As mentioned previously, Pseudomonas aeruginosa produces a host of virulence factors in concert, under the control of the quorum sensing system. Many studies show that inhibiting quorum sensing down-regulates the pathogenicity of Pseudomonas aeruginosa. However, it has been shown that rhamnolipids specifically are a key virulence determinant in Pseudomonas aeruginosa. A variety of virulence factors were analysed in Pseudomonas aeruginosa strains isolated from pneumonia patients. Rhamnolipids were found to be the only virulence factor that was associated with the deterioration of the patients to ventilator-associated pneumonia. Several other reports also support the role of rhamnolipids in lung infections. The effect of rhamnolipids in Pseudomonas aeruginosa virulence has been further noted in corneal infections (Alarcon et al., 2009; Zhu et al., 2004). It has been shown that rhamnolipids are able to integrate into the epithelial cell membrane and disrupt tight-junctions. This study used reconstituted epithelial membranes and purified rhamnolipids to demonstrate this mechanism. In addition to inhibition and killing of epithelial cells, rhamnolipids are able to kill polymorphonuclear (PMN) leukocytes and macrophages and inhibit phagocytosis. In summary, rhamnolipids have been shown unequivocally to be a potent virulence factor in the human host, however, they are also produced outside of the host, for example in a soil environment.
Rhamnolipids contribute to the establishment and maintenance of infection in cystic fibrosis patients in a number of ways, they disrupt the bronchial epithelium by disrupting the cell membranes, which promotes paracellular invasion of Pseudomonas aeruginosa and causes ciliostasis, further preventing the clearing of mucus. They also solubilise lung surfactant, allowing phospholipase C access to cell membranes and are necessary for correct biofilm formation.