No abstract

Two Lactobacillus plantarum strains of human intestinal origin, strains 299 ‫؍(‬ DSM 6595) and 299v ‫؍(‬ DSM 9843), have proved to be efficient colonizers of the human intestine under experimental conditions. These strains and 17 other L. plantarum strains were tested for the ability to adhere to cells of the human colonic cell line HT-29. L. plantarum 299 and 299v and nine other L. plantarum strains, including all six strains that belong to the same genetic subgroup as L. plantarum 299 and 299v, adhered to HT-29 cells in a manner that could be inhibited by methyl-␣-D-mannoside. The ability to adhere to HT-29 cells correlated with an ability to agglutinate cells of Saccharomyces cerevisiae and erythrocytes in a mannose-sensitive manner and with adherence to D-mannose-coated agarose beads. L. plantarum 299 and 299v adhered to freshly isolated human colonic and ileal enterocytes, but the binding was not significantly inhibited by methyl-␣-D-mannoside. Periodate treatment of HT-29 cells abolished mannose-sensitive adherence, confirming that the cell-bound receptor was of carbohydrate nature. Proteinase K treatment of the bacteria also abolished adherence, indicating that the binding involved protein structures on the bacterial cell surface. Thus, a mannose-specific adhesin has been identified in L. plantarum; this adhesin could be involved in the ability to colonize the intestine.

Rectal cultures from Swedish and Pakistani hospital-delivered newborn infants were analysed regarding the early acquisition of enterobacteria. Swedish infants were delivered vaginally, Pakistani infants were delivered either vaginally or by caesarean section. The Swedish infants were all breast-fed, whereas breastfeeding was incomplete and often started late among the Pakistani infants. Both groups of Pakistani infants were more rapidly colonized with enterobacteria than were the Swedish infants. Cultures from Swedish infants seldom yielded more than one kind of enterobacteria; E. coli and Klebsiella were most frequently isolated. E. coli dominated in both Pakistani groups, but especially caesarean section delivered infants were in addition often colonized with Proteus, Klebsiella, Enterobacter or Citrobacter species. Breastfeeding from the first day of life reduced colonization with Klebsiella/Enterobacter/Citrobacter. The results suggest that environmental exposure, delivery mode and early feeding habits all influence the early intestinal colonization with enterobacteria.

Type 1 fimbriae with mannose-specific lectins are widely distributed among members of the family Enterobacteriaceae and confer the ability to attach to a range of host cells, including colonic epithelial cells. The mucosal surfaces are protected by secretory immunoglobulin A (IgA), which agglutinates microorganisms and prevents their attachment to host epithelial cells. This action has been attributed to a specificity of the antigen-combining site of mucosal immunoglobulins for bacterial and viral surface components. Here, we report a novel mechanism for the antibacterial effect of secretory IgA. Secretory IgA and IgA myeloma proteins, especially those of the IgA2 subclass, were shown to possess carbohydrate receptors for the mannose-specific lectin of type 1-fimbriated Escherichia coli. The presence of the high-mannose oligosaccharide chain Manal-6(Manal-3)Manxl-6(Manal-3)Man,ll-4GlcNAcIl-4GlcNAc correlated with binding activity. The interaction between bacterial mannose-specific lectins and IgA receptor oligosaccharide resulted in agglutination of the bacteria and in inhibition of bacterial attachment to colonic epithelial cells. Thus, this interaction could form the basis for a broad antibacterial function of secretory IgA against enterobacteria regardless of the specificity of antibody molecules.

Staphylococcus aureus has been isolated at an increasing rate from infants' stools during the last decades, but it is not known whether this species can colonize and persist in the intestinal microflora. To investigate this, 49 Swedish infants were followed prospectively from birth until 12 months of age. S. aureus was identified in a rectal swab obtained 3 d after delivery and in quantitative cultures of fecal samples collected at 1, 2, 4, and 8 weeks and at 6 and 12 months of age. A random amplified polymorphic DNA (RAPD) method was developed to distinguish individual S. aureus strains from one another and the strains were tested for production of enterotoxins A-D and TSST-1. By 3 days of age, 16% of infants had S. aureus in their intestines, which increased to 73% by 2-6 months, whereafter it decreased slightly to 53%. At the same time S. aureus population counts in colonized infants declined from an average 10 6.8 CFU/g feces during the first months of life to 10 4.0 CFU/g feces by 12 months. Colonized infants usually harbored one or two S. aureus strains in their microflora for long periods of time. Few strains were transient passengers and the median time of persistence of S. aureus strains in the microflora was several months. Of the 75 S. aureus strains identified, 43% produced one or more toxins: 13% SEA, 7% SEB, 23% SEC, 4% SED, and 11% TSST-1. Altogether, 47% of the investigated infants were colonized by a toxin-producing S. aureus during their first year of life. Despite this they were apparently healthy and did not have more gastrointestinal problems than noncolonized infants. This report is the first to show that S. aureus may be a resident member of the normal intestinal microflora in infancy. Abbreviations CFU, colony-forming units TSST-1, toxic shock syndrome toxin-1 RAPD, random amplified polymorphic DNA Bacteria start to colonize the skin, respiratory tract, and intestines as soon as the newborn has left the sterile womb. With time, a complex ecosystem develops known as the normal microflora (1). Staphylococcus aureus colonizes the anterior nares of more than 50% of young infants (2-5). During the last decades, S. aureus has also been isolated at an increasing rate from fecal samples of infants in Western societies. Thus, only 1 out of 13 infants had S. aureus in their stools in a study performed in England in the 1980s (6), but 30% in a Swedish study published 1985 (7) and 53% in Sweden in the late 1990s (8). It is not known whether staphylococci persist and replicate in the intestines or if S. aureus in the stools represent bacteria transiently passing the intestines after having been swallowed. If infants are colonized by S. aureus in their intestines, it may have medical consequences. S. aureus strains can produce a range of different exotoxins, among them the enterotoxins, which cause vomiting with or without diarrhea and are responsible for staphylococcal food poisoning (9). The enterotoxins, together with toxic shock syndrome toxin-1, also function as "superantigens." By binding to both...