Bovine salmonellosis

Wray, C.; Sojka, W.J.

doi:10.1017/s0022029900020355

Cited by 88 publications

(16 citation statements)

References 170 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…elegans and Bacterial Stains-C. elegans strains were grown and maintained as previously described (19). The following bacterial strains were used in this study: Escherichia coli OP50 (20), Enterococcus faecalis OG1RF (21), Pseudomonas aeruginosa PA14 (22), Staphylococcus aureus NCTC8325 (45), and Salmonella enterica SL1344 (23). The following C. elegans strains were used in this study: wild-type N2, GF12 hsf-1(sy441), and AM141: N2rmIs133 (P(unc-54) Q40::YFP) (16).…”

Section: Methodsmentioning

confidence: 99%

Insulin Signaling and the Heat Shock Response Modulate Protein Homeostasis in the Caenorhabditis elegans Intestine during Infection

Mohri‐Shiomi

Garsin

2008

Journal of Biological Chemistry

101

View full text Add to dashboard Cite

During infection, damage can occur to the host as an outcome of both pathogen virulence mechanisms and host defense strategies. Using aggregation of a model polyglutamine-containing protein as an indicator in Caenorhabditis elegans, we show that protein damage occurs specifically at the site of the host-pathogen interaction, the intestine, in response to various bacterial pathogens. We demonstrate that the insulin signaling pathway and the heat shock transcription factor (HSF-1) influence the amount of aggregation that occurs, in addition to heat shock proteins and oxidative stress enzymes. We also show that addition of the antioxidants epigallocatechin gallate and ␣-lipoic acid reduces polyglutamine aggregation. The influence of oxidative stress enzymes and exogenous antioxidants on protein aggregation suggests that reactive oxygen species produced by the host are a source of protein damage during infection. We propose a model in which heat shock proteins and oxidative stress enzymes regulated by insulin signaling and HSF-1 are required for tissue protection during infection, to minimize the effects of protein damage occurring as a result of host-pathogen interactions.Innate immunity is comprised of strategies that allow an organism to immediately defend itself against an invading pathogen. In addition to mechanisms that actively destroy the infecting agent, the organism must protect itself from damage. Damage to the host can occur from virulence mechanisms of the pathogen, but also as a side effect of the immune response of the host. One pathway that we have shown contributes greatly to pathogen resistance in the model host Caenorhabditis elegans is insulin signaling (1). In addition to increased pathogen resistance, loss of insulin signaling in C. elegans results in several cytoprotective phenotypes such as stress resistance (oxidative stress, heat stress) and long lifespan. The insulin signaling pathway consists of a receptor, DAF-2, that when stimulated activates a phosphatidylinositol 3-kinase signaling cascade that culminates in the phosphorylation and down-regulation of the transcription factor DAF-16. A mutation in DAF-2, or any of the other upstream signaling components prevents inhibition of DAF-16, causing greater transcriptional activity (reviewed in Refs. 2-5).It was previously shown that pathogen resistance mediated by increased DAF-16 activity is dependent, at least in part, on the heat shock transcription factor HSF-1. 2 The loss of hsf-1 in a daf-2 mutant, or a mutant that overexpresses daf-16, causes a reduction in pathogen resistance and the overexpression of hsf-1 increases pathogen resistance (6). HSF-1 likely mediates these effects by controlling the expression of genes encoding heat shock proteins (HSPs). HSPs are protein chaperones that bind to unfolded or damaged proteins and prevent aggregation until they can be refolded or recycled (7-11). HSPs regulated by HSF-1 were demonstrated to be protective against bacterial pathogens (6) and we showed that ROS, a possible source of cellular da...

show abstract

Section: Methodsmentioning

confidence: 99%

Insulin Signaling and the Heat Shock Response Modulate Protein Homeostasis in the Caenorhabditis elegans Intestine during Infection

Mohri‐Shiomi

Garsin

2008

Journal of Biological Chemistry

101

View full text Add to dashboard Cite

show abstract

“…Para Mee (1995) o sorovar Dublin é mais invasivo que o Thyphimurium podendo ainda causar meningoencefalite, artrite séptica e necrose gangrenosa das extremidades distais. De acordo com Wray & Sojka (1977) habitualmente os animais ficam septicêmi-cos, apresentando sinais respiratórios e febre.…”

