An oral<i>Salmonella</i>vaccine promotes the down-regulation of cell surface Toll-like receptor 4 (TLR4) and TLR2 expression in mice

Eguchi, M.; Sekiya, Yukie; Suzuki, Masato; Yamamoto, Tomoko; Matsui, Hidenori

doi:10.1111/j.1574-695x.2007.00240.x

Cited by 10 publications

(9 citation statements)

References 39 publications

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“…Thus, 7-week-old mice were s.c. infected with a total of 1 ϫ 10 7 CFU of stationary-growth-phase GAS into both hind footpads (5 ϫ 10 6 CFU per footpad). After s.c. infection, the survival rates were observed every 24 h for 336 h postinfection, or the number of bacteria in the blood and tissue samples including the popliteal lymph nodes (PLN), spleen, and liver were determined by plating onto sheep blood agar (11,27). All mice were bred at the animal facility at the Kitasato Institute, and all mouse experiments were performed in accordance with institutional protocol guidelines under an approved protocol.…”

Section: Mouse Model For Gas Infectionmentioning

confidence: 99%

CD46 Transgenic Mouse Model of Necrotizing Fasciitis Caused by Streptococcus pyogenes Infection

et al. 2009

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We developed a human CD46-expressing transgenic (Tg) mouse model of subcutaneous (s.c.) infection into both hind footpads with clinically isolated 11 group A streptococcus (GAS) serotype M1 strains. When the severity levels of foot lesions at 72 h and the mortality rates by 336 h were compared after s.c. infection with 1 ؋ 10 7 CFU of each GAS strain, the GAS472 strain, isolated from the blood of a patient suffering from streptococcal toxic shock syndrome (STSS), induced the highest severity levels and mortality rates. GAS472 led to a 100% mortality rate in CD46 Tg mice after only 168 h postinfection through the supervention of severe necrotizing fasciitis (NF) of the feet. In contrast, GAS472 led to a 10% mortality rate in non-Tg mice through the supervention of partial necrotizing cutaneous lesions of the feet. The footpad skin sections of CD46 Tg mice showed hemorrhaging and necrotic striated muscle layers in the dermis, along with the exfoliation of epidermis with intracellular edema until 48 h after s.c. infection with GAS472. Thereafter, the bacteria proliferated, reaching a 90-fold or 7-fold increase in the livers of CD46 Tg mice or non-Tg mice, respectively, for 24 h between 48 and 72 h after s.c. infection with GAS472. As a result, the infected CD46 Tg mice appeared to suffer severe liver injuries. These findings suggest that human CD46 enhanced the progression of NF in the feet and the exponential growth of bacteria in deep tissues, leading to death.Group A streptococci (GAS), which are among the most common human pathogens, can cause a variety of uncomplicated superficial skin infections such as impetigo/pyoderma or throat infections, including streptococcal pharyngitis (sore throat) and tonsillitis (3). In addition, patients suffering from acute and complicated GAS infections, in particular streptococcal toxic shock syndrome (STSS) associated with severe necrotizing fasciitis (NF), have high mortality rates (4). M proteins, which attach to the cell wall, are one of the important virulence factors that GAS possess (15). The various GAS strains have more than 100 different antigenically distinguishable M proteins (46), and GAS serotype M1 strains are regarded as a highly virulent group (3).Membrane cofactor protein (MCP; CD46), which is expressed in every cell type except erythrocytes, is implicated as a receptor for at least six human pathogens (four viruses and two bacteria), including measles virus (9, 31, 35), herpesvirus 6 (40), adenovirus groups B (17, 41) and D (48), pathogenic Neisseria (23), and GAS (37). Human CD46-expressing transgenic (Tg) mice are susceptible to streptococcal disease (30). When CD46 Tg and non-Tg mice were infected intravenously (i.v.) with GAS, the bacteremia levels, frequency of arthritis, and mortality rate were higher in CD46 Tg mice than in non-Tg mice (30). Unfortunately, this animal model does not reflect the natural infection process in the human host. Consequently, we have attempted to establish a CD46 Tg mouse model of skin and soft tissue infection with GAS that...

