Difference between revisions of "Chlamydia muridarum"

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==Pathology==
 
==Pathology==
Chlamydia muridarum lives within the cells of infected mice and hamsters.  It is known to cause pharyngitis, bronchitis, and pneumonitis.  One way that the disease is thought to spread is by BAX dependent apoptosis.  BAX plays a crucial role in regulating apoptosis. This BAX dependent apoptosis in turn releases Chlamydia containing apoptic cells from the infected cells which are then uptaken by uninfected cells, thus the disease begins a whole new cycle of infection and spreading.
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Chlamydia muridarum lives within the cells of infected mice and hamsters.  It is known to cause pharyngitis, bronchitis, and pneumonitis.  One way that the disease is thought to spread is by BAX dependent apoptosis.  Chlamydia are known to replicate in a vacuole known as an inclusion.  BAX is then able to enter this inclusion, inducing mitochondrial dependent apoptosis. This BAX dependent apoptosis in turn releases Chlamydia containing apoptic cells from the infected cells which are then uptaken by uninfected cells, thus the disease begins a whole new cycle of infection and spreading.
  
 
==Application to Biotechnology==
 
==Application to Biotechnology==

Revision as of 22:42, 1 June 2007

A Microbial Biorealm page on the genus Chlamydia muridarum

Classification

Higher order taxa

Bacteria

Genus

chlamydiae; chlamydiales; chlamydiaceae; chlamydia; chlamydia muridarum nigg



NCBI: Taxonomy

Description and significance

Chlamydia muridarum is included in a broad range of gram negative bacteria. It is rod shaped and lives in the cells of vertebrates, particularly mice and hamsters. It lives at an optimal host body temperature of 37 degrees Celcius and has a mesophilic range. Chlamydia muridarum was isolated in 1942 from the lungs of albino Swiss mice which all had similar symptoms. The MoPn strain was isolated in the mice and an SFPD strain of the same bacteria was isolated in hamsters. The chromosome and extrachromosomal plasmid of MoPn was sequenced and was discovered to bind a molecule known as mAbs which also binds to the bacteria Chlamydia trachomatis, which is the sexually transmitted disease seen in humans. The SFPD strain was also seen to bind mAbs. Thus it was important to sequence the Chlamydia muridarum genome to parallel its similarities with the human bacteria Chlamydia trachomatis.

Genome structure

Chlamydia muridarum contains one circular chromosome of double stranded DNA, consisting of 1,072,950 nt. It contains 40% GC content and 89% coding genes. It contains 955 genes, 904 of which are protein coding genes and 43 structural RNA's. It contains an extrachromosomal plasmid pMoPn which is 7501 nt in length, has a 35% GC content, is 78% coding, and contains 7 genes all of which are protein coding genes. This plasmid binds to the molecule mAbs within the host, thus allowing the bacteria to begin its infection.

Cell structure and metabolism

Describe any interesting features and/or cell structures; how it gains energy; what important molecules it produces.

Ecology

Chlamydia muridarum live in oviduct epithelial cells in female mice and prostate epithelial cells in male mice. When the cells become infected with this pathogen they increase uptake of various cytokines and chemokine genes such as TLR4, CD14, TLR2, and the adaptor molecule MyD88 that help recruit immune cells.

Pathology

Chlamydia muridarum lives within the cells of infected mice and hamsters. It is known to cause pharyngitis, bronchitis, and pneumonitis. One way that the disease is thought to spread is by BAX dependent apoptosis. Chlamydia are known to replicate in a vacuole known as an inclusion. BAX is then able to enter this inclusion, inducing mitochondrial dependent apoptosis. This BAX dependent apoptosis in turn releases Chlamydia containing apoptic cells from the infected cells which are then uptaken by uninfected cells, thus the disease begins a whole new cycle of infection and spreading.

Application to Biotechnology

Does this organism produce any useful compounds or enzymes? What are they and how are they used?

Current Research

One such study concerning Chlamydia muridarum surrounded the fact that epithelial cells play an important part in host defense against microbial pathogens. A murine oviduct epithelial cell line was constructed to observed how epithelial cells conduct adaptive immune responses to Chlamydia muridarum infection. The infected epithelial cells produced a variety of chemokines such as CXCL16 and regulators of the acute-phase response including interleukin-1a and tumor necrosis factor alpha. The infected epithelial cells also expressed cytokines that augment gamma interferon production such as IL-12-p70. This is the first account of a non-myeloid/lymphoid cell making IL-12-p70 as a response to infection. The infected cells also began transforming growth factor alpha precursor expression which may lead to the pathological scarring seen from Chlamydia infections. Thus infected epithelium cells contribute greatly to the host's adaptive defenses but also contribute the immunopathology associated with Chlamydia infections.

Another study was done to see if chlamydia muridarum can infect and replicate in a rat adenocarcinoma cell line with characteristics of prostate epithelial cells (MAT-LU) and in a PPEC line which is a nontransformed rat prostate epithelial cell line. Infection of both types of cells resulted in formation of chlamydia contained inclusions detected by staining with an anit-Chlamydia antibody followed by flourescence microscopy. The infection rates ranged from 20 to 30% for MAT-LU cells and 30 to 40% for PPEC.

References

Brunham RC; Shen C; Gill SR; Heidelberg JF; White O; Hickey EK; Peterson J; Utterback T; Barry K; Bass S; Linher K; Weidman J; Kouri H; Craven B; Bowman C; Dodson R; Gwinn M; Nelson W; Deboy R; Kolonay J; McClarty G; Salzberg SL; Eisen J; Fraiser GM. "Chlamydia muridarum Nigg project at TIGR". 2000 Mar 15;28(6):1397-406. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=genomeprj&cmd=Retrieve&dopt=Overview&list_uids=229 http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=genome&cmd=Retrieve&dopt=Overview&list_uids=15275 http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=genome&cmd=Retrieve&dopt=Overview&list_uids=153

Perfettini, Jean-Luc; Ojcius, DAvid M.; Andrews, Charles W. Jr.; Korsmeyer; Stanley J.; Rank, Roger G.; Darville, Toni. "Role of Proapoptotic BAX in Propagation of Chlamydia muridarum (the mouse pneomonitis strain of Chlamydia trachomatis) and the Host Inflammatory Response". http://www.jbc.org/cgi/content/abstract/278/11/9496

Johnson, Raymond M. "Murine Oviduct Epithelial Cell Cytokine Responses to Chlamydia muridarum Infection Include Interleukin-12-p70 Secretion". Infection and Immunity. 2004 Jul;72(7): 3952-3960. http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=427409

Mackern-Oberti,Juan Pablo; Maccioni, Marinana; Cuffini, Cecilia; Gatti, Gerardo; Rivero, Virginia E. "Susceptibility of Prostate Epithelial Cells to Chlamydia muridarum Infection and Their Role in Innate Immunity by Recruitment of Intracellular Toll-Like Receptors 4 and 2 and MyD88 to the Inclusion". http://iai.asm.org/cgi/content/full/74/12/6973

Edited by Marina Christou student of Rachel Larsen and Kit Pogliano