The role of bacterial adhesion in cystic fibrosis including the staphylococcal aspect

Abstract

The bacteriology of cystic fibrosis shows a unique and predictable progression of colonizing micro-organisms. The reason for this sequence is still not known, but thought must be given to the idea that it may be related to the genetic disorder in some way. If this were to be true, an understanding of the colonization mechanisms at all stages in this progression could provide valuable insights for the development of novel therapies. As far as can be ascertained from published studies, mucus is the site of colonization in cystic fibrosis. While there is no doubt that the major pathogen, Pseudomonas aeruginosa, adheres to injured cells more avidly than to intact cells, the overwhelming evidence indicates that it also attaches more avidly to mucus than to intact airway cells by means of specific adhesin-receptor mechanisms. Studies with Staphylococcus aureus, the other major pathogen, are also in progress. These indicate that this organism also has an affinity for mucus. At this time the studies suggest a lesser affinity than P. aeruginosa, at least with adult mucins. These two organisms do not however appear to share the same receptor. In addition to these two major pathogens, Haemophilus influenzae and Streptococcus pneumoniae, pathogens of lesser importance also adhere to mucus. Therefore adhesion to mucus or mucins may be a recurring theme in all airway colonization. A knowledge of the factors which control these tropisms ought to provide insights into the bacterial specificity seen in cystic fibrosis and other diseases.