Comparative genomes of Chlamydia pneumoniae and C. trachomatis

Abstract

Chlamydia are obligate intracellular eubacteria that are phylogenetically separated from other bacterial divisions. C. trachomatis and C. pneumoniae are both pathogens of humans but differ in their tissue tropism and spectrum of diseases. C. pneumoniae is a newly recognized species of Chlamydia that is a natural pathogen of humans1, and causes pneumonia and bronchitis. In the United States, approximately 10% of pneumonia cases and 5% of bronchitis cases are attributed to C. pneumoniae infection2. Chronic disease may result following respiratory-acquired infection, such as reactive airway disease3, adult-onset asthma4 and potentially lung cancer5. In addition, C. pneumoniae infection has been associated with atherosclerosis6,7,8,9,10,11. C. trachomatis infection causes trachoma, an ocular infection that leads to blindness, and sexually transmitted diseases such as pelvic inflammatory disease, chronic pelvic pain, ectopic pregnancy and epididymitis12. Although relatively little is known about C. trachomatis biology13, even less is known concerning C. pneumoniae. Comparison of the C. pneumoniae genome with the C. trachomatis genome14 will provide an understanding of the common biological processes required for infection and survival in mammalian cells. Genomic differences are implicated in the unique properties that differentiate the two species in disease spectrum. Analysis of the 1,230,230-nt C. pneumoniae genome revealed 214 protein-coding sequences not found in C. trachomatis, most without homologues to other known sequences. Prominent comparative findings include expansion of a novel family of 21 sequence-variant outer-membrane proteins, conservation of a type-III secretion virulence system, three serine/threonine protein kinases and a pair of parologous phospholipase-D-like proteins, additional purine and biotin biosynthetic capability, a homologue for aromatic amino acid (tryptophan) hydroxylase and the loss of tryptophan biosynthesis genes.

Access optionsAccess options

Rent or Buy article

Get time limited or full article access on ReadCube.

from$8.99

All prices are NET prices.

Figure 2: Amino acid identity (%) among functionally assigned sets of protein-coding sequences with predicted orthologues between C. pneumoniae and C. trachomatis.
Figure 3: Comparative C. pneumoniae and C. trachomatis gene organization.
Figure 4: Relationship of the predicted C. pneumoniae amino acid hydroxylase (Aro-OHase) to eukaryotic tryptophan (Trp-OHase), tyrosine (Tyr-OHase) and phenylalanine (Phe-OHase) hydroxylases.

Accession codes

Accessions

GenBank/EMBL/DDBJ

References

  1. 1

    Grayston, J.T., Kuo, C.C., Campbell, L.A. & Wang, S.P. Chlamydia pneumoniae sp. nov. for Chlamydia strain TWAR. Int. J. Syst. Bacteriol. 39, 88 ( 1989).

  2. 2

    Kuo, C.C., Jackson, L.A., Campbell, L.A. & Grayston, J.T. Chlamydia pneumoniae (TWAR). Clin. Microbiol. Rev. 8, 451–461 (1995).

  3. 3

    Emre, U., Sokolovskaya, N., Roblin, P.M., Schachter, J. & Hammerschlag, M.R. Detection of anti-Chlamydia pneumoniae IgE in children with reactive airway disease. J. Infect. Dis. 172, 265–267 (1995).

  4. 4

    Hahn, D.L., Anttila, T. & Saikku, P. Association of Chlamydia pneumoniae IgA antibodies with recently symptomatic asthma. Epidemiol. Infect. 117, 513–517 (1996).

  5. 5

    Laurila, A.L. et al. Serological evidence of an association between Chlamydia pneumoniae infection and lung cancer. Int. J. Cancer 74, 31–34 (1997).

  6. 6

    Kuo, C.C. et al. Demonstration of Chlamydia pneumoniae in atherosclerotic lesions of coronary arteries. J. Infect. Dis. 167, 841–849 (1993).

