Fisiopatología de la sepsis por bacterias gram negativas: bases moleculares
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Fisiopatología de la sepsis por bacterias gram negativas: bases moleculares
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Sumario:

La sepsis constituye un complejo síndrome en el que a consecuencia de una respuesta anómala del huésped frente a una infección se desencadenan una serie de mecanismos fi siopatológicos celulares y moleculares que se traducirán en el daño multiorgánico del paciente y su respectivas manifestaciones clínicas. Las bacterias gram negativas, gracias al lipopolisacárido (LPS), principal constituyente de su membrana externa son reconocidas por moléculas como la proteína de unión al lipopolisacàrido (LBP) y por complejos de receptores de membrana celular en el huésped que reconocen su estructura antigénica como son el TLR4, el CD14 y la MD2, dando lugar, por medio de diferentes vías de señalización mieloide dependiente (MyD88) y mieloide independien... Ver más

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Revista Cuarzo

0121-2133

2500-7181

Méndez Fandiño, Yardani Rafael

Barrera C., María Claudia

FUNDACION UNIVERSITARIA JUAN N. CORPAS

10.26752/cuarzo.v21.n2.138

21

2015-12-15

88

103

Colombia

sepsis

bacterias gram-negativas

molecular

factores de virulencia

patología clínica

Revista Cuarzo - 2015

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spelling Fisiopatología de la sepsis por bacterias gram negativas: bases moleculares
Pathophysiology of sepsis by gram negative bacteria: Molecular bases
La sepsis constituye un complejo síndrome en el que a consecuencia de una respuesta anómala del huésped frente a una infección se desencadenan una serie de mecanismos fi siopatológicos celulares y moleculares que se traducirán en el daño multiorgánico del paciente y su respectivas manifestaciones clínicas. Las bacterias gram negativas, gracias al lipopolisacárido (LPS), principal constituyente de su membrana externa son reconocidas por moléculas como la proteína de unión al lipopolisacàrido (LBP) y por complejos de receptores de membrana celular en el huésped que reconocen su estructura antigénica como son el TLR4, el CD14 y la MD2, dando lugar, por medio de diferentes vías de señalización mieloide dependiente (MyD88) y mieloide independiente o TRIF, a la activación de una serie de kinasas que fi nalmente a través de vías de señalización intracelular como NF – kB, generarán cambios transcripcionales que inducirán la producción de citocinas pro infl amatorias, que explican el Síndrome de respuesta inflamatoria sistémica (SIRS) y las antinfl amatorias, que explican el síndrome de repuesta anti infl amatorio compensatorio (CARS), ambos constituyen las fases de la sepsis a través de los cuales pasa el paciente séptico en diferentes momentos del proceso. Todos estos procesos fisiopatológicos moleculares de la sepsis son los que darán como resultado cambios en el endotelio, la microvasculatura, el sistema del complemento, la coagulación y finalmente en cada uno de los órganos del paciente las diferentes manifestaciones clínicas que desde scores de valoración del paciente, como el SOFA, permiten identificar al paciente en sepsis, su pronóstico y directrices acerca del tratamiento. Es así como la comprensión de las bases fisiopatológicas moleculares de las sepsis por gram negativos constituyen hoy en día la base para su definición, la comprensión de la clínica y el punto de partida para mejoras terapéuticas en el manejo de la sepsis, traducida en la supervivencia del paciente.
