Chlamydia muridarum

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A Microbial Biorealm page on the genus Chlamydia muridarum


Higher order taxa

Bacteria (1)


group:chlamydiae; class: chlamydiales; order: chlamydiaceae; genus: chlamydia; species: chlamydia muridarum nigg (1)

Description and significance

Chlamydia muridarum is included in a broad range of Gram-negative bacteria. It is rod shaped and lives in the epithelial cells of vertebrates, particularly mice and hamsters. It lives at an optimal host body temperature of 37 degrees Celcius. 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. (1)

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. (1)

Cell structure and metabolism

Chlamydia muridarum is a Gram-negative bacteria, thus it contains an inner and outer cell wall. It spends most of its developmental stage in a vacuole known as an inclusion. The chlamydia possesses a specialized type III secretion apparatus which allows it to inject virulence factors from the bacteria into the host cytosol. This may activate a number of stress responses including mitogen activated protein kinases. These stress responses then produce the necessary metabolic molecules needed by the bacteria in which it is then able to uptake these molecules from the host cytoplasm into its inclusion and convert it into energy. (5)


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.


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. (2)

Application to Biotechnology

Chlamydia muridarum does not synthesize its own useful compounds or enzymes, however, it does allow infected cells to recruit cytokines which are small signaling molecules similar to hormones. These cytokines allow the infected cells to communicate with one another and begin an immune response to fight the bacteria.

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. (3)

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. (4)

The antibiotic novobiocin was added in small amounts to the Chlamydia muridarum Nigg strain to monitor its effects on the bacteria's plasmid. Consequentially it was determined that this antibiotic worked well against the plasmid. As a result, the bacteria was no longer able to accumulate glycogen, thus losing all intake of energy. The drug was also seen to decrease the bacteria's ability for plaque formation in cultures. These findings suggest that novobiocin is an appropriate curing agent against the Chlamydia muridarum plasmid and that this plasmid may encode for a regulator or co-factor necessary for the expression of these genes. (6)


(1) 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.

(2) 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".

(3) 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.

(4) 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".

(5) Verbeke, Philippe; Welter-Stahl, Lynn; Ying, Songmin; Hansen, Jon; Häcker, Georg; Darville,Toni; David M. "Recruitment of BAD by the Chlamydia trachomatis Vacuole Correlates with Host-Cell Survival".

(6) O'Connell, Catherine M.; Nicks, Kristy M. "A plasmid-cured Chlamydia muridarum strain displays altered plaque morphology and reduced infectivity in cell culture ". Microbiology 152 (2006), 1601-1607.

Edited by Marina Christou student of Rachel Larsen and Kit Pogliano