Triacylated lipoproteins derived from <i>Mycoplasma pneumoniae</i> activate nuclear factor‐κB through toll‐like receptors 1 and 2

Shimizu, Takashi; Kida, Yutaka; Kuwano, Koichi

doi:10.1111/j.1365-2567.2007.02594.x

Cited by 92 publications

(83 citation statements)

References 47 publications

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“…Therefore, lipoproteins, which are ligands for TLR2, are possible candidates for an inflammation-inducing factor in M. genitalium. In fact, we previously demonstrated that lipoproteins derived from M. pneumoniae induce NF-〉 through TLR2 (41,44). To elucidate whether M. genitalium induces NF-B through TLR2, we initially performed TX-114 phase partitioning of M. genitalium.…”

Section: Resultsmentioning

confidence: 99%

A Triacylated Lipoprotein fromMycoplasma genitaliumActivates NF-κB through Toll-Like Receptor 1 (TLR1) and TLR2

2008

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Mycoplasma genitalium is a sexually transmitted bacterial pathogen that causes nongonococcal chlamydianegative urethritis, mucopurulent cervicitis, endometritis, pelvic inflammatory disease, and tubal factor infertility in humans. However, pathogenic agents that induce inflammatory responses have not been identified in M. genitalium. In this study, we examined the involvement of Toll-like receptors ( Mycoplasma genitalium is an important, emerging sexually transmitted bacterial pathogen that is capable of eliciting a wide range of reproductive tract disease syndromes (3,19,20,28). M. genitalium has been identified as a causative agent of nongonococcal, chlamydia-negative urethritis (8, 50, 51) in men and of mucopurulent cervicitis, endometritis, pelvic inflammatory disease, and tubal factor infertility in women (6,7,24,33,34,45). However, pathogenic agents that induce an inflammatory response, such as endotoxin and exotoxin, have not been identified in M. genitalium.Recently, it has been reported that Toll-like receptors (TLRs) with a pattern recognition receptor function play a critical role in early innate recognition and in the inflammatory responses by the host defense against invading microbes (1, 21). Of 10 TLR family members reported, TLR2, TLR4, TLR5, and TLR9 have been implicated in the recognition of different bacterial components. Peptidoglycan, lipoarabinomannan, zymosan, and lipoproteins from various microorganisms are recognized by TLR2 (2,4,22,26,46,47,49,52). On the other hand, lipopolysaccharide, bacterial flagellin, and bacterial DNA are recognized by TLR4, TLR5, and TLR9, respectively (12,13,16,35). These TLR family members have been shown to activate NF-B via interleukin-1R-associated signal molecules, including myeloid differentiation protein (MyD88), interleukin-1R-activated kinase, tumor necrosis factor receptor-associated factor 6, and NF-B-inducing kinase (27).In this study, we examined the involvement of TLRs in activation of the immune response by lipoproteins from M. genitalium and their active components responsible for NF-B activation. MG149, a triacylated lipoprotein, was found to activate NF-B through TLR1 and TLR2. MATERIALS AND METHODSCells. Cells of a human kidney cell line, 293T, were cultured in Dulbecco modified Eagle medium containing 10% fetal calf serum, 2 mM L-glutamine, 100 U/ml penicillin G, and 100 g/ml streptomycin. To exclude the possibility of mycoplasma infections in the cell cultures, the cell suspensions were inoculated onto pleuropneumonialike organism agar medium once a month. To check the contamination of mycoplasma, cells were also stained with 4Ј,6-diamidino-2-phenylindole (DAPI) once a week. Synthesis of lipopeptide. Lipopeptide was synthesized by Bio-Synthesis (Lewisville, TX).TX-114 phase partitioning. M. genitalium G37 was cultured in SP-4 medium to the beginning of the stationary phase and then pelleted by centrifugation for 10 min at 12,000 ϫ g. M. genitalium cells were inactivated by incubation at 60°C for 30 min. Triton X-114 (TX-114) phase partitio...