Sepsis is a complex syndrome in which as a consequence of an abnormal response of the host against an infection, a series of cellular and molecular pathophysiological mechanisms are triggered, resulting in the multiorgan damage of the patient and their respective clinical manifestations. Gram-negative bacteria, due to the presence of lipopolysaccharide (LPS), the main constituent of its outer membrane, are recognized by molecules such as lipopolysaccharide binding protein (LBP) and complexes of cell membrane receptors in the host that recognize its structure Antigenic as are the TLR4, CD14 and MD2, giving rise, through different pathways of signaling dependent myeloid (MyD88) and independent myeloid or TRIF, to the activation of a series of kinases that fi nally through intracellular signaling pathways Such as NF - kB, will generate transcriptional changes that will induce the production of pro - infl ammatory cytokines, which explain the Systemic Inflammatory Response Syndrome (SIRS) and the anti - inflammatory drugs that explain the compensatory anti infl ammatory response syndrome (CARS) of the sepsis through which the septic patient passes in different moments of the process or. All these molecular pathophysiological processes of sepsis are those that will result in changes in the endothelium, the microvasculature, the complement system, the coagulation and fi nally in each one of the organs of the patient the different clinical manifestations that from scores of the patient’s evaluation, such as the SOFA, identify the patient in sepsis, their prognosis and treatment guidelines. Thus, the understanding of the molecular pathophysiological bases of gram-negative sepsis is nowadays the basis for its defi nition, the understanding of the clinic and the starting point for therapeutic improvements in the management of sepsis, translated into survival of the patient.
Méndez Fandiño, Yardani Rafael
Barrera C., María Claudia
sepsis
gram-negative bacteria
molecular
virulence factors
clinical pathology
sepsis
bacterias gram-negativas
molecular
factores de virulencia
patología clínica
21
2
Artículo de revista
Journal article
2015-12-15T00:00:00Z
2015-12-15T00:00:00Z
2015-12-15
application/pdf
Fundación Universitaria Juan N. Corpas
Revista Cuarzo
0121-2133
2500-7181
https://revistas.juanncorpas.edu.co/index.php/cuarzo/article/view/138
10.26752/cuarzo.v21.n2.138
https://doi.org/10.26752/cuarzo.v21.n2.138
spa
https://creativecommons.org/licenses/by-nc-sa/4.0/
Revista Cuarzo - 2015
88
103
Singer M, Deutschman C, Warren C, Shankar-Hari M, Annane D,Bauer M, et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016; 315(8): 801-810.
Ramachandran, G. Gram-positive and gram-negative bacterial toxins in sepsis A brief review. Virulence. 2014; 5(1): 213–218.
Rabirad N, Mohammadpoor M, Lari AR, Shojaie A, Bayat R, et al. Antimicrobial susceptibility patterns of the gram-negative bacteria isolated from septicemia in Children’s Medical Center, Tehran, Iran. J Prev Med Hyg. 2014;55(1):23-6.
Pérez M, Sánchez J.J. Actualización de la Sepsis en Adultos. Código Sepsis [Internet]. Universidad Internacional de Andalucía. [20 Mayo 2016] 2014. Disponible en: http://dspace.unia.es/bitstream/handle/10334/3418/0607_P%C3%A9rez.pdf?sequence=3
Mak T, Brüggemann H. Vimentin in Bacterial Infections. Cells. 2016;5(2):1-8.
Do Vale A, Cabanes D, Sousa. Bacterial Toxins as Pathogen Weapons Against Phagocytes. Frontiers in Microbiology. 2016;7(42):1-21.
Adams P, Lamoureux L, Swingle L, Mukundan K, Montan G. Lipopolysaccharide-Induced Dynamic Lipid Membrane Reorganization: Tubules, Perforations, and Stacks. Biophysical Journal. 2014;106:2395–2407.
Steimle A, Autenrieth I, Frick J.S. Structure and function: Lipid A modifications in commensals and pathogens. Int. J. Med. Microbiol. 2016; 306(5):290-301.
