Biology and pathology of urinary tract infections.
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Adolescent↗
Biomedical subjects
C Svanborg Edén
Publications and source records attributed to C Svanborg Edén.
The secretory IgA system in the neonatal period.
It is still not known when the secretory IgA response, important for defence of the mucous membranes, becomes fully competent in the human infant. The infant is, however, provided with 0.25--0.5 g of secretory IgA/day via the maternal milk. The milk contains secretory IgA antibodies against a wide variety of antigens from microorganisms, including bacteria, viruses and parasites. Many of the antibodies are directed against important virulence factors such as bacterial pili, enterotoxins, capsular polysaccharides and endotoxic lipopolysaccharides. The passive transfer of antibodies through the milk may explain why breast-fed infants are resistant to enteric infections in particular. The antibodies in the milk are often directed against antigens in the mother's milieu and intestine. An entero-mammary gland link, possibly consisting of lymphoid cells homing from the Peyer's patches in the intestine to the mammary gland, has been suggested. A limited selective uptake of oligomeric IgA from serum in exocrine glands, including the mammary glands, has also been indicated. Whichever the mechanism, the antibodies transferred via breast milk are composed to meet the needs of the infant.
Adolescent↗
Recent progress in the understanding of the role of bacterial adhesion in the pathogenesis of urinary tract infection.
There is extensive evidence indicating that the capacity of Escherichia coli to attach to the mucosal lining of the urinary tract is a virulence factor in acute pyelonephritis in the unobstructed state. In vitro results using human uroepithelial cells and clinical E. coli isolates as well as in vivo work on ascending urinary tract infection in mice and E. coli strains with genetically defined adhesins support this notion. The biochemical characterization of the bacterial ligands and epithelial cell receptors important for the attachment of most pyelonephritogenic E. coli provides a more sophisticated means of evaluating the role of bacterial adhesion in urinary tract infection: 1) It allows precise diagnosis of the receptor specificity of clinical isolates; 2) The receptor can be used to isolate the relevant bacterial adhesins; 3) The localization and quantity of the receptor in the patient may be of prognostic importance; 4) The administration of soluble receptor analogues or antibodies to the adhesins may be useful for prophylactic and/or therapeutic purposes.
Adhesins, Escherichia coli↗
Defence of mucous membranes by antibodies, receptor analogues and non-specific host factors.
Most infections reach man via the mucosal membranes, and more than half of the lymphoid system is found in connection with mucosae. The major antibodies found on mucous membranes are secretory IgA, which function primarily by binding microorganisms and thereby preventing their contact with the host tissues. The optimal mode of immunization to obtain a secretory IgA response is not well defined. Repeated mucosal exposure with antigen may result in oral tolerance, with decreasing circulating antibodies but a remaining secretory IgA response. The secretory IgA response is usually short-lived and can be difficult to boost. IgM as well as IgG antibodies may add to host defence at the mucosal level, but when engaged, they usually induce inflammation in host tissues. Analogues to bacterial receptors on mucosal epithelium may be present in exocrine secretions such as human milk. During an attack on the host, it is possible that such receptor analogues may aid in the prevention of attachment of bacteria to mucous membranes used as an initial site. A number of non-specific host factors support mucosal defence. One of them is lactoferrin. Lactoferrin deficiency seems to result in recurrent bacterial infections, suggesting its importance in normal host defence.
Administration, Oral↗
Genetic factors in host resistance to urinary tract infection.
In patients with recurrent pyelonephritis, the pathogenetic events proceed through intestinal colonization, spread to the urinary tract and persistence, seemingly uninterrupted by host defense mechanisms. The factors responsible for the deficient bacterial clearence from the kidneys of these patients, and the genetic control, have not been identified. The susceptibility to colonization has been linked to an increased receptivity for attaching bacteria of the uroepithelia, and to an overrepresentation of the P1 blood group phenotype. To evaluate the role of defects in host defense for the susceptibility to pyelonephritis, experimental UTI in mouse strains with known deficiencies was used. A highly significant increase in susceptibility was noted for C3H/HeJ compared to C3H/HeN mice. The bacterial recovery was inversely correlated to the mitogenic response to LPS. Back-cross analysis revealed a linkage of susceptibility to the Lpsd/Lpsd genotype. In contrast, T and B lymphocyte and complement (C5) defects had little effect on the clearance of Escherichia coli from the kidneys. It is concluded that the inflammatory mechanisms induced by LPS are essential for resistance to experimental pyelonephritis.
Animals↗
Non-antibiotic prevention of urinary tract infection.
The identification of several glycoconjugates as receptors for attaching bacteria has resulted in optimism regarding the use of receptor analogues in preventing infection. The structure of receptor-active oligosaccharides and the patient groups which might benefit from such treatment are most thoroughly understood for urinary tract infections. Prevention of adhesion and delay or decrease of infection was achieved using oligosaccharides from the globoseries of glycolipids containing Gal alpha 1----4Gal. This minimal receptor structure as a free saccharide was, however, not sufficient. It was the intact P, P1 and pk determinants which showed optimal activity in vitro. In addition, protection against experimental UTI results from previous exposure to whole bacteria or isolated antigens. The mechanism(s) of protection and their relevance in clinical UTI remain to be defined.
Animals↗
The secretory IgA system.
The secretory IgA system is common to all mucosal membranes and is presumably of great importance for their defense. In addition to the secretory IgA antibodies produced in a mucosa in response to a local antigenic stimulus there is a spread of this type of IgA response via committed lymphocytes. They originate from central lymphoid organs in the intestinal (Peyer's patches) and bronchial mucosa (bronchus-associated lymphoid tissue, BALT) which they leave after antigenic exposure. They migrate, or "home", to exocrine glands such as the lacrimal, salivary, mammary and prostatic glands and mucosal membranes of the respiratory, gastrointestinal and genito-urinary tract. Almost half of all lymphocytes may be involved in the production of IgA antibodies. The secretory IgA antibodies are the dominating immunoglobulins in exocrine secretions on mucous membranes. They function primarily by preventing contact between the microbe and the host tissue most commonly attacked in infections, the mucous membrane. The fact that breast-feeding protects the infant against intestinal infections is one good example of the clinical significance of secretory IgA antibodies. This mode of protection can be enhanced by vaccination.
Breast Feeding↗