The Gram-negative bacterium Chlamydia trachomatis L2 stimulates tumor necrosis factor secretion by innate immune cells independently of its endotoxin.

The endotoxin of Chlamydia trachomatis L(2), the causative agent of lymphogranuloma venerum, has been described as an endotoxin with an atypical structure and weak stimulatory activity. It is, however, unclear whether chlamydial endotoxin plays a role in the stimulation of innate immune cells upon contact with the whole microorganism C. trachomatis L(2).

Role of IgG-seropositivity to Chlamydia pneumoniae in early thrombotic events after coronary stent placement.

Aims: Since infection of endothelial or smooth muscle cells with Chlamydia pneumoniae increased expression of tissue factor and plasminogen activator inhibitor I (PAI-1), C. pneumoniae might be involved in triggering acute thrombotic events in patients with coronary artery disease. Therefore, we explored a potential relationship between IgG-seropositivity to C.

Role of chlamydial heat shock protein 60 in the stimulation of innate immune cells by Chlamydia pneumoniae.

Chlamydia pneumoniae stimulates potently maturation of and cytokine secretion by bone marrow-derived dendritic cells (BMDDC). BMDDC responses depend mainly on Toll-like receptor (TLR)2 and to a minor extent on TLR4. We demonstrate here using C.

Chlamydia pneumoniae activates IKK/I kappa B-mediated signaling, which is inhibited by 4-HNE and following primary exposure.

Chlamydia pneumoniae may be involved in atherosclerosis by inducing inflammation as well as LDL oxidation. The transcription factor NF-kappa B is found in an active state in atherosclerotic lesions. This study examined the effect of C.