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Biomedical subjects

A G Cummins

Publications and source records attributed to A G Cummins.

44 records · Page 3Linked to original sources
PubMed1986

The effect of methionine and protein deficiency in delaying expulsion of Nippostrongylus brasiliensis in the rat.

Three protein-deficient diets containing 5%, 6%, or 7% casein, with and without 0.3% methionine supplementation, were fed to Wistar rats from weaning for 6 wk. Animals were infected subcutaneously with 1500 larvae of Nippostrongylus brasiliensis and killed after 14 days when nutritionally normal animals have expelled more than 97% of the worm burden. There was a delay in worm expulsion that was related to both the protein content (p = 0.0006) and to methionine content (p less than 0.0001). Methionine supplementation significantly reduced the worm burden in animals fed the 7% protein diet from a geometric mean of 32.4 to 5.2 (p = 0.0408) and in rats fed the 6% protein diet from a mean of 162 to 8.1 (p = 0.0002) but had no effect in rats on the 5% casein diet. Thus, addition of methionine overcame the adverse effect of protein deficiency in these less severely affected groups.

Animals↗
PubMed1978

Histopathology in giardiasis: a correlation with diarrhoea.

There is controversy both in regard to the severity of small bowel mucosal damage attributable to giardiasis and to the causal relationship of these changes to the associated diarrhoea. In this series of 17 consecutive patients with giardiasis, small bowel histology and diarrhoea were independently assessed and compared. Disaccharidase assays were performed in 16 of these patients and a repeat biopsy obtained in seven cases. On histological examination the villous architecture varied from normal to sub-total villous atrophy. When these changes were compared with the severity of diarrhoea, a direct correlation was obtained, the more severe symptoms being associated with the more severe villous changes. Repeat biopsy after treatment demonstrated improvement in the histology which correlated with improvement in diarrhoea. Lactase activity was low in all patients with moderate or severe diarrhoea as well as in some patients with mild diarrhoea, two of whom had normal histology. This series demonstrates the occurrence of a spectrum of mucosal changes in giardiasis and supports the concept that these changes mediate the diarrhoea associated with this gut parasite.

Adolescent↗
PubMed1978

Suppression of rejection of Nippostrongylus brasiliensis in iron and protein deficient rats: effect of syngeneic lymphocyte transfer.

Rejection of Nippostrongylus brasiliensis is impaired in iron and protein deficient rats and this suggests that iron and protein deficiency directly or indirectly suppresses the immune response. The site of the immunological defect in deficient rats was investigated using the technique of cellular transfer of resistance. The functional activity of immune mesenteric lymph node cells obtained from iron and protein deficient donors was not depressed as measured by their capacity to cause parasite rejection in nutritionally sufficient recipients. In contrast, immune lymph node cells obtained from either sufficient or deficient donors did not result in parasite rejection in iron and protein deficient recipients. These results indicate that there is no permanent defect of lymphocyte function in iron and protein deficient rats and suggest that either some other component of the rejection mechanism is defective, or that lymphocyte function is blocked in an iron and protein deficient environment.

Animals↗
PubMed1977

Effect of iron and protein deficiency on the expulsion of Nippostrongylus brasiliensis from the small intestine of the rat.

The relationship between iron deficiency and protein deficiency and infestation of the rat with the nematode Nippostrongylus brasiliensis was investigated. There was a significant delay in the expulsion of N. brasiliensis from the small intestine of both iron deficient and protein deficient animals and those with a combined deficiency of iron and protein. Iron repletion returned the time of worm expulsion to normal and this would appear to be related to iron deficiency per se rather than to anaemia. Antibody initiated damage to worms was normal in the control animals and in animals with nutritional deficiencies. This suggests that the defect in worm expulsion occurs either in the cell-mediated immune system or in one of the other mediators of expulsion. Extrapolation to the human situation has important therapeutic implications in that iron and protein deficiency may play an important role in the perpetuation of helminth infestations. Thus, to be successful antihelminth therapy should be accompanied by iron and protein supplementation.