Harm S, Gabor F, Hartmann J. Low-dose polymyxin: an option for therapy of Gram-negative sepsis. Innate Immunity. 2016;22(4):274–283.
Band V, Weiss D. Mechanisms of Antimicrobial Peptide Resistance in Gram-Negative Bacteria. Antibiotics. 2015;4:18-41.
Carrillo R.C, Tapia J, Peña C.A, Kim Kohd M.J, Jaime A.R, Montalvo E. Bases moleculares de la sepsis. Revista de la Facultad de Medicina de la UNAM. 2014;57(3):1-13.
Castillo-Juárez I, Maeda T, Mandujano-Tinoco E, Tomás M, Pérez- Eretza B, García-Contreras S.J, et al. Role of quorum sensing in bacterial infections. World J Clin Cases. 2015;3(7):575-598.
March Rossello´ a G.A, Eiros Bouza J.M. Quorum sensing en bacterias y levaduras. Med Clin (Barc). 2013;141(8):353–357.
Reuter K, Steinbach A, Helms V. Interfering with Bacterial Quorum Sensing. Perspectives in Medicinal Chemistry 2016;8:1-15.
Prieto A, Urcola I, Blanco J, Dahbi G, Muniesa M, Quirós P, et al. Tracking bacterial virulence: global modulators as indicators. Scientifi c Reports. 2016;6(25973):1-11.
Yamamoto H, Oda M, Kanno M, Tamashiro S, Tamura I, Yoneda T, et al. Chemical Hybridization of Vizantin and Lipid A to Generate a Novel LPS Antagonist. Chem. Pharm. Bull. 2016;64:246–257.
Oda M, Yamamoto H, Shibutani M, Nakano M, Yabiku K, Tarui T, et al. Vizantin Inhibits Endotoxin-Mediated Immune Responses via the TLR 4/MD-2 Complex. J Immunol. 2014;193:4507-4514.
Martinez de Tejada G, Heinbockel L, Ferrer-Espada R, Heine H, Alexander C, Bárcena-Varela S, et al. Lipoproteins/peptides are sepsisinducing toxins from bacteria that can be neutralized by synthetic anti-endotoxin peptides. Scientifi c Reports. 2015;5(14292):1-15.
Chang Y, Tsai M, Huey-Herng Sheu W, Hsieh S, Chiang A. The Therapeutic Potential and Mechanisms of Action of Quercetin in Relation to Lipopolysaccharide-Induced Sepsis In Vitro and In Vivo. PLOS ONE. November 2013;8(11):1-13.
Takashima K, Matsushima M, Hashimoto K, Nose H, Sato M, Hashimoto N, et al. Protective effects of intratracheally administered quercetin on lipopolysaccharide-induced acute lung injury. Takashima et al. Respiratory Research 2014;15(150):1-10.
Chen K.F, Chaou C.H, Jiang J.Y, Yu H.W, Meng Y.H, Tang W.C, et al. Diagnostic Accuracy of Lipopolysaccharide-Binding Protein as Biomarker for Sepsis inAdult Patients: A Systematic Review and Meta-Analysis. PLOS ONE. 2016;11(4):1-13.
Krasity B, Troll J, Lehnert E, Hackett K, Dillard J, Apicella M, et al. Structural and Functional Features of a Developmentally Regulated Lipopolysaccharide-Binding Protein. mBio. 2015;6(5):1-10.
Dupont A, Heinbockel L, Brandenburg K, Hornef M. Antimicrobial peptides and the enteric mucus layer act in concert to protect the intestinal mucosa. Gut Microbes Deecember 2014;5(6):761-765.
Fang L, Xu Z, Wang G.S, Ji F, Mei C, Liu J, et al. Directed Evolution of an LBP/CD14 Inhibitory Peptide and Its Anti-Endotoxin Activity. PLoS One. 2014;9(7):1-10.
Płóciennikowska A, Hromada-Judycka A, Borzecka K, Kwiatkowska K. Co-operation of TLR4 and raft proteins in LPSinduced pro-infl ammatory signaling. Cell. Mol. Life Sci. 2015;72:557–581.
Yang H, Wang H, Ju Z, Ragab A.A, Lundbäck P, Long W. MD-2 is required for disulfi de HMGB1– dependent TLR4 signaling. J Exp Med. 2015;212(1):5-14
Wang H, Wei Y, Zeng Y, Qin Y, Xiong B, Qin G, et al. The association of polymorphisms of TLR4 and CD14 genes with susceptibility to sepsis in a Chinese population. BMC Med Genet. 2014;15(123):1-9.
Mukherjee S, Karmakar S, Sinha Babu S.P. TLR2 and TLR4 mediated host immune responses in major infectious diseases: a review. braz j infect dis. 2016; 20(2):193–204.
