Effect of glutamine and protein supplementation on exercise-induced decreases in salivary IgA.

Postexercise immune impairment has been linked to exercise-induced decrease in plasma glutamine concentration. This study examined the possibility of abolishing the exercise-induced decrease in salivary IgA through glutamine supplementation during and after intense exercise. Eleven athletes performed cycle ergometer exercise for 2 h at 75% of maximal oxygen uptake on 3 separate days. Glutamine (a total of 17.5 g), protein (a total of 68.5 g/6.2 g protein-bound glutamine), and placebo supplements were given during and up to 2 h after exercise. Unstimulated, timed saliva samples were obtained before exercise and 20 min, 140 min, 4 h, and 22 h postexercise. The exercise protocol induced a decrease in salivary IgA (IgA concentration, IgA output, and IgA relative to total protein). The plasma concentration of glutamine was decreased by 15% 2 h postexercise in the placebo group, whereas this decline was abolished by both glutamine and protein supplements. None of the supplements, however, was able to abolish the decline in salivary IgA. This study does not support that postexercise decrease in salivary IgA is related to plasma glutamine concentrations.

Immunomodulation of human blood cells following the ingestion of lactic acid bacteria.

Because of the lack of data that convincingly show immunomodulatory properties of lactic acid bacteria in humans, a study was performed in which healthy volunteers were divided into two groups and given a fermented milk product supplemented with Lactobacillus acidophilus strain La1 or Bifidobacterium bifidum strain Bb 12 for 3 wk. Blood was sampled throughout the study to assess changes in lymphocyte subsets or leukocyte phagocytic activity following consumption of the fermented products. No modifications of lymphocyte subpopulations were detected. In contrast, phagocytosis of Escherichia coli sp. in vitro was enhanced after the administration of both fermented products. The increment in phagocytosis was coincident with fecal colonization by the lactic acid bacteria and persisted for 6 wk after ingestion of the fermented products. By this time, the fecal lactobacilli and bifidobacteria had returned to concentrations prior to consumption. Nonspecific, anti-infective mechanisms of defense can be enhanced by the ingestion of specific lactic acid bacteria strains. These strains can be used as nutritional supplements to improve the immune function of particular age groups, i.e., the neonate or the elderly, for which these functions are diminished.

Modulation of a specific humoral immune response and changes in intestinal flora mediated through fermented milk intake.

This study was undertaken to elucidate whether eating a fermented milk containing Lactobacillus acidophilus La1 and bifidobacteria could induce changes in intestinal flora and modulate the immune response in man. Volunteers consumed a fermented milk containing L. acidophilus La1 and bifidobacteria over a period of three weeks during which an attenuated Salmonella typhi Ty21a was administered to mimic an enteropathogenic infection. A control group ate no fermented foods but received the S. typhi Ty21a. Faecal flora analyses showed an increase in L. acidophilus and bifidobacterial counts during fermented milk intake. The specific serum IgA titre rise to S. typhi Ty21a in the test group was > 4-fold and significantly higher (P = 0.04) than in the control group. An increase in total serum IgA was also observed. These results indicate that lactic acid bacteria which can persist in the gastrointestinal tract can act as adjuvants to the humoral immune response.

Field trial of an infant formula containing anti-rotavirus and anti-Escherichia coli milk antibodies from hyperimmunized cows.

Two groups of 124 and 108 children, respectively, living in urban Santiago, Chile in low socioeconomic conditions were prospectively followed for 6 months for their incidence of diarrhea. Each cohort was divided into two subgroups receiving either a commercial milk formula or the same formula containing 1% (wt/wt) bovine milk immunoglobulin concentrate from cows hyperimmunized with human rotaviruses and the major enteropathogenic Escherichia coli (EPEC) serogroups. Neither group differed with respect to incidence of diarrhea (98 episodes in 117 treated children versus 95 episodes in 115 control children), duration and clinical symptoms of diarrhea, and weight gain. Furthermore, neither group differed with respect to isolation of rotavirus (14 and 13 isolates in treatment and control groups, respectively) and isolation of enteropathogenic E. coli (14 and 15 isolates in treatment and control groups, respectively). The treatment but not the control formula contained neutralizing antibody against all human rotavirus serotypes. Titers were comparable to human breast milk samples. All isolated EPEC serogroups were included in the vaccine used for the immunization of the cows. The treatment, but not the control formula, protected mice against a lethal challenge with an EPEC strain. In conclusion, feeding an antibody-supplemented formula had no positive effect on diarrheal diseases under the conditions of a fairly well-controlled small-scale field trial.

Adhesion of colonization factor antigen II-positive enterotoxigenic Escherichia coli strains to human enterocytelike differentiated HT-29 cells: a basis for host-pathogen interactions in the gut.

Enterotoxigenic Escherichia coli are the most common cause of travelers' and infant diarrhea in less-developed countries. In the present work, among several metabolically labeled human diarrheagenic E. coli strains, enterotoxigenic strains expressing colonization factor antigen II were shown to bind to HT-29 intestinal cell monolayers when these cells were grown in conditions promoting their enterocytic differentiation. Indirect immunofluorescence with fimbrial antisera revealed that pathogen attachment was associated with the production of a specific bacterial adhesin, the E. coli surface antigen CS3. Scanning and transmission electron micrographs showed an apical pattern of colonization, characteristic of enterotoxigenic E. coli infections. The above data were consistent with all observations previously made with human enterocytes obtained from intestinal biopsies. The lectin-carbohydrate nature of this cell-cell recognition mechanism was also established. Bacterial binding to differentiated HT-29 cells was inhibited by a mixture of newborn meconium glycopeptides. By coating the cell layers with the plant agglutinin from Evonymus europaea, pathogen attachment was also prevented. Binding of 125I-labeled CS3 adhesin and E. europaea agglutinin to brush border membrane proteins separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and transferred to nitrocellulose revealed three bands of about 30, 20, and 13 kilodaltons, which acted as receptors for both bacterial and plant lectins. These data suggest that the sugar units to which the bacterial colonization factor CS3 binds are synthesized as carbohydrate chains of three brush border membrane glycoproteins in HT-29 cells by a differentiation-specific pathway.