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Chlamydia pneumoniae infection of the central nervous system worsens experimental allergic encephalitis.

Du C, Yao SY, Ljunggren-Rose A, Sriram S - J. Exp. Med. (2002)

Bottom Line: Experimental allergic encephalitis (EAE) is considered by many to be a model for human multiple sclerosis.Inoculation with Chlamydia trachomatis did not worsen EAE and infectious organisms were not seen in the CNS.These observations suggest that dissemination of C. pneumoniae results in localized infection in CNS tissues in animals with EAE.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology, Multiple Sclerosis Research Center, Vanderbilt University Medical Center, Nashville, TN 37212, USA.

ABSTRACT
Experimental allergic encephalitis (EAE) is considered by many to be a model for human multiple sclerosis. Intraperitoneal inoculation of mice with Chlamydia pneumoniae, after immunization with neural antigens, increased the severity of EAE. Accentuation of EAE required live infectious C. pneumoniae, and the severity of the disease was attenuated with antiinfective therapy. After immunization with neural antigens, systemic infection with C. pneumoniae led to the dissemination of the organism into the central nervous system (CNS) in mice with accentuated EAE. Inoculation with Chlamydia trachomatis did not worsen EAE and infectious organisms were not seen in the CNS. These observations suggest that dissemination of C. pneumoniae results in localized infection in CNS tissues in animals with EAE. We propose that infection of the CNS by C. pneumoniae can amplify the autoreactive pool of lymphocytes and regulate the expression of an autoimmune disease.

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RT-PCR analysis of C. pneumoniae gene transcription in the CNS of mice with EAE. Mice were immunized with MSCH and infected with either C. pneumoniae or C. trachomatis as described in Fig. 1 A. Mice were killed on day 18 and total RNA was isolated from PBS-perfused spinal cords, and then analyzed for the presence of mRNA of C. pneumoniae 16S RNA gene by RT-PCR. Lanes 1–5, uninfected mice immunized with MSCH alone; lanes 6–10 mice infected with C. trachomatis and immunized with MSCH; lanes 11–14 mice infected with C. pneumoniae and immunized with MSCH. Lane 15 internal negative control, lane 16 internal positive control for each of the primers. Arrows indicate the size of PCR product. Top panel, RT-PCR performed with primers for 16SRNA of C. pneumoniae, middle panel RT-PCR performed with primers for 16SRNA of C. trachomatis, and bottom panel, GAPDH primers.
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fig2: RT-PCR analysis of C. pneumoniae gene transcription in the CNS of mice with EAE. Mice were immunized with MSCH and infected with either C. pneumoniae or C. trachomatis as described in Fig. 1 A. Mice were killed on day 18 and total RNA was isolated from PBS-perfused spinal cords, and then analyzed for the presence of mRNA of C. pneumoniae 16S RNA gene by RT-PCR. Lanes 1–5, uninfected mice immunized with MSCH alone; lanes 6–10 mice infected with C. trachomatis and immunized with MSCH; lanes 11–14 mice infected with C. pneumoniae and immunized with MSCH. Lane 15 internal negative control, lane 16 internal positive control for each of the primers. Arrows indicate the size of PCR product. Top panel, RT-PCR performed with primers for 16SRNA of C. pneumoniae, middle panel RT-PCR performed with primers for 16SRNA of C. trachomatis, and bottom panel, GAPDH primers.

Mentions: Three groups of mice (five/group) were immunized with MSCH in CFA and infected with either C. pneumoniae or C. trachomatis on day 7. The third group of mice was left untreated. 18 d after immunization, the mice were killed, and an RT-PCR analysis of RNA obtained from the spinal cord were performed. As shown in Fig. 2 , all four mice from which RNA was available showed an RT-PCR signal for the presence of replicating C. pneumoniae. None of the mice infected with C. trachomatis showed a signal to primers that were specific for the C. trachomatis 16sRNA gene. These studies suggest that C. pneumoniae but not C. trachomatis is capable of infecting the CNS in mice with EAE.


