Metabolic adaptation of human pathogenic and related nonpathogenic bacteria to extra- and intracellular habitats
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作者:
Fuchs, Thilo M.
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Tech Univ Munich, Abt Mikrobiol, Zent Inst Ernahrungs & Lebensmittelforsch ZIEL, Weihenstephan, GermanyUniv Munich, Max Von Pettenkofer Inst Hyg & Med Mikrobiol, D-80336 Munich, Germany
Fuchs, Thilo M.
[2
]
Eisenreich, Wolfgang
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Tech Univ Munich, Lehrstuhl Biochem, D-8046 Garching, GermanyUniv Munich, Max Von Pettenkofer Inst Hyg & Med Mikrobiol, D-80336 Munich, Germany
Eisenreich, Wolfgang
[3
]
Heesemann, Juergen
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Univ Munich, Max Von Pettenkofer Inst Hyg & Med Mikrobiol, D-80336 Munich, GermanyUniv Munich, Max Von Pettenkofer Inst Hyg & Med Mikrobiol, D-80336 Munich, Germany
Heesemann, Juergen
[1
]
Goebel, Werner
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Univ Munich, Max Von Pettenkofer Inst Hyg & Med Mikrobiol, D-80336 Munich, GermanyUniv Munich, Max Von Pettenkofer Inst Hyg & Med Mikrobiol, D-80336 Munich, Germany
Goebel, Werner
[1
]
机构:
[1] Univ Munich, Max Von Pettenkofer Inst Hyg & Med Mikrobiol, D-80336 Munich, Germany
Most bacteria pathogenic for humans have closely related nonpathogenic counterparts that live as saprophytes, commensals or even symbionts (mutualists) in similar or different habitats. The knowledge of how these bacteria adapt their metabolism to the preferred habitats is critical for our understanding of pathogenesis, commensalism and symbiosis, and in the case of bacterial pathogens could help to identify targets for new antimicrobial agents. The focus of this review is on the metabolic potentials and adaptations of three different groups of human extra- and intracellular bacterial pathogens and their nonpathogenic relatives. All bacteria selected have the potential to reach the interior of mammalian host cells. However, their ability to replicate intracellularly differs significantly. The question therefore arises whether there are specific metabolic requirements that support stable intracellular replication. Furthermore, we discuss whenever relevant data for the pathogenic representatives are available the possible effect of the metabolism on the expression of virulence genes.