Birzeit University’s Biology and Biochemistry Department sponsored a lecture on how the rare Legionnaire’s Disease infects humans. The research was presented by postdoctoral researcher at the University of Kentucky Arwa Abu Khweek on March 23, 2013.

Abu Khweek described how legionella pneumophila, the causative agent of Legionnaire’s disease, replicates in human alveolar macrophages to establish infection in humans. The infection occurs without  human-to-human transmission, with its main source being L. pneumophila biofilms established in air conditioners, water fountains, and hospital equipment. The biofilm structure provides protection for the organism from disinfectants and antibacterial agents.

The L. pneumophila infection in humans is characterized by a subtle initial immune response, giving time for the organism to establish infection before the patient succumbs to pneumonia. Planktonic L. pneumophila elicits a strong immune response in murine, but not in human macrophages, enabling control of the infection.

Interactions between planktonic L. pneumophila and murine or human macrophages have been studied for years, yet the interface between biofilm-derived L. pneumophila and macrophages has not been explored. Abu Kwaik’s research demonstrates that biofilm-derived L. pneumophila replicates significantly more in murine macrophages than planktonic bacteria. In contrast to planktonic L. pneumophila, biofilm-derived L. pneumophila lacks flagellin expression, do not activate caspase-1 or 7 and trigger less pyroptosis. In addition, while planktonic L. pneumophila is promptly delivered to lysosomes for degradation, biofilm-derived bacteria were enclosed in a vacuole that did not fuse with lysosomes in murine macrophages.

The study has advanced understanding of the innate immune response to biofilm-derived L. pneumophila and closely reproduces the natural mode of infection in human beings.