Paramo T, Tomasio S.M, Irvine K.L, Bryant C.E, Bond P.J. Energetics of Endotoxin Recognition in the Toll-Like Receptor 4 Innate Immune Response. Sci Rep. 2015;5(17997):1-13.
Zhang S, Yu M, Guo Q, Li1 R, Li G, Tan S, et al. Annexin A2 binds to endosomes and negatively regulates TLR4- triggered inflammatory responses via the TRAM-TRIF pathway. Sci Rep. 2015;5(15859):1-15.
Tsirigotis P, Chondropoulos S, Gkirkas K, Meletiadis J, Dimopoulou I. Balanced control of both hyper and ypo-infl ammatoryphases as a new treatment paradigm in sepsis. J Thorac Dis. 2016;8(5):E312-E316.
Boomer JS, Green JM, Hotchkiss RS. The changing immune system in sepsis: is individualized immuno-modulatory therapy the answer?. Virulence. 2014;5(1):45-56.
Kajiwara Y, Schiff T, Voloudakis G, Gama Sosa M.A, Elder G, Bozdagi O, et al. A Critical Role for Human Caspase-4 in Endotoxin Sensitivity. J Immunol. 2014;193(1):335-43.
Smith C, Wang X, Yin H. Caspases come together over LPS. Trends Immunol. 2015;36(2):59–61.
Aziz , Jacob A, Wang P. Revisiting caspases in sepsis. Cell Death Dis. 2014;20(5):1-12.
Jorgensen I, Miao E.A. Pyroptotic cell death defends against intracellular pathogens. Immunol Rev. 2015;265(1):130–142.
Wiersinga W.J, Leopold S.J, Cranendonk D.R, Van der Poll T. Host innate immune responses to sepsis. Virulence. 2014;5(1):36–44.
ManS.M, Kanneganti T.D. Regulation of infl ammasome activation. Immunol Rev. 2015;265(1):6–21.
Suárez R, Buelvas N. El infl amosoma: mecanismos de activación. Invest Clin. 2015;56(1):74 – 99.
Gómez H.G, Rugeles M.T, Jaimes F.A. Características inmunológicas claves en la fi siopatología de la sepsis Infectio. 2015;19(1):40-46.
Yu Y, Tang D, Kang R. Oxidative stress-mediated HMGB1 biology. Front Physiol. 2015;6:93:1-9.
Wang H, Ward MF, Sama AE. Targeting HMGB1 in the treatment of sepsis. Expert Opin Ther Targets. 2014;18(3):257-68.
Lee SA, Kwak MS, Kim S, Shin JS. The role of high mobility group box 1 in innate immunity. Yonsei Med J. 2014;55(5):1165-76.
Luo L, Zhang S, Wang Y, Rahman M, Syk I, Zhang E, Thorlacius H. Proinfl ammatory role of neutrophil extracellular traps in abdominal sepsis. Am J Physiol Lung Cell Mol Physiol. 2014;307(7):L586-96.
Zhang J, Yang J, Xu X, Liang L, Sun H, Liu G, et al. The influence of genetic polymorphisms in TLR4 and TIRAP, and their expression levels in peripheral blood, on susceptibility to sepsis. Exp Ther Med. 2016;11(1):131-139.
Bataille A, Galichon P, Ziliotis MJ, Sadia I, Hertig A. Epigenetic changes during sepsis: on your marks!. Crit Care. 2015;19(358):1-3.
Arens C, Bajwa SA, Koch C, Siegler BH, Schneck E, Hecker A, et al. Sepsis-induced long-term immuneparalysis - results of adescriptive, explorative study. Crit Care. 2016;20(93)1-11
Schulte W1, Bernhagen J, Bucala R. Cytokines in sepsis: potent immunoregulators and potential therapeutic targets--an updated view. Mediators Infl amm. 2013;2013(165974):1-16.
Yan J, Li S, Li S. The role of the liver in sepsis. . Int Rev Immunol. 2014;33(6):498-510.
Minemura M, Tajiri K, Shimizu Y. Liver involvement in systemic infection. World J Hepatol. 2014;6(9):632-42.
Sônego F, Castanheira FV, Ferreira RG, Kanashiro A, Leite CA, Nascimento DC, et al. Paradoxical Roles of the Neutrophil in Sepsis: Protective and Deleterious. Front Immunol. 2016;7(155):1-7.
Allen KS, Sawheny E, Kinasewitz GT. Anticoagulant modulation of inflammation in severe sepsis. World J Crit Care Med. 2015 May 4;4(2):105-15.
Lupu F, Keshari RS, Lambris JD, Coggeshall KM. Crosstalk between the coagulation and complement systems in sepsis. Thromb Res. 2014;133(01):S28-31.
Charchafl ieh J, Rushbrook J, Worah S, Zhang M. Activated Complement Factors as Disease Markers for Sepsis. Dis Markers. 2015;2015(382463):1-9.