  7. 7

    Kuo, C.C., Gown, A.M., Benditt, E.P. & Grayston, J.T. Detection of Chlamydia pneumoniae in aortic lesions of atherosclerosis by immunocytochemical stain. Arterioscler. Thromb. 13, 1501–1504 (1993).

  8. 8

    Kuo, C.C. et al. Chlamydia pneumoniae (TWAR) in coronary arteries of young adults (15-34 years old). Proc. Natl Acad. Sci. USA 92, 6911–6914 (1995).

  9. 9

    Mlot, C. Chlamydia linked to atherosclerosis. Science 272 , 1422 (1996).

  10. 10

    Muhlestein, J.B. et al. Increased incidence of Chlamydia species within the coronary arteries of patients with symptomatic atherosclerotic versus other forms of cardiovascular disease. J. Am. Coll. Cardiol. 27, 1555–1561 (1996).

  11. 11

    Fong, I.W. et al. Rabbit model for Chlamydia pneumoniae infection. J. Clin. Microbiol. 35, 48–52 (1997).

  12. 12

    Schachter, J. Chlamydial infections. West. J. Med. 153, 523–534 (1990).

  13. 13

    Stephens, R.S. Challenge of Chlamydia research. Infect. Agents Dis. 1, 279–293 (1992).

  14. 14

    Stephens, R.S. et al. Genome sequence of an obligate intracellular pathogen of humans: Chlamydia trachomatis. Science 282, 754–759 (1998).

  15. 15

    Campbell, L.A., Kuo, C.C. & Grayston, J.T. Characterization of the new Chlamydia agent, TWAR, as a unique organism by restriction endonuclease analysis and DNA-DNA hybridization. J. Clin. Microbiol. 25, 1911 –1916 (1987).

  16. 16

    Mitchell, W.P. & Stephens, R.S. in Chlamydial Infections: Proceedings of the Ninth International Symposium on Human Chlamydial Infection (eds Stephens, R.S. et al.) 543– 546 (International Chlamydia Symposium, San Francisco, 1998).

  17. 17

    Rockey, D.D., Heinzen, R.A. & Hackstadt, T. Cloning and characterization of a Chlamydia psittaci gene coding for a protein localized in the inclusion membrane of infected cells. Mol. Microbiol. 15, 617– 626 (1995).

  18. 18

    Rockey, D.D. & Rosquist, J.L. Protein antigens of Chlamydia psittaci present in infected cells but not detected in the infectious elementary body. Infect. Immun. 62, 106– 112 (1994).

  19. 19

    Rasmussen, S.J. et al. Secretion of proinflammatory cytokines by epithelial cells in response to Chlamydia infection suggests a central role for epithelial cells in chlamydial pathogenesis. J. Clin. Invest. 99, 77–87 (1997).

  20. 20

    Longbottom, D., Findlay, J., Vretou, E. & Dunbar, S.M. Immunoelectron microscopic localisation of the OMP90 family on the outer membrane surface of Chlamydia psittaci. FEMS Microbiol. Lett. 164, 111–117 (1998).

  21. 21

    Altschul, S.F. et al. Gapped BLAST and PSI-BLAST: a new generation of protein database search programs. Nucleic Acids Res. 25, 3389–3402 (1997).

  22. 22

    Thompson, J.D., Higgins, D.G. & Gibson, T.J. CLUSTAL W: improving the sensitivity of progressive multiple sequence alignment through sequence weighting, position-specific gap penalties and weight matrix choice. Nucleic Acids Res. 22, 4673–4680 (1994).

  23. 23

    Salzberg, S., Delcher, A., Kasif, S. & White, O. Microbial gene identification using interpolated Markov models. Nucleic Acids Res. 26, 544–548 (1997).

Download references

Acknowledgements

We thank C. Black for providing the C. pneumoniae strain and Incyte Pharmaceuticals, Inc. for financial support.

Author information

Correspondence to Richard Stephens.

Supplementary information

Table 1 (PDF 35 kb)

Figure 1 (PDF 25 kb)

Rights and permissions

Reprints and Permissions

About this article

Further reading