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Section: Resultsmentioning

confidence: 99%

A Triacylated Lipoprotein fromMycoplasma genitaliumActivates NF-κB through Toll-Like Receptor 1 (TLR1) and TLR2

2008

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“…The others were predicted to be lipoproteins MPN611 and MPN162 and designated NF-Bactivating lipoprotein 1 (N-ALP1) and N-ALP2, respectively. N-ALP1 and N-ALP2 activated TLR signaling through TLR1 and TLR2, indicating that both are triacylated lipoproteins (9). Because mycoplasmas lack cell walls, they do not contain known pathogen-associated molecular patterns (PAMPS) such as those corresponding to lipopolysaccharide (LPS), peptidoglycan (PGN), or lipoteichoic acid.…”

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Cytadherence of Mycoplasma pneumoniae Induces Inflammatory Responses through Autophagy and Toll-Like Receptor 4

et al. 2014

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“…Such LAMPs are a subunit of the F 0 F 1 -type ATPase and are diacylated [144]. In addition other triacylated lipoproteins signal through TLR 1 and 2 but are independent of TLR6 [145]. As expected by these data, an in vivo model of pulmonary mycoplasma infection is heavily reliant on TLR2 [146].…”

Section: Cell Wall Free Bacteriamentioning

confidence: 58%

Pathogen Associated Molecular Patterns, Pattern Recognition Receptors and Pediatric Sepsis

Doughty¹

2011

TOINFJ

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Abstract:The mortality of septic shock in the pediatric population has improved over the last 2 decades with better supportive care however it still remains unacceptably high. Exaggerated inflammatory responses early in septic shock have been associated with poor outcomes. Regulation of the magnitude of the early inflammatory response is not well understood. The earliest aspect of the inflammatory response to pathogens is the innate immune response which is important to pathogen containment. Elements of the innate immune system activate the adaptive immune system in an antigen-specific way which leads to pathogen-specific protection and lasting immunologic memory to prevent subsequent infection. Pattern recognition receptors (PRRs) are evolutionarily conserved receptors on multiple types of innate immune cells and are capable of responding to highly conserved components of pathogens called pathogen associated molecular patterns (PAMPs). Numerous PRRs have been defined and are present on the cell surface as well as in the cytosol. These receptors fall into several classes called Toll-like receptors which are expressed on the cell surface or on the endosomal plasma membrane, C type lectin receptors and scavenger receptors which are only present on the cell surface. Other PRRs are present in the cytosol and including NOD-like receptors which can aggregate to form inflammasomes and RIG1 like receptors. Pathogenic microorganisms are extremely diverse however there are some common patterns repeated in components of structures such as the cell wall. PRRs can respond to PAMPs comprised of proteins, lipids, and carbohydrates, DNA and RNA. Numerous PAMPs have been described for many classes of pathogenic microorganisms such as Gram negative bacteria, Gram positive bacteria, viruses, fungi, and protozoa. The interactions between PRRs and PAMPs comprise the earliest immune responses to foreign substances and are critical for pathogen containment and amplification of the full repertoire of the immune response. There are developmental differences in the immune systems of infants and children compared to adults. The innate immune system matures much earlier than the adaptive immune response and as a result infants and young children may be more reliant on their innate immune system. For this reason it important to fully understand the key elements of the innate immune response including the many categories of PRRs and their cognate PAMPs. As these interactions are very early in the immune response, they are particularly relevant targets for therapeutic intervention. Below is a discussion of the major classes of PRRs, their expression, ligands, and signaling pathways as well as the major classes of PAMPs that activate them.

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Triacylated lipoproteins derived from Mycoplasma pneumoniae activate nuclear factor‐κB through toll‐like receptors 1 and 2

Cited by 92 publications

References 47 publications

A Triacylated Lipoprotein fromMycoplasma genitaliumActivates NF-κB through Toll-Like Receptor 1 (TLR1) and TLR2

A Triacylated Lipoprotein fromMycoplasma genitaliumActivates NF-κB through Toll-Like Receptor 1 (TLR1) and TLR2

Cytadherence of Mycoplasma pneumoniae Induces Inflammatory Responses through Autophagy and Toll-Like Receptor 4

Pathogen Associated Molecular Patterns, Pattern Recognition Receptors and Pediatric Sepsis

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