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title Fisiopatología de la sepsis por bacterias gram negativas: bases moleculares
spellingShingle Fisiopatología de la sepsis por bacterias gram negativas: bases moleculares
Méndez Fandiño, Yardani Rafael
Barrera C., María Claudia
sepsis
gram-negative bacteria
molecular
virulence factors
clinical pathology
sepsis
bacterias gram-negativas
molecular
factores de virulencia
patología clínica
title_short Fisiopatología de la sepsis por bacterias gram negativas: bases moleculares
title_full Fisiopatología de la sepsis por bacterias gram negativas: bases moleculares
title_fullStr Fisiopatología de la sepsis por bacterias gram negativas: bases moleculares
title_full_unstemmed Fisiopatología de la sepsis por bacterias gram negativas: bases moleculares
title_sort fisiopatología de la sepsis por bacterias gram negativas: bases moleculares
title_eng Pathophysiology of sepsis by gram negative bacteria: Molecular bases
description La sepsis constituye un complejo síndrome en el que a consecuencia de una respuesta anómala del huésped frente a una infección se desencadenan una serie de mecanismos fi siopatológicos celulares y moleculares que se traducirán en el daño multiorgánico del paciente y su respectivas manifestaciones clínicas. Las bacterias gram negativas, gracias al lipopolisacárido (LPS), principal constituyente de su membrana externa son reconocidas por moléculas como la proteína de unión al lipopolisacàrido (LBP) y por complejos de receptores de membrana celular en el huésped que reconocen su estructura antigénica como son el TLR4, el CD14 y la MD2, dando lugar, por medio de diferentes vías de señalización mieloide dependiente (MyD88) y mieloide independiente o TRIF, a la activación de una serie de kinasas que fi nalmente a través de vías de señalización intracelular como NF – kB, generarán cambios transcripcionales que inducirán la producción de citocinas pro infl amatorias, que explican el Síndrome de respuesta inflamatoria sistémica (SIRS) y las antinfl amatorias, que explican el síndrome de repuesta anti infl amatorio compensatorio (CARS), ambos constituyen las fases de la sepsis a través de los cuales pasa el paciente séptico en diferentes momentos del proceso. Todos estos procesos fisiopatológicos moleculares de la sepsis son los que darán como resultado cambios en el endotelio, la microvasculatura, el sistema del complemento, la coagulación y finalmente en cada uno de los órganos del paciente las diferentes manifestaciones clínicas que desde scores de valoración del paciente, como el SOFA, permiten identificar al paciente en sepsis, su pronóstico y directrices acerca del tratamiento. Es así como la comprensión de las bases fisiopatológicas moleculares de las sepsis por gram negativos constituyen hoy en día la base para su definición, la comprensión de la clínica y el punto de partida para mejoras terapéuticas en el manejo de la sepsis, traducida en la supervivencia del paciente.
description_eng Sepsis is a complex syndrome in which as a consequence of an abnormal response of the host against an infection, a series of cellular and molecular pathophysiological mechanisms are triggered, resulting in the multiorgan damage of the patient and their respective clinical manifestations. Gram-negative bacteria, due to the presence of lipopolysaccharide (LPS), the main constituent of its outer membrane, are recognized by molecules such as lipopolysaccharide binding protein (LBP) and complexes of cell membrane receptors in the host that recognize its structure Antigenic as are the TLR4, CD14 and MD2, giving rise, through different pathways of signaling dependent myeloid (MyD88) and