Legionella pneumophila is an intracellular pathogen that replicates within alveolar macrophages. Through its ability to activate multiple host innate immune components, L. pneumophila has emerged as a useful tool to dissect inflammatory signaling pathways in macrophages. However the resolution of L. pneumophila infection in the lung requires multiple cell types and abundant cross talk between immune cells. Few studies have examined the coordination of events that lead to effective immune control of the pathogen. Here we discuss L. pneumophila interactions with macrophages and dendritic cell subsets and highlight the paucity of knowledge around how these interactions recruit and activate other immune effector cells in the lung.
"Legionella pneumophila is an opportunistic intracellular pathogen of humans and the major cause of Legionnaires’ disease worldwide. Infection of mice with L. pneumophila has been widely utilised to investigate the contribution of both host and pathogen derived factors to infection and the resulting immune response
. A critical technique in these investigations is the quantification of pulmonary bacteria in infected mice. "
[Show abstract][Hide abstract] ABSTRACT: Background
Pulmonary load of Legionella pneumophila in mice is normally determined by counting serial dilutions of bacterial colony forming units (CFU) on agar plates. This process is often tedious and time consuming. We describe a novel, rapid and versatile flow cytometric method that detects bacteria phagocytosed by neutrophils.
Mice were infected with L. pneumophila via intratracheal or intranasal administration. At various times after bacteria inoculation, mouse lungs were harvested and analysed concurrently for bacterial load by colony counting and flow cytometry analysis. The number of L. pneumophila-containing neutrophils correlated strongly with CFU obtained by bacteriological culture.
This technique can be utilised to determine pulmonary bacterial load and may be used in conjunction with other flow cytometric based analyses of the resulting immune response.
BMC Research Notes 08/2012; 5(1):448. DOI:10.1186/1756-0500-5-448
"The current model is that L. pneumophila replication is restricted due to flagellin dependent caspase-1 activation through Naip5- Ipaf and early macrophage cell death by pyroptosis. However, although depletion or inhibition of caspase-1 activity leads to decreased targeting of bacteria to lysosomes, the mechanism of caspase-1-dependent restriction of L. pneumophila replication in macrophages and in vivo is not fully understood (Schuelein et al., 2011). "
[Show abstract][Hide abstract] ABSTRACT: Although best known for its ability to cause severe pneumonia in people whose immune defenses are weakened, Legionella pneumophila and Legionella longbeachae are two species of a large genus of bacteria that are ubiquitous in nature, where they parasitize protozoa. Adaptation to the host environment and exploitation of host cell functions are critical for the success of these intracellular pathogens. The establishment and publication of the complete genome sequences of L. pneumophila and L. longbeachae isolates paved the way for major breakthroughs in understanding the biology of these organisms. In this review we present the knowledge gained from the analyses and comparison of the complete genome sequences of different L. pneumophila and L. longbeachae strains. Emphasis is given on putative virulence and Legionella life cycle related functions, such as the identification of an extended array of eukaryotic like proteins, many of which have been shown to modulate host cell functions to the pathogen's advantage. Surprisingly, many of the eukaryotic domain proteins identified in L. pneumophila as well as many substrates of the Dot/Icm type IV secretion system essential for intracellular replication are different between these two species, although they cause the same disease. Finally, evolutionary aspects regarding the eukaryotic like proteins in Legionella are discussed.
Frontiers in Microbiology 10/2011; 2:208. DOI:10.3389/fmicb.2011.00208 · 3.99 Impact Factor
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