Trefoil peptides are expressed near endodermal ulcerations and may modulate epithelial repair. The trefoil pancreatic spasmolytic polypeptide (PSP) was tested for growth activity in vitro on epithelial cells and in vivo following intragastric or intravenous infusion in parenterally fed intact rats. Ion transport was assessed a s changes in short-circuit current in rat intestine and adenocarcinoma cells in Ussing chambers. PSP stimulated growth of MCF-7 and Colo-357 cells, but only in the presence of extracellular glutathione (GSH). The effect was attenuated by GSH depletion with buthionine sulphoximine, even in GSH-containing media. When GSH-reduced PSP was carboxymethylated with iodoacetic acid, it still depended on extracellular GSH for its growth effect. Intestinal epithelial proliferation in rats was not affected by either intravenous or intraluminal infusion. PSP had no effect on basal or stimulated ion flux in rat jejunum or epithelial monolayers. The peptide did not compete with 'ZsI-labeled epidermal growth factor for its receptor. ["CC]Iodoacetamide treatment of PSP, followed by prolonged tryptic digestion yielded predominantly a "iC-labeled tetrapeptide fragment containing Cysl04, with a lesser quantity of a '"C-labeled 1 Samino-acid peptide containing Cys9S (molar ratio 15: 1). GSH may predominantly reduce the Cys6-CyslO4 terminal disulphide bond in PSP. We conclude that some epithelia may exhibit a growth response to PSP if extracellular GSH is present. Reduction of PSP by GSH is not necessary for this response, suggesting that the trefoil receptor or its signal transduction is GSH sensitive. PSP could assist wound healing by interactions with epithelial cells exposed concurrently to a local high GSH concentration.

Flow cytometry was used to analyse the cord blood T cells of 33 babies at high risk 'HR' for developing allergy (born to at least one atopic, asthmatic parent), and 10 low risk 'LR' babies (born to non-atopic parents), following normal term deliveries. Significantly lower numbers of CD25+, (activated) T cells (p < 0.005) were seen in the cord blood of the HR babies who had developed both allergic symptoms and positive skin prick tests by one year of age when compared with the LR group. CD45RO+ (memory) T cells were detected in both HR and LR babies with a trend for lower numbers of memory cells to be detected in HR infants who later developed allergic symptoms and/or positive skin prick tests. Significantly lower numbers of CD4+/CD45RO+ were seen in the cord blood of HR babies who developed allergic symptoms compared to HR babies who showed no sign of allergy by one year and to the LR babies (p < 0.05 and p < 0.005). The presence of activated and memory T cells at birth implies intra-uterine priming. The significantly lower numbers of memory T cells in the HR babies suggests a suppression of T cell activation or lack of antigenic priming in this group. This prenatal influence on babies born to atopic parents may have important implications with regard to the mechanisms underlying atopic sensitisation.

No abstract

A simple trivalent colour test, developed for the rapid detection and identification of streptococci belonging to Lancefield groups A, C and G, was evaluated for sensitivity and specificity with cultures and when directly used with wound and throat swabs. In tests performed on cultures, all of 94 group A, 78 group C and 94 group G cultures were correctly identified. In direct tests on wound swabs, 49 of 52 group A, 17 of 19 group C and 48 of 51 group G streptococci were detected and correctly identified; no false positives were observed. With throat swabs from pharyngitis patients 34 of 36 group A, 3 of 6 group C and 5 of 8 group G streptococci gave positive results. Almost 10% of these swabs gave false positive reactions with the group C component of the test system. Samples taken from uninfected individuals indicated that the false positives were probably associated with blood group A. The test system gives rapid and reliable results with streptococcal cultures, but when directly applied to clinical samples the results must be interpreted with caution, particularly if the patient's blood group is not known.

A panel of monoclonal antibodies specific for TcR V gene families was used to study TcR V region expression in 28 cases of malignant and reactive T-cell expansions including four cases of mixed cellularity Hodgkin's disease (HD) and five reactive cases. TcR V beta 5 gene products were represented in three cases of lymphoblastic malignancy (V beta 5.1, V beta 5.2) and two cases of peripheral T-cell lymphoma (PTCL) (V beta 5.1). In the PTCL cases, the expanded family was found in the absence of clonal TcR gene rearrangements and in one of these cases with Ig JH and Ck clonal gene rearrangements consistent with the presence of a phenotypically and histologically undetectable clonal B-cell population. In a third PTCL case not investigated for genotype, the TCR V alpha 12 family was overrepresented. Expanded TcR V alpha 2 and V beta 5.1 families were identified in HD and V beta 8 and V beta 5.2/V beta 5.3 families in a reactive lymph node and CD3 and CD8-positive blood lymphocytosis respectively. Further study of PTCL and related entities are needed to establish whether expanded TcR families are common in those cases that fail to exhibit clonal TcR gene rearrangement.