Extract of Pelargonium sidoides (EPs® 7630) displays anti-infective properties by enhanced phagocytosis and differential modulation of host – bacteria interactions

Background: EPs® 7630 is an extract derived from the roots of Pelargonium sidoides DC. Clinical trials have shown that the preparation is effective in the treatment of respiratory tract infections such as acute bronchitis. Objectives: In-vitro study to assess the impact of EPs® 7630 on human peripheral blood phagocytes (PBP) and on the host-bacteria interaction using A-Streptococci (GAS) as a model. Methods: A whole-blood based flow cytometric assay was used to analyze phagocytosis of C. albicans and oxidative burst. Intracellular killing of yeast cells was assessed by a microbiological assay. Adhesion of GAS on human HEp-2 and buccal epithelial cells (BEC) was determined by flow cytometry and GAS invasion of HEp-2 cells was analyzed by a penicillin/gentamicin-protection assay. EPs® 7630 was applied at concentrations between 0 and 30µg/ml. Results: EPs® 7630 increased the number of phagocytosing PBP with a maximum effect of 56% at 2min and led to an increase of burst-active PBP (up to 120% at 4min). Intracellular killing was enhanced, as demonstrated by a 31% reduction in the number of surviving target organisms after 120min. Interestingly, EPs® 7630 displayed a differential effect with respect to adhesion of GAS to HEp-2 cells and BEC. While adhesion to HEp-2 cells was inhibited with a maximum effect of 46% at 120min, adhesion to BEC was increased up to 7-fold. EPs® 7630-pre-treatment of HEp-2 cells or GAS revealed that the preparation targets GAS rather than epithelial cells. In addition, EPs® 7630 significantly reduced GAS invasion of HEp-2 cells at 60, 120, and 180min. Conclusions: The essential anti-infective properties of EPs® 7630 can explain its clinical effect. Thus, the enhanced function of phagocytes represents an important effector mechanism in order to repel pathogens. Furthermore, modulated host-bacteria interaction may prevent from bacterial super- and recurrent infections. Reduced bacterial adhesion to intact epithelia (HEp-2) protects from bacterial colonization and infection/super-infection whereas enhanced attachment of bacteria to decaying BEC may inactivate pathogens by swallowing. Thus the inhibition of GAS invasion of epithelial cells prevents from microorganisms that evade host defences and antibiotic treatment.