Ancylostomatoidea↗
PubMedDate not supplied

Association of maturation of the small intestine at weaning with mucosal mast cell activation in the rat.

Maturation of the small intestine at weaning has some features in common with immunological reactions involving the gut mucosa. Mucosal mast cell (MMC) activation is a prominent feature of both IgE and cell-mediated mucosal immune responses. MMC activation was therefore studied during the weaning period by measurement of rat mucosal mast cell protease II (RMCPII) release into the systemic circulation as well as MMC counts and jejunal RMCPII content. Maturation of the small intestine was measured by changes in villus and crypt length, and in crypt cell production rate (CCPR). At 3 weeks of age, serum RMCPII increased 17-fold and MMC showed features of degranulation. At the time of weaning (2-4 weeks), villus and crypt length and CCPR increased progressively to adult values. After weaning, serum RMCPII declined slowly to normal adult levels and MMC regained a normal appearance. This study showed a close association between MMC activation and maturation of the small intestine during the weaning period.

Animals↗
PubMedDate not supplied

Recovery of the small intestine in coeliac disease on a gluten-free diet: changes in intestinal permeability, small bowel morphology and T-cell activity.

Intestinal permeability was assessed before and 1, 2, 4, 8 and 12 weeks after commencing a gluten-free diet (GFD) in eight coeliac subjects. Intestinal morphology was quantified in six coeliac subjects on a normal diet, six coeliac subjects on a GFD, and 21 normal subjects. T-cell activity was measured in the eight coeliac subjects by soluble interleukin-2 receptor (sIL-2R) concentration (normal less than 477 U/mL). Intestinal permeability was increased 10-fold with a geometric mean value of 0.72 on a normal diet, and decreased to 0.17 at 4 weeks (P = 0.04), to 0.07 at 8 weeks (P = 0.010), and to 0.20 at 12 weeks (P = 0.015) of a GFD. Two of the eight subjects showed a poor response to gluten withdrawal. Quantitative intestinal morphology showed no significant improvement after 3 to 6 months of a GFD. Mean +/- s.d. sIL-2R concentrations in the eight subjects were increased 5-fold higher than control values at 1400 +/- 530 U/mL on a normal diet and decreased to 750 +/- 200 U/mL after 12 weeks of a GFD (P = 0.004). We conclude that intestinal permeability improves rapidly in the majority of coeliac subjects after commencing a GFD, although some abnormal permeability and increased T-cell activity persists. This may be due to varying degrees of gluten ingestion resulting in continued immune activation.

Adult↗
PubMedDate not supplied

The interactive role of mucosal T lymphocytes in intestinal growth, development and enteropathy.

Over the past 15-20 years, research has progressively focused on the mucosal T cell as the central factor in the initiation of physiological or pathological changes, first in the growth and maturation of the early (postnatal) intestine, and second in adult-type enteropathies resulting from sensitivity to either food or pathogen-derived antigens. T cell-mediated events may be measured, for example, in terms of specific immunopathologic patterns of change and injury, such as type 1 (lymphocyte infiltration), type 2 (crypt hyperplasia) and type 3 (flat-destructive), which can be recognized and quantitated microscopically; by determination of lymphocyte reactivity through secretion of interleukin-2 receptors (IL-2R) into plasma or expression by mucosal lymphocytes; by quantitation of lymphocyte subsets emigrating into inflamed tissues by immunoperoxidase-labelled monoclonal antibodies; or by the determination of T cell receptor polymorphisms. Alterations in intestinal growth, structure and function at weaning are likely to be T cell-mediated as they are analogous to the same type 1/2 lesions that reflect modulation of adult mucosal architecture in food and parasite-induced hypersensitivity reactions. Enteropathies associated with HIV infection and T cell deficiency display a milder degree of villous flattening and impaired crypt hyperplasia than that typical of gluten-sensitivity, suggesting a reversion to lesser degrees of mucosal pathology (type 1/2). Clearly more information will accrue; meanwhile the remarks in this brief survey should provide a firm basis whereby clinician and scientist can meet, and together recognize and further dissect the modulatory effect of T lymphocytes on mucosal structure and function.

Animals↗