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Section: Mouse Model For Gas Infectionmentioning

confidence: 99%

CD46 Transgenic Mouse Model of Necrotizing Fasciitis Caused by Streptococcus pyogenes Infection

et al. 2009

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“…As bacterial Lon has been shown to be important for the infectivity and/or pathogenicity of certain species such as B. abortus and S. typhimurium, compounds that specifically block bacterial but not human Lon, hold promise for a new class of anti-microbial agents (8,31,33,34,99,102). In addition, mitochondrial Lon has been implicated in the response to oxidative stress and damage to proteins and mtDNA (7,46,103), which has direct relevance to aging.…”

Section: Inhibitors Of Lon Proteasesmentioning

confidence: 99%

Functional mechanics of the ATP-dependent Lon protease- lessons from endogenous protein and synthetic peptide substrates

Lee

Suzuki

2008

Biochimica et Biophysica Acta (BBA) - Proteins and Proteomics

101

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SUMMARYLon, also known as the protease La, is a homo-oligomeric ATP-dependent protease, which is highly conserved in archaea, eubacteria and eukaryotic mitochondria and peroxisomes. Since its discovery, studies have shown that Lon activity is essential for cellular homeostasis, mediating protein quality control and metabolic regulation. This article highlights the discoveries made over the past decade demonstrating that Lon selectively degrades abnormal as well as certain regulatory proteins and thus plays significant roles in maintaining bacterial and mitochondrial function and integrity. In addition, Lon is required in certain pathogenic bacteria, for rendering pathogenicity and host infectivity. Recent research endeavors have been directed towards elucidating the reaction mechanism of the Lon protease by different biochemical and structural biological techniques. In this mini-review, the authors survey the diverse biological roles of Lon, and also place special emphasis on recent discoveries that elucidate the mechanistic aspects of the Lon reaction cycle.

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“…TLR4 is often overexpressed in malignant and tumor-infiltrating immune cells, and the application of TLR4 ligands in cancer therapies is desirable for enhancement of antitumor immunity [38, 39]. PAX5 haploinsufficiency induced decreased expression of TLR4, and the downregulated TLR4 participated in immune tolerance [43, 44]. Fos was involved in inducing a large number of cytokine genes and other genes that were central to the productive immune response.…”

Section: Discussionmentioning

confidence: 99%

Identification of Significant Pathways Induced by PAX5 Haploinsufficiency Based on Protein-Protein Interaction Networks and Cluster Analysis in Raji Cell Line

Zhao

et al. 2017

BioMed Research International

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PAX5 encodes a transcription factor essential for B-cell differentiation, and PAX5 haploinsufficiency is involved in tumorigenesis. There were few studies on how PAX5 haploinsufficiency regulated genes expression to promote tumorigenesis. In this study, we constructed the cell model of PAX5 haploinsufficiency using gene editing technology in Raji cells, detected differentially expressed genes in PAX5 haploinsufficiency Raji cells, and used protein-protein interaction networks and cluster analysis to comprehensively investigate the cellular pathways involved in PAX5 haploinsufficiency. The clusters of gene transcription, inflammatory and immune response, and cancer pathways were identified as three important pathways associated with PAX5 haploinsufficiency in Raji cells. These changes hinted that the mechanism of PAX5 haploinsufficiency promoting tumorigenesis may be related to genomic instability, immune tolerance, and tumor pathways.

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An oralSalmonellavaccine promotes the down-regulation of cell surface Toll-like receptor 4 (TLR4) and TLR2 expression in mice

Cited by 10 publications

References 39 publications

CD46 Transgenic Mouse Model of Necrotizing Fasciitis Caused by Streptococcus pyogenes Infection

CD46 Transgenic Mouse Model of Necrotizing Fasciitis Caused by Streptococcus pyogenes Infection

Functional mechanics of the ATP-dependent Lon protease- lessons from endogenous protein and synthetic peptide substrates

Identification of Significant Pathways Induced by PAX5 Haploinsufficiency Based on Protein-Protein Interaction Networks and Cluster Analysis in Raji Cell Line

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