Caenorhabditis elegans as an Alternative Model Host for Legionella pneumophila, and Protective Effects of Bifidobacterium infantis

Department of Interdisciplinary Studies for Advanced Aged Society, Osaka City University Graduate School of Human Life Science, Osaka 558-8585, Japan.
Applied and Environmental Microbiology (Impact Factor: 3.67). 04/2010; 76(12):4105-8. DOI: 10.1128/AEM.03021-09
Source: PubMed


The survival times of Caenorhabditis elegans worms infected with Legionella pneumophila from day 7.5 or later after hatching were shorter than those of uninfected worms. However, nematodes fed bifidobacteria prior
to Legionella infection were resistant to Legionella. These nematodes may act as a unique alternative host for Legionella research.

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    • "Bacterivorous nematodes such as Caenorhabditis elegans are infected and killed by a number of human bacterial pathogens (Hilbi et al., 2007). Legionella pneumophila non-invasively colonizes and replicates in the intestinal tract of C. elegans, eventually leading to the death of the worm (Brassinga et al., 2009; Komura et al., 2010) (Fig. 1). While the bacterial Icm/Dot T4SS does not affect the survival of C. elegans, the susceptibility of the nematodes to L. pneumophila is regulated by innate immune signalling pathways involving p38 mitogenactivated protein kinase and insulin/insulin growth factor-1 receptor. "
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    ABSTRACT: Bacteria of the genus Legionella persist in a wide range of environmental habitats, including biofilms, protozoa and nematodes. Legionellaceae are 'accidental' human pathogens that upon inhalation cause a severe pneumonia termed 'Legionnaires' disease'. The interactions of L. pneumophila with eukaryotic hosts are governed by the Icm/Dot type IV secretion system (T4SS) and more than 150 'effector proteins', which subvert signal transduction pathways and promote the formation of the replication-permissive 'Legionella-containing vacuole'. The Icm/Dot T4SS is essential to infect free-living protozoa, such as the amoeba Dictyostelium discoideum, as well as the nematode Caenorhabditis elegans, or mammalian macrophages. To adapt to different niches, L. pneumophila not only responds to exogenous cues, but also to endogenous signals, such as the α-hydroxyketone compound LAI-1 (Legionella autoinducer-1). The long-term adaptation of Legionella spp. is based on extensive horizontal DNA transfer. In fact, Legionella spp. have acquired canonical 'genomic islands' of prokaryotic origin, but also a number of eukaryotic genes. Since many aspects of Legionella virulence against environmental predators and immune phagocytes are similar, an understanding of Legionella ecology provides valuable insights into the pathogenesis of legionellaceae for humans.
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    • "It is possible that L. pneumophila co-evolved with some as yet unrecognized lower metazoan. In support of this notion, two recent studies found that L. pneumophila can infect Caenorhabditis elegans (Brassinga et al., 2010; Komura et al., 2010), an organism with well-defined cell death pathways (Conradt, 2009). Alternatively, L. pneumophila can acquire genes specific for metazoan pathways from other more adapted mammalian pathogens which also are parasites of amebae (Moliner et al., 2010). "
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    ABSTRACT: Programmed cell death is considered the ultimate solution for the host to eliminate infected cells, leading to the abolishment of the niche for microbial replication and the ablation of infection. Thus, it is not surprising that successful pathogens have evolved diverse strategies to reprogram the cell death pathways for their proliferation. Using effector proteins translocated by the Dot/Icm type IV secretion system, the facultative intracellular pathogen Legionella pneumophila manipulates multiple host cellular processes to create a niche within host cells to support its replication. Investigation in the past decade has established that in mammalian cells this bacterium actively modulates two host cell death pathways, namely the canonical apoptotic pathway controlled by the mitochondrion and the pyroptotic pathway controlled by the Nod-like receptor Naip5 and the Ipaf inflammasome. In this review, I will discuss the recent progress in understanding the mechanisms the bacterium employs to interfere with these host cell death pathways and how such modulation contribute to the intracellular life cycle of the pathogen.
    Frontiers in Microbiology 02/2011; 2:36. DOI:10.3389/fmicb.2011.00036 · 3.99 Impact Factor
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    ABSTRACT: An emerging central concept in evolutionary biology suggests that symbiosis is a universal characteristic of living organisms that can help in understanding complex traits and phenotypes. During evolution, an integrative circuitry fundamental for survival has been established between commensal gut microbiota and host. On the basis of recent knowledge in worms, flies, and humans, an important role of the gut microbiota in aging and longevity is emerging. The complex bacterial community that populates the gut and that represents an evolutionary adapted ecosystem correlated with nutrition appears to limit the accumulation of pathobionts and infections in all taxa, being able of affecting the efficiency of the host immune system and exerting systemic metabolic effects. There is an urgent need to disentangle the underpinning molecular mechanisms, which could shed light on the basic mechanisms of aging in an ecological perspective. Thus, it appears possible to extend healthy aging and lifespan by targeting the host as a metaorganism by manipulating the complex symbiotic ecosystem of gut microbiota, as well as other possible ecosystems of the body.
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