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Luong, Truc Thanh,Kim, Eun-Hye,Bak, Jong Phil,Nguyen, Cuong Thach,Choi, Sangdun,Briles, David E.,Pyo, Suhkneung,Rhee, Dong-Kwon American Society for Microbiology 2015 Infection and immunity Vol.83 No.1
<P>Alcohol impairs the host immune system, rendering the host more vulnerable to infection. Therefore, alcoholics are at increased risk of acquiring serious bacterial infections caused by <I>Streptococcus pneumoniae</I>, including pneumonia. Nevertheless, how alcohol affects pneumococcal virulence remains unclear. Here, we showed that the <I>S. pneumoniae</I> type 2 D39 strain is ethanol tolerant and that alcohol upregulates alcohol dehydrogenase E (AdhE) and potentiates pneumolysin (Ply). Hemolytic activity, colonization, and virulence of <I>S. pneumoniae</I>, as well as host cell myeloperoxidase activity, proinflammatory cytokine secretion, and inflammation, were significantly attenuated in <I>adhE</I> mutant bacteria (Δ<I>adhE</I> strain) compared to D39 wild-type bacteria. Therefore, AdhE might act as a pneumococcal virulence factor. Moreover, in the presence of ethanol, <I>S. pneumoniae</I> AdhE produced acetaldehyde and NADH, which subsequently led Rex (redox-sensing transcriptional repressor) to dissociate from the <I>adhE</I> promoter. An increase in AdhE level under the ethanol condition conferred an increase in Ply and H<SUB>2</SUB>O<SUB>2</SUB> levels. Consistently, <I>S. pneumoniae</I> D39 caused higher cytotoxicity to RAW 264.7 cells than the Δ<I>adhE</I> strain under the ethanol stress condition, and ethanol-fed mice (alcoholic mice) were more susceptible to infection with the D39 wild-type bacteria than with the Δ<I>adhE</I> strain. Taken together, these data indicate that AdhE increases Ply under the ethanol stress condition, thus potentiating pneumococcal virulence.</P>
A Molecular Mucosal Adjuvant To Enhance Immunity Against Pneumococcal Infection In The Elderly
Yoshiko Fukuyama,Yorihiko Ikeda,Junichiro Ohori,Gen Sugita,Kazuyoshi Aso,Keiko Fujihashi,David E. Briles,Jerry R. McGhee,Kohtaro Fujihashi 대한면역학회 2015 Immune Network Vol.15 No.1
Streptococcus pneumoniae (the pneumococcus) causes amajor upper respiratory tract infection often leading to severeillness and death in the elderly. Thus, it is important toinduce safe and effective mucosal immunity against thispathogen in order to prevent pnuemocaccal infection. However, this is a very difficult task to elicit protective mucosalIgA antibody responses in older individuals. A combindnasal adjuvant consisting of a plasmid encoding the Flt3 ligandcDNA (pFL) and CpG oligonucleotide (CpG ODN) successfullyenhanced S. pneumoniae-specific mucosal immunityin aged mice. In particular, a pneumococcal surfaceprotein A-based nasal vaccine given with pFL and CpG ODNinduced complete protection from S. pneumoniae infection. These results show that nasal delivery of a combined DNAadjuvant offers an attractive potential for protection againstthe pneumococcus in the elderly.
A Molecular Mucosal Adjuvant To Enhance Immunity Against Pneumococcal Infection In The Elderly
Fukuyama, Yoshiko,Ikeda, Yorihiko,Ohori, Junichiro,Sugita, Gen,Aso, Kazuyoshi,Fujihashi, Keiko,Briles, David E.,McGhee, Jerry R.,Fujihashi, Kohtaro The Korean Association of Immunobiologists 2015 Immune Network Vol.15 No.1
Streptococcus pneumoniae (the pneumococcus) causes a major upper respiratory tract infection often leading to severe illness and death in the elderly. Thus, it is important to induce safe and effective mucosal immunity against this pathogen in order to prevent pnuemocaccal infection. However, this is a very difficult task to elicit protective mucosal IgA antibody responses in older individuals. A combind nasal adjuvant consisting of a plasmid encoding the Flt3 ligand cDNA (pFL) and CpG oligonucleotide (CpG ODN) successfully enhanced S. pneumoniae-specific mucosal immunity in aged mice. In particular, a pneumococcal surface protein A-based nasal vaccine given with pFL and CpG ODN induced complete protection from S. pneumoniae infection. These results show that nasal delivery of a combined DNA adjuvant offers an attractive potential for protection against the pneumococcus in the elderly.
