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

Prebeck, Sigrid; Brade, Helmut; Kirschning, Carsten J.; Costa, Clarissa Prazeres da; Dürr, Susanne; Wagner, Hermann; Miethke, Thomas

doi:10.1016/s1286-4579(03)00063-7

Cited by 41 publications

(38 citation statements)

References 24 publications

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“…However, recent reports for C. trachomatis serovar E (Heine et al, 2003) and serovar LGV-2 (Prebeck et al, 2003) have shown that these serovars signal via TLR4 and not TLR2. These are interesting observations, as we have also shown that serovar E but not serovar LGV-1 signals via TLR4 (S. Hosseinzadeh and A. Eley, unpublished), suggesting that there might be differences in TLR signalling between serovars of C. trachomatis.…”

Section: Resultsmentioning

confidence: 93%

“…Indeed, the idea that LPS of different serovars might signal via different TLRs is not without precedent, as different strains of Pseudomonas aeruginosa have already been shown to signal via different TLRs (Hajjar et al, 2002). Additionally, it is worth noting that the study of Prebeck et al (2003) involved challenge of murine macrophages. Murine TLRs can show distinct differences from human TLRs in responding to certain ligands -for example taxol and lipid IVa both stimulate murine TLR4 but do not activate human TLR4.…”

Section: Resultsmentioning

confidence: 99%

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Lipopolysaccharides of Bacteroides fragilis, Chlamydia trachomatis and Pseudomonas aeruginosa signal via Toll-like receptor 2

Erridge

Pridmore

Eley

et al. 2004

Journal of Medical Microbiology

164

132

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Recognition of bacterial lipopolysaccharide (LPS) is critical in the host defence against Gramnegative infection. While enterobacterial LPS signals via Toll-like receptor 4 (TLR4), it has recently been reported that the LPS of Leptospira interrogans, Legionella pneumophila, Rhizobium species Sin-1 and at least one strain of Porphyromonas gingivalis are capable of signalling via TLR2. Using a TLR transfection assay and measurement of an NF-kB-sensitive promoter region, the results show that the LPS of Bacteroides fragilis NCTC-9343, Chlamydia trachomatis LGV-1 and Pseudomonas aeruginosa PAC-611 also signal via TLR2 and it is pointed out that all TLR2-signalling LPS discovered to date demonstrate relatively weak endotoxicity in some models and structural features distinct from those LPS shown to signal via TLR4.

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Section: Resultsmentioning

confidence: 93%

Section: Resultsmentioning

confidence: 99%

Lipopolysaccharides of Bacteroides fragilis, Chlamydia trachomatis and Pseudomonas aeruginosa signal via Toll-like receptor 2

Erridge

Pridmore

Eley

et al. 2004

Journal of Medical Microbiology

164

132

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“…Chlamydia are gram-negative bacteria and purified endotoxin from C. trachomatis is able to stimulate macrophages via TLR4, albeit only at high concentrations [14]. In addition, TLR4 d/d BMDDC display a partial defect to produce IL-12p40 upon stimulation with C. pneumoniae [17].…”

Section: Resultsmentioning

confidence: 99%

“…First, the microorganism appears to synthesize TLR ligands of low affinity. For instance, chlamydial endotoxin stimulates macrophages via TLR4, but its activity is 100-1000-fold weaker compared to endotoxin derived from Enterobacteriaceae [13,14]. Furthermore, chlamydial DNA, a structure potentially recognized via TLR9, displays a low CpG-frequency (2.99%), which is only slightly higher than that of eukaryotic DNA (2.06%), but much lower than that of genomic DNA from E. coli (7.48%) or M. tuberculosis (12.73%).…”

Section: Introductionmentioning

confidence: 99%

Differential involvement of TLR2 and TLR4 in host survival during pulmonary infection with Chlamydia pneumoniae

Rodríguez

Wantia

Fend³

et al. 2006

Eur J Immunol

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The relevance of TLR2 and TLR4 for recognizing Chlamydia pneumoniae in vivo during pulmonary infection and to survive the infection was explored. We found that early immune responses triggered by C. pneumoniae partially depended on TLR2, but not on TLR4. The chemokines MIP-2 and MIP-1a were not induced, while IL-12p40 levels were higher in TLR2 -/-mice compared to wild-type mice. Secretion of TNF, keratinocytederived chemokine and monocyte chemoattractant protein-1 was attenuated in TLR2 -/-mice, while IFN-c was increased as in wild-type mice. The pulmonary cyto-and chemokine response of TLR2 -/-ÂTLR4 d/d was similar to TLR2 -/-mice. TLR2 -/-and TLR2 -/-ÂTLR4 d/d mice also attracted fewer polymorphonuclear neutrophils into the lung, while TLR4 d/d mice recruited them. Attenuated recruitment of polymorphonuclear neutrophils correlated with reduced weight loss in TLR2 -/-and TLR2 -/-ÂTLR4 d/d mice and a lower chlamydial burden 3 days post infection. At 9 days post infection, TLR2 -/-and TLR2 -/-ÂTLR4 d/d mice produced cyto-and chemokines as efficiently as wild-type mice, indicating that the involvement of TLR in inflammation varies over time. All TLR2 -/-ÂTLR4 d/d mice succumbed to the infection, while about 50% of TLR2 -/-mice died. Taken together, the function of TLR2 and TLR4 is required to survive pulmonary infection with C. pneumoniae.

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“…As with most bacteria, Chlamydia infections are detected by host pattern recognition receptors (PRRs) that recognize chlamydial LPS via TLR4 (Ingalls et al 1995;Prebeck et al 2001Prebeck et al , 2003Heine et al 2003) and heat shock protein Hsp60 through TLR2 and TLR4 (Kol et al 1999(Kol et al , 2000Vabulas et al 2001;Bulut et al 2002;Costa et al 2002;Bulut et al 2009). TLR2 appears to be the predominant receptor required for an inflammatory response to infection (Prebeck et al 2001;Darville et al 2003;O'Connell et al 2006).…”

Section: Modifying the Host Response Detection Of Chlamydia By The Hostmentioning

confidence: 99%

Chlamydial Intracellular Survival Strategies

Bastidas

Elwell

Engel

et al. 2013

Cold Spring Harbor Perspectives in Medicine

202

197

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Chlamydia trachomatis is the most common sexually transmitted bacterial pathogen and the causative agent of blinding trachoma. Although Chlamydia is protected from humoral immune responses by residing within remodeled intracellular vacuoles, it still must contend with multilayered intracellular innate immune defenses deployed by its host while scavenging for nutrients. Here we provide an overview of Chlamydia biology and highlight recent findings detailing how this vacuole-bound pathogen manipulates host -cellular functions to invade host cells and maintain a replicative niche.

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

Cited by 41 publications

References 24 publications

Lipopolysaccharides of Bacteroides fragilis, Chlamydia trachomatis and Pseudomonas aeruginosa signal via Toll-like receptor 2

Lipopolysaccharides of Bacteroides fragilis, Chlamydia trachomatis and Pseudomonas aeruginosa signal via Toll-like receptor 2

Differential involvement of TLR2 and TLR4 in host survival during pulmonary infection with Chlamydia pneumoniae

Chlamydial Intracellular Survival Strategies

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