Intracellular Life of Coxiella burnetii in Macrophages

Abstract

Coxiella burnetii, the agent of Q fever, is an obligate intracellular bacterium that is considered a potential biological weapon of category B. C. burnetii survives within myeloid cells by subverting receptor-mediated phagocytosis and preventing phagosome maturation. The intracellular fate of C. burnetii also depends on the functional state of myeloid cells. This review describes the mechanisms used by C. burnetii to circumvent uptake and trafficking events, and the role of cytokines on C. burnetii survival in myeloid cells.

Coxiella burnetii Infects Primary Bovine Macrophages and Limits Their Host Cell Response

“…Interestingly, this prominent difference between the strains was observed only in bovine MDM cultures but not when alveolar macrophage cultures were inoculated in which equally low numbers of C. burnetii bacteria expressing either LPS phase became cell bound. As opposed to what is seen with bovine macrophages, phase I particles are only poorly internalized by human monocytes, whereas phase II particles are better ingested (46). It remains to be determined whether these apparent species differences can be traced back to quantitative differences in the expression of ␣ V ␤ 3 , CR3, or other surface molecules like, e.g., Toll-like receptor 4 (TLR4) by phagocyte subsets.…”

Computational modeling and experimental validation of the Legionella and Coxiella virulence-related type-IVB secretion signal

“…pathogenomics | type-IV secretion | translocated substrates | Legionnaire disease | Q-fever T he bacteria Legionella pneumophila, the causative agent of Legionnaire disease, and Coxiella burnetii, the causative agent of Q-fever, are both human intracellular pathogens that multiply in alveolar macrophages (1,2). In nature, L. pneumophila multiplies in a broad range of amoebae, whereas C. burnetii infects various ruminants, such as cattle and sheep (3,4).…”

Hijacked phagosomes and leukocyte activation: an intimate relationship

“…In myeloid cells, which are the host cells of C. burnetii, phase I C. burnetii survive and replicate, whereas phase II organisms are eliminated (as reviewed in ref. [16]). In contrast, virulent and avirulent organisms replicate in non-microbicidal cells such as CHO, L929, Vero, and HeLa cells [41][42][43][44][45] or trophoblastic cell lines (unpublished results).…”

“…In contrast to virulent C. burnetii, avirulent variants of C. burnetii (phase II organisms) are eliminated in phagolysosomes of human monocytes and macrophages [16], and their replication is controlled in resident mouse peritoneal macrophages [64]. In non-microbicidal cells, phase II bacteria replicate within a compartment that displays all of the characteristics of phagolysosomes, as is decorated with Lamp-1, Lamp-2, M6PR, V-H ϩ -ATPase, Rab7, cathepsin D, and acid phosphatases (Table 4) [41][42][43]58].…”

“…[57][58][59]). At present, C. burnetii appears to survive within an acidic late phagosome in monocytes and macrophages by preventing phagolysosome biogenesis ( Table 4) [16]. The absence of phagosome-lysosome fusion in macrophages infected with C. burnetii has been discussed.…”