Chlamydia pneumoniae infection of the central nervous system worsens experimental allergic encephalitis.

Du C, Yao SY, Ljunggren-Rose A, Sriram S - J. Exp. Med. (2002)

RT-PCR analysis of C. pneumoniae gene transcription in the CNS of mice with EAE. Mice were immunized with MSCH and infected with either C. pneumoniae or C. trachomatis as described in Fig. 1 A. Mice were killed on day 18 and total RNA was isolated from PBS-perfused spinal cords, and then analyzed for the presence of mRNA of C. pneumoniae 16S RNA gene by RT-PCR. Lanes 1–5, uninfected mice immunized with MSCH alone; lanes 6–10 mice infected with C. trachomatis and immunized with MSCH; lanes 11–14 mice infected with C. pneumoniae and immunized with MSCH. Lane 15 internal negative control, lane 16 internal positive control for each of the primers. Arrows indicate the size of PCR product. Top panel, RT-PCR performed with primers for 16SRNA of C. pneumoniae, middle panel RT-PCR performed with primers for 16SRNA of C. trachomatis, and bottom panel, GAPDH primers.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2196067&req=5

fig2: RT-PCR analysis of C. pneumoniae gene transcription in the CNS of mice with EAE. Mice were immunized with MSCH and infected with either C. pneumoniae or C. trachomatis as described in Fig. 1 A. Mice were killed on day 18 and total RNA was isolated from PBS-perfused spinal cords, and then analyzed for the presence of mRNA of C. pneumoniae 16S RNA gene by RT-PCR. Lanes 1–5, uninfected mice immunized with MSCH alone; lanes 6–10 mice infected with C. trachomatis and immunized with MSCH; lanes 11–14 mice infected with C. pneumoniae and immunized with MSCH. Lane 15 internal negative control, lane 16 internal positive control for each of the primers. Arrows indicate the size of PCR product. Top panel, RT-PCR performed with primers for 16SRNA of C. pneumoniae, middle panel RT-PCR performed with primers for 16SRNA of C. trachomatis, and bottom panel, GAPDH primers.
Mentions: Three groups of mice (five/group) were immunized with MSCH in CFA and infected with either C. pneumoniae or C. trachomatis on day 7. The third group of mice was left untreated. 18 d after immunization, the mice were killed, and an RT-PCR analysis of RNA obtained from the spinal cord were performed. As shown in Fig. 2 , all four mice from which RNA was available showed an RT-PCR signal for the presence of replicating C. pneumoniae. None of the mice infected with C. trachomatis showed a signal to primers that were specific for the C. trachomatis 16sRNA gene. These studies suggest that C. pneumoniae but not C. trachomatis is capable of infecting the CNS in mice with EAE.

Bottom Line: Experimental allergic encephalitis (EAE) is considered by many to be a model for human multiple sclerosis.Inoculation with Chlamydia trachomatis did not worsen EAE and infectious organisms were not seen in the CNS.These observations suggest that dissemination of C. pneumoniae results in localized infection in CNS tissues in animals with EAE.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology, Multiple Sclerosis Research Center, Vanderbilt University Medical Center, Nashville, TN 37212, USA.

ABSTRACT
Experimental allergic encephalitis (EAE) is considered by many to be a model for human multiple sclerosis. Intraperitoneal inoculation of mice with Chlamydia pneumoniae, after immunization with neural antigens, increased the severity of EAE. Accentuation of EAE required live infectious C. pneumoniae, and the severity of the disease was attenuated with antiinfective therapy. After immunization with neural antigens, systemic infection with C. pneumoniae led to the dissemination of the organism into the central nervous system (CNS) in mice with accentuated EAE. Inoculation with Chlamydia trachomatis did not worsen EAE and infectious organisms were not seen in the CNS. These observations suggest that dissemination of C. pneumoniae results in localized infection in CNS tissues in animals with EAE. We propose that infection of the CNS by C. pneumoniae can amplify the autoreactive pool of lymphocytes and regulate the expression of an autoimmune disease.

Show MeSH
Related in: MedlinePlus