independent myeloid or TRIF, to the activation of a series of kinases that fi nally through intracellular signaling pathways Such as NF - kB, will generate transcriptional changes that will induce the production of pro - infl ammatory cytokines, which explain the Systemic Inflammatory Response Syndrome (SIRS) and the anti - inflammatory drugs that explain the compensatory anti infl ammatory response syndrome (CARS) of the sepsis through which the septic patient passes in different moments of the process or. All these molecular pathophysiological processes of sepsis are those that will result in changes in the endothelium, the microvasculature, the complement system, the coagulation and fi nally in each one of the organs of the patient the different clinical manifestations that from scores of the patient’s evaluation, such as the SOFA, identify the patient in sepsis, their prognosis and treatment guidelines. Thus, the understanding of the molecular pathophysiological bases of gram-negative sepsis is nowadays the basis for its defi nition, the understanding of the clinic and the starting point for therapeutic improvements in the management of sepsis, translated into survival of the patient.
author Méndez Fandiño, Yardani Rafael
Barrera C., María Claudia
author_facet Méndez Fandiño, Yardani Rafael
Barrera C., María Claudia
topic sepsis
gram-negative bacteria
molecular
virulence factors
clinical pathology
sepsis
bacterias gram-negativas
molecular
factores de virulencia
patología clínica
topic_facet sepsis
gram-negative bacteria
molecular
virulence factors
clinical pathology
sepsis
bacterias gram-negativas
molecular
factores de virulencia
patología clínica
topicspa_str_mv sepsis
bacterias gram-negativas
molecular
factores de virulencia
patología clínica
citationvolume 21
citationissue 2
publisher Fundación Universitaria Juan N. Corpas
ispartofjournal Revista Cuarzo
source https://revistas.juanncorpas.edu.co/index.php/cuarzo/article/view/138
language spa
format Article
rights https://creativecommons.org/licenses/by-nc-sa/4.0/
Revista Cuarzo - 2015
info:eu-repo/semantics/openAccess
http://purl.org/coar/access_right/c_abf2
references Singer M, Deutschman C, Warren C, Shankar-Hari M, Annane D,Bauer M, et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016; 315(8): 801-810.
Ramachandran, G. Gram-positive and gram-negative bacterial toxins in sepsis A brief review. Virulence. 2014; 5(1): 213–218.
Rabirad N, Mohammadpoor M, Lari AR, Shojaie A, Bayat R, et al. Antimicrobial susceptibility patterns of the gram-negative bacteria isolated from septicemia in Children’s Medical Center, Tehran, Iran. J Prev Med Hyg. 2014;55(1):23-6.
Pérez M, Sánchez J.J. Actualización de la Sepsis en Adultos. Código Sepsis [Internet]. Universidad Internacional de Andalucía. [20 Mayo 2016] 2014. Disponible en: http://dspace.unia.es/bitstream/handle/10334/3418/0607_P%C3%A9rez.pdf?sequence=3
Mak T, Brüggemann H. Vimentin in Bacterial Infections. Cells. 2016;5(2):1-8.
Do Vale A, Cabanes D, Sousa. Bacterial Toxins as Pathogen Weapons Against Phagocytes. Frontiers in Microbiology. 2016;7(42):1-21.
Adams P, Lamoureux L, Swingle L, Mukundan K, Montan G. Lipopolysaccharide-Induced Dynamic Lipid Membrane Reorganization: Tubules, Perforations, and Stacks. Biophysical Journal. 2014;106:2395–2407.
Steimle A, Autenrieth I, Frick J.S. Structure and function: Lipid A modifications in commensals and pathogens. Int. J. Med. Microbiol. 2016; 306(5):290-301.
Harm S, Gabor F, Hartmann J. Low-dose polymyxin: an option for therapy of Gram-negative sepsis. Innate Immunity. 2016;22(4):274–283.
Band V, Weiss D. Mechanisms of Antimicrobial Peptide Resistance in Gram-Negative Bacteria. Antibiotics. 2015;4:18-41.
