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

Abstract

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.

Pseudomonas aeruginosa flagellum is critical for invasion, cutaneous persistence and induction of inflammatory response of skin epidermis

“…These results are consistent with a previous study showing that TLR5 is essential to the recognition of P. aeruginosa flagellin both in vivo and ex vivo [38]. P. aeruginosa possesses other virulence factors such as LPS, which is recognized either by TLR2 or TLR4 depending on its structure [23,50]. It has been suggested that the most important system involved in the recognition of P. aeruginosa could be TLR and that TLR4 and TLR5 were redundant for the recognition of P. aeruginosa [38].…”

“…The innate immune system is able to detect P. aeruginosa products such as LPS, flagellin and CpG DNA via TLR4, TLR5 and TLR9 respectively [23–25] leading to the induction of large amounts of pro-inflammatory cytokines such as interleukin (IL)-6, granulocyte-colony stimulating factor (G-CSF), tumor necrosis factor (TNF)α [24,26] during lung infections in mouse model. Moreover, studies have suggested the role of TLR5 in induction of an early innate response and of T2SS and T3SS, in death, due to Pseudomonas infection in mouse lung infection model [18,26,27].…”

Pattern Recognition Molecules Activated by Chlamydia muridarum Infection of Cloned Murine Oviduct Epithelial Cell Lines

“…The recent finding that C. trachomatis LPS activates NF-B by signaling through TLR2 rather than TLR4 (63) and that C. trachomatis has a potential peptidoglycan synthesis pathway (64,65) suggest several possible Chlamydia PAMPs for TLR2.…”

Toll-like receptor 2 promotes bacterial clearance during the initial stage of pulmonary infection with Acinetobacter baumannii

“…This discrepancy may be due to the distinct bacterial origin and different experimental conditions. Although TLR4 is regarded as the main PRR of Gram-negative bacteria, TLR2 has also been reported to participate in the recognition of some Gram-negative bacteria, including Helicobacter pylori, Porphyromonas gingivalis and Bacteroides fragilis (11,26,27). Therefore, TLR2 serves as a functional receptor for Gram-positive and -negative bacteria and induces production of proinflammatory cytokines (28).…”