Cell membrane Complex Enzyme Eukaryotic cell or cell component Microbe-host cell complex Microorganism or its component Other Other -- ion Pathway or action Protein Protein or gene Protein or gene complex Protein or protein complex Bacterial membrane or virus envelope Cell membrane Cytoplasm Eukaryotic cell or cell component Extracellular Golgi Golgi membrane Intercellular Intracellular Mitochondria Nucleocapsid/Cytoplasm Organelle Organelle -- Cell membrane Organelle -- Endoplasmic reticulum Organelle -- ER Organelle -- Golgi Organelle -- Golgi membrane Organelle -- Nucleus Organelle -- Phagolysosome Organelle -- Phagosome Organelle -- Ribosome Other Phagolysosome Phagosome Chaperone Defense, immunity protein Enzyme Enzyme activator Enzyme inhibitor Genomic S segment Infection Ligand binding or carrier Motor Nucleic acid binding Other Signal transducer Toxicity Transcription factor binding Transcription regulation Transporter Unknown IC Inferred by Curator IDA Inferred from Direct Assay IEA Inferred from Electronic Annotation IEP Inferred from Expression Pattern IGI Inferred from Genetic Interaction IMP Inferred from Mutant Phenotype IPI Inferred from Physical Interaction ISS Inferred from Sequence or Structural Similarity NAS Non-traceable Author Statement ND No biological Data available RCA inferred from Reviewed Computational Analysis TAS Traceable Author Statement NR Not Recorded Winkler HH, Miller ET Infection and immunity Phospholipase A and the interaction of Rickettsia prowazekii and mouse fibroblasts (L-929 cells) 1982 6815087 PubMed Winkler HH, Daugherty RM Infection and immunity Phospholipase A activity associated with the growth of Rickettsia prowazekii in L929 cells 1989 2491840 PubMed Hackstadt T Infectious agents and disease The biology of rickettsiae 1996 8805076 PubMed Teysseire N, Boudier JA, Raoult D Infection and immunity Rickettsia conorii entry into Vero cells 1995 7806381 PubMed Silverman DJ, Santucci LA, Meyers N, Sekeyova Z Infection and immunity Penetration of host cells by Rickettsia rickettsii appears to be mediated by a phospholipase of rickettsial origin 1992 1612741 PubMed Walker DH, Valbuena GA, Olano JP Annals of the New York Academy of Sciences Pathogenic mechanisms of diseases caused by Rickettsia 2003 12860594 PubMed Adhesin Function: Ligand binding or carrier. >Evidence that rickettsial outer membrane protein A (OmpA) is an adhesin of R. rickettsii and that OmpA and OmpB are adhesins of R. japonica has been documented. Rickettsiae attach to a protein-dependent receptor on the host cell membrane and induce focal host cell cytoskeletal rearrangements at the site of attachment, resulting in their entry into the host cell even in nonprofessional phagocytes by a mechanism requiring rickettsial metabolic activity (Walker, et al., 2003).(Walker et al., 2003) Protein-dependent Receptor Function: Ligand binding or carrier. Rickettsia attach to a protein dependent receptor on the host cell membrane and induce focal host cell cytoskeletal rearrangements at the site of attachment, resulting in their entry into the host cell even in nonprofessional phagocytes by a mechanism requiring rickettsial metabolic activity (Walker et al., 2003).Important unidentified elements of the rickettsia-host cell interaction include the host cell membrane receptor for the rickettsial adhesin(s) (Walker et al., 2003).(Walker et al., 2003) Rickettsia in Phagosome Function: . The entry of rickettsiae into eukaryotic cells is mediated by an induced phagocytosis, but rickettsiae have never been observed in a closed phagocytic vacuole. In this study, Rickettsia conorii entry into Vero cells was observed by transmission electron microscopy during a period of 3 to 20 min after bacterium-cell contact. The entry occurred within 3 min after bacterium-cell contact, and R. conorii was observed in the process of engulfment, within a phagocytic vacuole, or free in the cytosol. Escape from the phagosome is a very rapid step since phagosome lysis was only occasionally observed. By 12 min, 90% of bacteria were internalized and half were free in the cytosol. This report confirms that rickettsiae penetrate nonphagocytic cells by induced phagocytosis and is the first demonstration of rickettsiae within a complete phagocytic vacuole (Teysseire et al., 1995).Internalization of obligate intracellular bacteria belonging to the genus Rickettsia by eukaryotic cells requires participation of both the parasitized host and the microorganism. The term"induced phagocytosis" has been used specifically to describe the entry of Rickettsia prowazekii, although a similar mechanism is likely for R. rickettsii. A role for a phospholipase in the internalization process has been proposed for both of these organisms, with the strongest supporting evidence provided for R. prowazekii. Despite general acceptance of the notion that phospholipase activity is involved in the internalization process of these bacteria, the origin of the enzyme is not known (Silverman et al., 1992).(Teysseire et al., 1995)(Silverman et al., 1992) Rickettsia in Cytoplasm Function: . Rickettsia rapidly lyse the phagosomal membrane and escape into the cytosol prior to phagolysomal fusion avoiding exposure to the lysosomal enzymes. In the cytosol they acquire their nutrients (e.g., glutamate), a part of their energy requirements (ADP/ATP transporter), and many components required for growth (e.g., amino acids) (Walker et al., 2003).Whereas R. rickettsii rarely grows to number greater than 100 organisms per cell before lysis occurs, R. prowazekii will achieve levels of greater than 800 organisms per cell (Hackstadt, 1996).(Walker et al., 2003)(Hackstadt, 1996) Extracellular Rickettsia Function: . During the exponential growth of R. prowazekii, very few bacteria exit from the infected cell to set up secondary infections in neighboring cells. Instead, R. prowazekii grows and fills the cytoplasm until, presumably, the host can no longer support the growth of the parasite. The host cell then bursts and a bolus of hundreds of R. prowazekii organisms are released to initiate infections in many new host cells. The mechanism by which R. prowazekii exits from the host cell as a burst, late in infection, has not been elucidated (Winkler and Daugherty, 1989).The typhus-group rickettsia do not produce such dramatic effects on the host cell and characteristically accumulate to very large numbers within the cytoplasm until lysis occurs. The ultrastructural damage seen in R. rickettsii-infected cells is not observed in R. prowazekii-infected cells (Hackstadt, 1996).(Winkler et al., 1989)(Hackstadt, 1996)