Li, Jie,Wang, Jennifer P.,Ghiran, Ionita,Cerny, Anna,Szalai, Alexander J.,Briles, David E.,Finberg, Robert W. American Society for Microbiology 2010 Infection and immunity Vol.78 No.7
<B>ABSTRACT</B><P>Complement-containing immune complexes can be presented to phagocytes by human erythrocytes bearing complement receptor 1 (CR1). Although this has long been assumed to be a mechanism by which humans are able to protect themselves from “extracellular” bacteria such as pneumococci, there is little direct evidence. In these studies we have investigated this question by comparing results for erythrocytes from transgenic mice expressing human CR1 on their erythrocytes to the results for wild-type mouse erythrocytes that do not express CR1. We demonstrate that human CR1 expression on murine erythrocytes allows immune adherence to beads opsonized with either mouse or human serum as a source of complement. The role of CR1 in immune adherence was supported by studies showing that it was blocked by the addition of antibody to human CR1. Furthermore, human CR1 expression enhances the immune adherence of opsonized pneumococci to erythrocytes <I>in vitro</I>, and the pneumococci attached to erythrocytes via CR1 can be transferred <I>in vitro</I> to live macrophages. Even more importantly, we observed that if complement-opsonized pneumococci are injected intravenously with CR1<SUP>+</SUP> mouse erythrocytes into wild-type mice (after a short <I>in vitro</I> incubation), they are cleared faster than opsonized pneumococci similarly injected with wild-type mouse erythrocytes. Finally, we have shown that the intravenous (i.v.) injection of pneumococci into CR1<SUP>+</SUP> mice also results in more rapid blood clearance than in wild-type mice. These data support that immune adherence via CR1 on erythrocytes likely plays an important role in the clearance of opsonized bacteria from human blood.</P>
Inhibition of Autolysis by Lipase LipA in Streptococcus pneumoniae Sepsis
김규리,Truc Thanh Luong,박상상,이승엽,하정아,Cuong Thach Nguyen,안지혜,박기태,백만정,표석능,David E. Briles,이동권 한국분자세포생물학회 2017 Molecules and cells Vol.40 No.12
More than 50% of sepsis cases are associated with pneumonia. Sepsis is caused by infiltration of bacteria into the blood via inflammation, which is triggered by the release of cell wall components following lysis. However, the regulatory mechanism of lysis during infection is not well defined. Mice were infected with Streptococcus pneumoniae D39 wild-type (WT) and lipase mutant (∆lipA) intranasally (pneumonia model) or intraperitoneally (sepsis model), and survival rate and pneumococcal colonization were determined. LipA and autolysin (LytA) levels were determined by qPCR and western blotting. S. pneumoniae Spd_1447 in the D39 (type 2) strain was identified as a lipase (LipA). In the sepsis model, but not in the pneumonia model, mice infected with the ∆lipA displayed higher mortality rates than did the D39 WT-infected mice. Treatment of pneumococci with serum induced LipA expres-sion at both the mRNA and protein levels. In the presence of serum, the ∆lipA displayed faster lysis rates and higher LytA expression than the WT, both in vitro and in vivo. These results indicate that a pneumococcal lipase (LipA) represses autolysis via inhibition of LytA in a sepsis model.
Inhibition of Autolysis by Lipase LipA in Streptococcus pneumoniae Sepsis
Kim, Gyu-Lee,Luong, Truc Thanh,Park, Sang-Sang,Lee, Seungyeop,Ha, Jung Ah,Nguyen, Cuong Thach,Ahn, Ji Hye,Park, Ki-Tae,Paik, Man-Jeong,Pyo, Suhkneung,Briles, David E.,Rhee, Dong-Kwon Korean Society for Molecular and Cellular Biology 2017 Molecules and cells Vol.40 No.12
More than 50% of sepsis cases are associated with pneumonia. Sepsis is caused by infiltration of bacteria into the blood via inflammation, which is triggered by the release of cell wall components following lysis. However, the regulatory mechanism of lysis during infection is not well defined. Mice were infected with Streptococcus pneumoniae D39 wild-type (WT) and lipase mutant (${\Delta}lipA$) intranasally (pneumonia model) or intraperitoneally (sepsis model), and survival rate and pneumococcal colonization were determined. LipA and autolysin (LytA) levels were determined by qPCR and western blotting. S. pneumoniae Spd_1447 in the D39 (type 2) strain was identified as a lipase (LipA). In the sepsis model, but not in the pneumonia model, mice infected with the ${\Delta}lipA$ displayed higher mortality rates than did the D39 WT-infected mice. Treatment of pneumococci with serum induced LipA expression at both the mRNA and protein levels. In the presence of serum, the ${\Delta}lipA$ displayed faster lysis rates and higher LytA expression than the WT, both in vitro and in vivo. These results indicate that a pneumococcal lipase (LipA) represses autolysis via inhibition of LytA in a sepsis model.