Phagocytosis of the bacteria (its elimination by phagocytes) has been shown to require that
specific antibodies are first created in order to help opsonise them [1; 2]. As humans
generally have no pre-existing Legionella antibodies  they will take time following
initial infection to develop. Verbrugh  found that human sera generally did not contain
sufficient concentrations of opsonins to facilitate phagocytosis. Whereas experimental animal
sera that had previously been exposed to Legionella were sufficient to facilitate
opsonisation and phagocytosis by virtue of the antibody-mediated activation of the classical
complement pathway, therefore pointing to a deficiency of the innate system to mediate
phagocytosis [5; 6]. Indeed, human phagocytes ingested Legionella substantially less
efficiently than other typically resistant bacteria such as E. coli [5; 7].
The mammalian immune response to a Legionella infection can be summarised as follows:
Innate immune response - When Legionella pneumophilla enters the lungs they are
engulfed by macrophages where they are able to replicate. The Legionella replication
causes the macrophage to release cytokines which attract the attention of Natural Killer
cells. These then stimulate the macrophages, by releasing IFN-γ, enabling them to
restrict Legionella growth.
Adaptive immune response - Immature dendritic cells (DCs) present in the lung are infected by the
Legionella bacteria. The bacteria inside the DC are not destroyed but are prevented from further
growth. The DC then goes
through a process of maturation enabling it to produce Legionella antigens. The
DCs then present the
intracellularly produced antigen to T-cells thus allowing the T-cells to produce IFN-γ
and assist in the removal of the infection.
In a wide variety of mammals this system works well enough to prevent an infection of
Legionella pneumophilla from becoming a fully symptomatic disease. However in the case
of humans and Guinea-pigs there is no natural protection (innate response) thus allowing the
bacteria to gain a foothold in the lungs until the adaptive response is able to react.
- NEILD A. L. & ROY C.R. (2003) Legionella reveal dendritic cell functions that
facilitate selection of antigens for MHC class II presentation Immunity 18, pp.813 - 823
- NEILD A. L. & ROY C. R. (2004) Immunity to vacuolar pathogens: What can we learn from
legionella? Cellular Microbiology 6, pp.1011 - 10 18 http
- COLLINS M. T., CHO S. N. & REIF J. S. (1982) Prevalence of antibodies to Legionella
pneumophila in animal populations Journal of Clinical Microbiology 15, pp. 130 - 136
- VERBRUGH H. A., LEE D. A., ELLIOTT G. R., KAEANE W. F., HOIDAL J. R. & PETERSON P. K.
(1985) Opsonization of Legionella pneumophila in human serum: key roles for specific antibodies
and the classical complement pathway Immunology 54, pp.643 - 653 http pdf
- HORWITZ M. A. & SILVERSTEIN S. C. (1981) Interaction of the Legionnaires' disease
bacterium (Legionella pneumophila) with human phagocytes. II. Antibody promotes binding of L.
pneumophila to monocytes but does not inhibit intracellular multiplication. Journal of
Experimental Medicine 153, pp.386 - 397 http pdf
- WEERATNA R., STAMLER D. A., EDELSTEIN P. H., RIPLEY M., MARRIE T., HOSKIN D. & HOFFMAN
P. S. (1994) Human and guinea pig immune responses to Legionella pneumophila protein antigens
OmpS and Hsp60. Infection and Immunity 62, pp.3454 - 3462 http pdf
- NASH T. W., LIBBY D. M. & HORWITZ M. A. (1984) Interaction between the Legionnaires'
disease bacterium (Legionella pneumophila) and human alveolar macrophages. Influence of
antibody, lymphokines, and hydrocortisone. Journal of Clinical Investigation 74, pp.771
- 782 http
 Legionella bacteria are naturally resistant to phagocytes, and so need to be put
through what is called an opsonisation process to make them more susceptible to phagocytosis.