Carrillo R.C, Tapia J, Peña C.A, Kim Kohd M.J, Jaime A.R, Montalvo E. Bases moleculares de la sepsis. Revista de la Facultad de Medicina de la UNAM. 2014;57(3):1-13.
Castillo-Juárez I, Maeda T, Mandujano-Tinoco E, Tomás M, Pérez- Eretza B, García-Contreras S.J, et al. Role of quorum sensing in bacterial infections. World J Clin Cases. 2015;3(7):575-598.
March Rossello´ a G.A, Eiros Bouza J.M. Quorum sensing en bacterias y levaduras. Med Clin (Barc). 2013;141(8):353–357.
Reuter K, Steinbach A, Helms V. Interfering with Bacterial Quorum Sensing. Perspectives in Medicinal Chemistry 2016;8:1-15.
Prieto A, Urcola I, Blanco J, Dahbi G, Muniesa M, Quirós P, et al. Tracking bacterial virulence: global modulators as indicators. Scientifi c Reports. 2016;6(25973):1-11.
Yamamoto H, Oda M, Kanno M, Tamashiro S, Tamura I, Yoneda T, et al. Chemical Hybridization of Vizantin and Lipid A to Generate a Novel LPS Antagonist. Chem. Pharm. Bull. 2016;64:246–257.
Oda M, Yamamoto H, Shibutani M, Nakano M, Yabiku K, Tarui T, et al. Vizantin Inhibits Endotoxin-Mediated Immune Responses via the TLR 4/MD-2 Complex. J Immunol. 2014;193:4507-4514.
Martinez de Tejada G, Heinbockel L, Ferrer-Espada R, Heine H, Alexander C, Bárcena-Varela S, et al. Lipoproteins/peptides are sepsisinducing toxins from bacteria that can be neutralized by synthetic anti-endotoxin peptides. Scientifi c Reports. 2015;5(14292):1-15.
Chang Y, Tsai M, Huey-Herng Sheu W, Hsieh S, Chiang A. The Therapeutic Potential and Mechanisms of Action of Quercetin in Relation to Lipopolysaccharide-Induced Sepsis In Vitro and In Vivo. PLOS ONE. November 2013;8(11):1-13.
Takashima K, Matsushima M, Hashimoto K, Nose H, Sato M, Hashimoto N, et al. Protective effects of intratracheally administered quercetin on lipopolysaccharide-induced acute lung injury. Takashima et al. Respiratory Research 2014;15(150):1-10.
Chen K.F, Chaou C.H, Jiang J.Y, Yu H.W, Meng Y.H, Tang W.C, et al. Diagnostic Accuracy of Lipopolysaccharide-Binding Protein as Biomarker for Sepsis inAdult Patients: A Systematic Review and Meta-Analysis. PLOS ONE. 2016;11(4):1-13.
Krasity B, Troll J, Lehnert E, Hackett K, Dillard J, Apicella M, et al. Structural and Functional Features of a Developmentally Regulated Lipopolysaccharide-Binding Protein. mBio. 2015;6(5):1-10.
Dupont A, Heinbockel L, Brandenburg K, Hornef M. Antimicrobial peptides and the enteric mucus layer act in concert to protect the intestinal mucosa. Gut Microbes Deecember 2014;5(6):761-765.
Fang L, Xu Z, Wang G.S, Ji F, Mei C, Liu J, et al. Directed Evolution of an LBP/CD14 Inhibitory Peptide and Its Anti-Endotoxin Activity. PLoS One. 2014;9(7):1-10.
Płóciennikowska A, Hromada-Judycka A, Borzecka K, Kwiatkowska K. Co-operation of TLR4 and raft proteins in LPSinduced pro-infl ammatory signaling. Cell. Mol. Life Sci. 2015;72:557–581.
Yang H, Wang H, Ju Z, Ragab A.A, Lundbäck P, Long W. MD-2 is required for disulfi de HMGB1– dependent TLR4 signaling. J Exp Med. 2015;212(1):5-14
Wang H, Wei Y, Zeng Y, Qin Y, Xiong B, Qin G, et al. The association of polymorphisms of TLR4 and CD14 genes with susceptibility to sepsis in a Chinese population. BMC Med Genet. 2014;15(123):1-9.
Mukherjee S, Karmakar S, Sinha Babu S.P. TLR2 and TLR4 mediated host immune responses in major infectious diseases: a review. braz j infect dis. 2016; 20(2):193–204.
Paramo T, Tomasio S.M, Irvine K.L, Bryant C.E, Bond P.J. Energetics of Endotoxin Recognition in the Toll-Like Receptor 4 Innate Immune Response. Sci Rep. 2015;5(17997):1-13.
Zhang S, Yu M, Guo Q, Li1 R, Li G, Tan S, et al. Annexin A2 binds to endosomes and negatively regulates TLR4- triggered inflammatory responses via the TRAM-TRIF pathway. Sci Rep. 2015;5(15859):1-15.
