphoma and associated immune hemolysis due to an anti-Pr2 cold autoantibody. Two of the eight clones producing this autoantibody were used to immunize mice for the establishment of hybridomas, and four monoclonal anti-idiotypic antibodies were isolated (2 IgG1 kappa and 2 IgM kappa). By the use of these anti-idiotypic antibodies, strong crossreactivity was seen on enzyme-linked immunosorbent assay with other anti-Pr2-producing clones from the same patient, but no cross-reactivity was seen with RBC autoantibodies from other individuals having anti-Pr or different specificities. Each of the anti-idiotypic antibodies inhibited hemagglutination (HA) by the patient's anti-Pr2 but failed to inhibit HA by antisera of a different RBC specificity. Cross-competition experiments indicated that all of the anti-idiotypic antibodies may recognize the same or a closely related idiotope on the anti-Pr2 autoantibody. These studies suggested that the four anti-idiotypic antibodies are directed against the same (or closely related) idiotypic determinant(s), unique to this patient's anti-Pr2 and located at or near the antigen-binding site. These anti-idiotypic antibodies may be useful tools for the study of this autoimmune response or for the development of immune therapeutic agents.(ABSTRACT TRUNCATED AT 250 WORDS)     

Acidosis and severe megaloblastic anaemia

Ten patients with severe megaloblastic anaemia were studied to investigate whether the causative metabolic defects might predispose them to lactic or other acidosis. One patient had compensated acidosis with hyperlactataemia before treatment but there were obvious causes other than anaemia. No other patient developed an acidosis. Neither anaemia per se nor the metabolic defects of vitamin B₁₂ or folic acid deficiency are likely to cause clinically significant lactic acidosis or hyperlactataemia.     

A comparative laboratory diagnosis of malaria: microscopy versus rapid diagnostic test kits

Objective

To compare the two methods of rapid diagnostic tests (RDTs) and microscopy in the diagnosis of malaria.

Methods

RDTs and microscopy were carried out to diagnose malaria. Percentage malaria parasitaemia was calculated on thin films and all non-acute cases of plasmodiasis with less than 0.001% malaria parasitaemia were regarded as negative. Results were simply presented as percentage positive of the total number of patients under study. The results of RDTs were compared to those of microscopy while those of RDTs based on antigen were compared to those of RDTs based on antibody. Patients'' follow-up was made for all cases.

Results

All the 200 patients under present study tested positive to RDTs based on malaria antibodies (serum) method (100%). 128 out of 200 tested positive to RDTs based on malaria antigen (whole blood) method (64%), while 118 out of 200 patients under present study tested positive to visual microscopy of Lieshman and diluted Giemsa (59%). All patients that tested positive to microscopy also tested positive to RDTs based on antigen. All patients on the second day of follow-up were non-febrile and had antimalaria drugs.

Conclusions

We conclude based on the present study that the RDTs based on malaria antigen (whole blood) method is as specific as the traditional microscopy and even appears more sensitive than microscopy. The RDTs based on antibody (serum) method is unspecific thus it should not be encouraged. It is most likely that Africa being an endemic region, formation of certain levels of malaria antibody may not be uncommon. The present study also supports the opinion that a good number of febrile cases is not due to malaria. We support WHO''s report on cost effectiveness of RDTs but, recommend that only the antigen based method should possibly, be adopted in Africa and other malaria endemic regions of the world.