Morphological and immune response alterations in the intestinal mucosa of the mouse after short periods on a low-magnesium diet.

The importance of Mg for the immune function is well recognized; however, there is no information available about the effect of Mg intake on the modulation of local immune response in the intestine. Thus, in the present study the hypothesis that short periods of Mg deprivation can affect intestinal mucosa and local immune response was tested. For this purpose, OF1 female mice were fed a semipurified diet (1000 mg Mg/kg diet). For 3 d before immunization and 1 d after, half of the animals were fed a Mg-deficient diet (30 mg Mg/kg diet), three immunizations per os were performed every 3 weeks with Escherichia coli producing the CS31A capsule-like protein (1010 or bacteria per animal). Mice were killed 10 d after the last immunization. The level of specific anti CS31A immunoglobulin (Ig) G and IgA in the serum and secretory IgA in the intestinal secretions and faeces were measured by ELISA. The results indicated that administration of a high dose of immunogen with a low-Mg diet led to lower specific IgA levels in the intestinal mucus and serum. Administration of a low dose of immunogen with a low-Mg diet led to lower IgA and IgG levels in the serum and secretory IgA coproantibodies. To assess alterations of intestinal mucosa caused by a low-Mg diet for a short period, histological and scanning electron microscopy analyses were performed on samples from mice (not submitted to the vaccination protocol) after 3 d on the Mg-deficient diet. These analyses showed several alterations, suggesting perturbations in the growth of the intestinal mucosa. These changes were accompanied by modifications in the expression of several genes involved in cell growth and stress response. From this present work, it may be concluded that short periods of Mg deprivation can affect the intestinal mucosa and local immune response of the intestine.

Septicaemic Escherichia coli and experimental infection of calves.

Three strains of Escherichia coli with a common surface antigen, 31a, capable of adhering to calf enterocytes in vitro were compared to reference strains of septicaemic E. coli (RVC 330 and vir E. coli). The surface antigen 31a was present in the RVC 330 reference strain. E. coli vir had a surface antigen which was not present in E. coli 31a or E. coli RVC 330. The RVC 330 and vir reference strains also adhered to calf enterocytes in vitro. Oral infection of calves not receiving colostrum with E. coli 31a was generally followed by septicaemia and death in less than 48 h. Post-mortem examination revealed pneumonia and oedema of the kidneys and gall bladder. Oral infection of calves receiving colostrum had no effect, but intravenous inoculation produced arthritis within 15 days. The comparison of these results with those previously described by other workers did not lead to the identification of pathognomonic characteristics, which could be clearly correlated with properties specific to E. coli 31a. It is suggested that, like ColV and vir, antigen 31a may be a virulence marker for certain strains of bovine septicaemic E. coli. Furthermore, the 31a antigen appears to be carried on a plasmid.

Additive protective effects of colostral antipili antibodies in calves experimentally infected with enterotoxigenic Escherichia coli.

With oral infection of calves by an enterotoxigenic Escherichia coli strain carrying K99, F41, and FY adhesins, colostrums from cows vaccinated against either K99+F41 or FY did not provide protection, but a mixture of the two colostrums did. The association of antibodies directed against the different adhesins is more effective than antibodies directed against one adhesin alone for colostral protection against enterotoxigenic E. coli carrying several adhesins.

[Anti-K99 vaccination and colostric protection of calves infected experimentally with Escherichia coli K99]. / Vaccination anti-K99 et protection colostrale des veaux infectés expérimentalement avec Escherichia coli K99.

Colostral antibodies of cows vaccinated with E. coli B41 (O101: K99, F41) protect completely B41 experimentally infected calves. In order to know more precisely the role of K99, F41 antibodies in protection, calves receiving the colostrum of B41 vaccinated cows are infected with E. coli B44 (O9: K30: H-K99, F41). Vaccination multiplies K99 antibodies in colostrum by seven. In B44 infected calves, specific K99, F41 antibodies protect only 3 out of 6 calves completely. Additive effect of antibodies against K99 and other surface antigens of enterotoxigenic E. coli seems desirable for a more complete protection.

Intestinal K99+ escherichia coli adhesion and absorption of colostral IgG1 in the newborn lamb: effect of fetal infusion of thyroid hormones.

Continuous infusion of thyroid hormones during the last 12 days of gestation in ovine fetuses was associated with: a reduction of the rate of appearance of blood IgG1 after colostrum feeding in the newborn lambs; an important reduction of the number of jejunal cells filled with IgG1, 12 hours post partum, suggesting a premature closure of the intestinal permeability to IgG1; and a significant reduction of the K99+ Escherichia coli adhesion on the intestinal villi. These results could partly explain relationships observed previously between perinatal thyroid function abnormalities and the occurrence of neonatal diseases.

Specific protection by colostrum from cows vaccinated with the K 99 antigen in newborn calves experimentally infected with E. coli Ent+ K99+.

We have measured the protective effect of colostrum of vaccinated cows with the K99 antigen comparatively with the colostrum of non vaccinated cows, in calves receiving at birth 2 liters of colostrum and just after 5 times 10(10) to 1 times 10(11) E. coli Ent+, K99+. The K99 antigen was prepared from E coli B41 (0101:K99:H-) cultured in a fermentor. Cows were vaccinated subcutaneously with 100 mg or 300 mg (wet weight) in emulsion in Freund uncomplete adjuvant 45 and 15 days before parturition. Of 4 calves receiving a colostrum of non vaccinated cows 4 had a diarrhoea, 3 became dehydrated and 2 died. Of 6 calves receiving colostrum of vaccinated cows, 5 were healthy and the 6th calf had a mild diarrhoea for few hours and became again healthy. Control and protected calves excreted E. coli K99+, 24 HOURS AFTER INFECTION. The protection is probably due to K99 antibodies which inhibit adhesion of E. coli K99+ to the intestinal epithelium.