Ragnar Lindstedt

Anti-adhesive activity of human casein against Streptococcus pneumoniae and Haemophilus influenzae.

The casein fraction of human milk was found to inhibit the attachment of Streptococcus pneumoniae and Haemophilus influenzae human respiratory tract epithelial cells. The inhibitory activity for S. pneumoniae remained after heat and trypsin treatment of the casein and was found in oligosaccharides released from casein. kappa-Casein, which is the most highly glycosylated casein component, inhibited pneumococcal attachment at concentrations similar to the whole casein fraction. The results are consistent with the known recognition of GlcNAc beta 1-3Gal by S. pneumoniae, since human milk and bovine colostrum, which contain GlcNAc, inhibited attachment, but mature bovine milk lacking GlcNAc did not. The effect on H. influenzae was similar to that on S. pneumoniae in that the attachment was inhibited by human casein and bovine colostrum, but not by either mature bovine milk or by the bovine casein fraction. The kappa-casein component of human milk was a less efficient inhibitor of H. influenzae attachment than the whole casein fraction and the free oligosaccharides were inactive. This anti-microbial effect of human casein represents a new mechanism for the protection by breast-milk against respiratory tract infection.

Bacterial Adherence and Mucosal Cytokine Production

1. Uropathogenic E. coli adhere to mucosal sites. 2. In the urinary tract, adherence is followed by inflammation, including a mucosal cytokine response. 3. Bacteria activate epithelial cells to secrete IL-6 and IL-8. IL-6 may cause the fever and acute phase response that accompany systemic urinary tract infections. IL-8 may function as a neutrophil chemoattractant. 4. E. coli up-regulate adhesion molecule expression on epithelial cell lines and neutrophil migration through epithelial cell monolayers. This process is inhibited by antibodies to CD18 and ICAM-1. 5. Cytokines released by nonepithelial cells (T cells and monocytes) modify the epithelial cell cytokine response to bacteria.

Globo-A--a new receptor specificity for attaching Escherichia coli.

Uropathogenic Escherichia coli strains designated as ONAP, based on their O negative A positive agglutination of human P1 erythrocytes, were shown to prefer the globo‐A glycolipid as a receptor structure. The dependence on both the A terminal and the globoseries chain was confirmed by agglutination of human AP1, but not A or OP1, erythrocytes and by binding to the globo‐A glycolipid on TLC plates. Neither Galαl→Ga1β nor the A trisaccharide GalNAcαl→ 3(Fucαl→2)Galβ alone functioned as receptors. The bacteria thus appeared to recognize an epitope resulting from the combination of the terminal and internal structures.

Mechanism of adherence of Moraxella(Branhamella)catarrhalis.

We examined the mechanisms of adherence of Moraxella catarrhalis to nasopharyngeal epithelial cells. Fimbriae were detected by electron microscopy on most of the strains studied. A role of fimbriae in adherence was supported by the reduction in adherence by treatments denaturing the fimbriae or by antifimbrial antibodies. There was, however, no significant difference in adhesive capacity or hemagglutination between fimbriated and non-fimbriated strains. Furthermore, there was no correlation between hemagglutination and adherence. The possibility that receptor epitopes were provided by cell surface glycolipids was examined by thin-layer chromatography. Glycolipids from various sources, including nasopharyngeal cells were separated by thin layer chromatography plates and overlayed with bacteria. No binding was detected. The results suggest that lectin-glycolipid interactions do not explain the attachment of M. catarrhalis to epithelial cells.

[18] Strategies for studying bacterial adhesion in Vivo

Publisher Summary The ultimate goal of studies on microbial adhesion is to understand what molecular interactions between the host and microbe occur in vivo and the impact of these interactions on disease processes. With this goal in mind, the problem can be approached at four levels. At the biochemical level, the host receptors at the relevant colonization site are identified; at the cell biology level, consequences of bacterial binding to host epithelial cells are studied in cell culture; at the physiological level, the consequences of bacterial binding are studied in experimental animals or humans; and at the population level, the consequences of receptor binding for colonization are studied by epidemiological methods. This chapter provides an example of studies at each level and discusses the implications for what might occur in vivo .