MyD88-dependent changes in the pulmonary transcriptome after infection with Chlamydia pneumoniae

Physiol Genomics. 2007 Jul 18;30(2):134-45. doi: 10.1152/physiolgenomics.00011.2007. Epub 2007 Mar 20.


Chlamydia pneumoniae, an intracellular bacterium, causes pneumonia in humans and mice. Toll-like receptors and the key adaptor molecule myeloid differentiation factor-88 (MyD88) play a critical role in inducing immunity against this microorganism and are crucial for survival. To explore the influence of MyD88 on induction of immune responses in vivo on a genome-wide level, wildtype (WT) or MyD88(-/-) mice were infected with C. pneumoniae on anesthesia, and the pulmonary transcriptome was analyzed 3 days later by microarrays. We found that the infection caused pulmonary cellular infiltration in WT but not MyD88(-/-) mice. Furthermore, it induced the transcription of 360 genes and repressed 18 genes in WT mice. Of these, 221 genes were not or weakly induced in lungs of MyD88(-/-) mice. This cluster contains primarily genes encoding for chemokines and cytokines like MIP-1alpha, MIP-2, MIP-1gamma, MCP-1, TNF, and KC and other immune effector molecules like immunoresponsive gene-1 and TLR2. Arginase was highly induced after C. pneumoniae infection and was MyD88 dependent. Genes induced by interferons were abundant in a cluster of 102 genes that were only partially MyD88 dependent. Also, lcn2 (lipocalin-2) and timp1 were represented within this cluster. Interestingly, a set of 37 genes including sprr1a was induced more strongly in MyD88(-/-) mice, and most of them are involved in the regulation of cellular replication. In summary, ex vivo analysis of the pulmonary transcriptome on infection with C. pneumoniae demonstrated a major impact of MyD88 on inflammatory responses but not on interferon-type responses and identified MyD88-independent genes involved in cellular replication.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Base Sequence
  • Blotting, Northern
  • Chlamydia Infections / genetics*
  • Chlamydia Infections / immunology
  • Chlamydia Infections / microbiology
  • Chlamydophila pneumoniae / isolation & purification*
  • DNA Primers
  • Lung / cytology
  • Lung / metabolism*
  • Lung / microbiology
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Myeloid Differentiation Factor 88 / physiology*
  • RNA, Messenger / genetics*
  • Reverse Transcriptase Polymerase Chain Reaction


  • DNA Primers
  • Myd88 protein, mouse
  • Myeloid Differentiation Factor 88
  • RNA, Messenger