Section: Discussão E Conclusõesunclassified

Surto de salmonelose pelo sorovar Dublin em bezerros no Maranhão

et al. 2013

View full text Add to dashboard Cite

Pesq. Vet. Bras. 33(8):983-988, agosto 2013 983 RESUMO.-Um surto de salmonelose em bezerros causado pela Salmonella enterica subsp. enterica sorovar Dublin é relatado em uma fazenda no município de Timon, Maranhão. De um total de 62 bezerros, 22 (35,5%) adoeceram e destes nove (40,9%) morreram. Os sinais clínicos incluíram febre, depressão, anorexia e, em alguns casos, sinais respiratórios, neurológicos, entéricos ou artrites, com curso clínico hiperagudo ou subagudo. As principais lesões macroscópicas foram hepatomegalia com áreas pálidas multifocais a coalescentes, esplenomegalia e líquido nas cavidades torácica e abdominal. Histologicamente foram observados granulomas paratifoides no fígado, rim e baço, além de trombos e agregados bacterianos em vasos sanguíneos de diversos órgãos. O surto foi controlado com a adoção de antibioticoterapia adequada aliada a correção de algumas medidas sanitárias na propriedade.

show abstract

“…Further studies indicate that increased expression of the water channel Aquaporin is responsible for the deleterious effects of excessive DAF-16-mediated immune response. (12), Pseudomonas aeruginosa-strain PA14 (13), Salmonella enterica strain 1344 (14) Yersinia pestis strain KIM5 (15), and Staphylococcus aureus MSSA476 (16) were used. C. elegans strains utilized were wild-type N2, TJ356-daf-16::gfp (zIs356 (pDAF-16::DAF-16-GFP;rol-6)), and daf-2(e1370).…”

mentioning

confidence: 99%

Regulation of DAF-16-mediated Innate Immunity in Caenorhabditis elegans

Singh

Aballay

2009

Journal of Biological Chemistry

View full text Add to dashboard Cite

Activation of the innate immune system results in a rapid microbicidal response against microorganisms, which needs to be fine-tuned because uncontrolled immune responses can lead to infection and cancer, as well as conditions such as Crohn disease, atherosclerosis, and Alzheimer disease. Here we report that excessive activity of the conserved FOXO transcription factor DAF-16 enhances susceptibility to bacterial infections in Caenorhabditis elegans. We found that increased temperature activates not only DAF-16 nuclear import but also a control mechanism involved in DAF-16 nuclear export. The nuclear export of DAF-16 requires heat shock transcription factor HSF-1 and Hsp70/HSP-1. Furthermore, we show that increased expression of the water channel Aquoporin-1 is responsible for the deleterious consequences of excessive DAF-16-mediated immune response. These studies reveal a stress-inducible mechanism involved in the regulation of DAF-16 and indicate that uncontrolled DAF-16 activity and water homeostasis are a cause of the deleterious effects of excessive immune responses.The inflammatory response is a physiological process that takes place in the presence of a variety of noxious stimuli, including bacterial infections. A hallmark of inflammation is the increased tissue permeability, which allows components of the innate immune system to execute an inflammatory response at the site of infection. In addition to cellular immune effectors, humoral factors such as antimicrobial peptides, lysozymes, and reactive oxygen species accumulate at the site of infection to control invading microorganisms. Whereas this myriad of immune effectors plays a key role in the control of infections, they have the potential to damage host tissues. To provide insights into the mechanisms by which excessive immune responses may be deleterious to an infected host, we have taken advantage of the simple innate immune system of the genetically tractable nematode Caenorhabditis elegans.Dauer formation abnormal (DAF) 2 -16 is a key FOXO transcription factor that controls innate immunity in C. elegans (1-3). DAF-16 is closely related to mammalian FOXO3a, which has been linked to inflammation in response to infection (4, 5). Like FOXO3a, the activity of DAF-16 is tightly regulated by a wide variety of external stimuli such as nutrients, oxidative stress, and heat stress (6 -9). The activity of DAF-16 is tightly controlled at the level of subcellular localization and posttranslational modifications of the protein, including phosphorylation (7,8,10,11). The presence of such tight control suggests that there may be a stress-inducible mechanism that prevents the deleterious consequences of a hyperactive DAF-16.Here we studied the effect of hyperactivation of DAF-16 in the context of C. elegans immunity. We found that while DAF-16 overexpression protects C. elegans from bacterial infections, its excessive activation has deleterious effects. Even though increased temperature promotes DAF-16 nuclear import, it also turns on a control mechanism that prom...

show abstract

Bovine salmonellosis

Abstract: Introduction Incidence of salmonellosis in cattle Epidemic-logical considerations Epidemic-logical differences between

Cited by 88 publications

References 170 publications

Insulin Signaling and the Heat Shock Response Modulate Protein Homeostasis in the Caenorhabditis elegans Intestine during Infection

Insulin Signaling and the Heat Shock Response Modulate Protein Homeostasis in the Caenorhabditis elegans Intestine during Infection

Surto de salmonelose pelo sorovar Dublin em bezerros no Maranhão

Regulation of DAF-16-mediated Innate Immunity in Caenorhabditis elegans

Contact Info

Product

Resources

About