Tsirigotis P, Chondropoulos S, Gkirkas K, Meletiadis J, Dimopoulou I. Balanced control of both hyper and ypo-infl ammatoryphases as a new treatment paradigm in sepsis. J Thorac Dis. 2016;8(5):E312-E316.
Boomer JS, Green JM, Hotchkiss RS. The changing immune system in sepsis: is individualized immuno-modulatory therapy the answer?. Virulence. 2014;5(1):45-56.
Kajiwara Y, Schiff T, Voloudakis G, Gama Sosa M.A, Elder G, Bozdagi O, et al. A Critical Role for Human Caspase-4 in Endotoxin Sensitivity. J Immunol. 2014;193(1):335-43.
Smith C, Wang X, Yin H. Caspases come together over LPS. Trends Immunol. 2015;36(2):59–61.
Aziz , Jacob A, Wang P. Revisiting caspases in sepsis. Cell Death Dis. 2014;20(5):1-12.
Jorgensen I, Miao E.A. Pyroptotic cell death defends against intracellular pathogens. Immunol Rev. 2015;265(1):130–142.
Wiersinga W.J, Leopold S.J, Cranendonk D.R, Van der Poll T. Host innate immune responses to sepsis. Virulence. 2014;5(1):36–44.
ManS.M, Kanneganti T.D. Regulation of infl ammasome activation. Immunol Rev. 2015;265(1):6–21.
Suárez R, Buelvas N. El infl amosoma: mecanismos de activación. Invest Clin. 2015;56(1):74 – 99.
Gómez H.G, Rugeles M.T, Jaimes F.A. Características inmunológicas claves en la fi siopatología de la sepsis Infectio. 2015;19(1):40-46.
Yu Y, Tang D, Kang R. Oxidative stress-mediated HMGB1 biology. Front Physiol. 2015;6:93:1-9.
Wang H, Ward MF, Sama AE. Targeting HMGB1 in the treatment of sepsis. Expert Opin Ther Targets. 2014;18(3):257-68.
Lee SA, Kwak MS, Kim S, Shin JS. The role of high mobility group box 1 in innate immunity. Yonsei Med J. 2014;55(5):1165-76.
Luo L, Zhang S, Wang Y, Rahman M, Syk I, Zhang E, Thorlacius H. Proinfl ammatory role of neutrophil extracellular traps in abdominal sepsis. Am J Physiol Lung Cell Mol Physiol. 2014;307(7):L586-96.
Zhang J, Yang J, Xu X, Liang L, Sun H, Liu G, et al. The influence of genetic polymorphisms in TLR4 and TIRAP, and their expression levels in peripheral blood, on susceptibility to sepsis. Exp Ther Med. 2016;11(1):131-139.
Bataille A, Galichon P, Ziliotis MJ, Sadia I, Hertig A. Epigenetic changes during sepsis: on your marks!. Crit Care. 2015;19(358):1-3.
Arens C, Bajwa SA, Koch C, Siegler BH, Schneck E, Hecker A, et al. Sepsis-induced long-term immuneparalysis - results of adescriptive, explorative study. Crit Care. 2016;20(93)1-11
Schulte W1, Bernhagen J, Bucala R. Cytokines in sepsis: potent immunoregulators and potential therapeutic targets--an updated view. Mediators Infl amm. 2013;2013(165974):1-16.
Yan J, Li S, Li S. The role of the liver in sepsis. . Int Rev Immunol. 2014;33(6):498-510.
Minemura M, Tajiri K, Shimizu Y. Liver involvement in systemic infection. World J Hepatol. 2014;6(9):632-42.
Sônego F, Castanheira FV, Ferreira RG, Kanashiro A, Leite CA, Nascimento DC, et al. Paradoxical Roles of the Neutrophil in Sepsis: Protective and Deleterious. Front Immunol. 2016;7(155):1-7.
Allen KS, Sawheny E, Kinasewitz GT. Anticoagulant modulation of inflammation in severe sepsis. World J Crit Care Med. 2015 May 4;4(2):105-15.
Lupu F, Keshari RS, Lambris JD, Coggeshall KM. Crosstalk between the coagulation and complement systems in sepsis. Thromb Res. 2014;133(01):S28-31.
Charchafl ieh J, Rushbrook J, Worah S, Zhang M. Activated Complement Factors as Disease Markers for Sepsis. Dis Markers. 2015;2015(382463):1-9.
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url https://revistas.juanncorpas.edu.co/index.php/cuarzo/article/view/138
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citationstartpage 88
citationendpage 103
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