Consulta por: Publicación seriada
Autor: Santeliz Casavilca, Joanna V. (Comienzo)
2 registros cumplieron la condición especificada en la base de información BOLMED. ()
Registro 1 de 2, Base de información BOLMED
Portada
Artículos de éste númeroArtículos de éste número
Autor: Santeliz Casavilca, Joanna V. jsanteliz@ucla.edu.ve
Oprima aquí para enviar un correo electrónico a esta dirección
Título: ARTÍCULO DE REVISIÓN: MICROBIOTA PULMONAR Y EPOC: UNA RELACIÓN CASUAL?
LUNG MICROBIOTA AND COPD: A CAUSAL RELATIONSHIP?
ISSN: 0798-0361
Fecha: 2016
Páginas/Colación: pp. 144-152
En:/ BOLETÍN MÉDICO DE POSTGRADO Vol. 32 Nro. 2 Mayo - Junio 2016
Información de existenciaInformación de existencia
Categoría Temática: Palabras: MED01 MED01
Palabras Claves del Autor: Palabras: ÉPOC ÉPOC, Palabras: MICROBIOMA MICROBIOMA, Palabras: MICROBIOTA MICROBIOTA, Palabras: PULMÓN PULMÓN
Documentos asociados
Oprima aquí para visualizar el documento PDF:Documento en formato PDF Documento en formato PDF

RESUMEN


PALABRAS CLAVE: EPOC. Microbiota. Microbioma. Pulmón.

RESUMEN

La Enfermedad Pulmonar Obstructiva Crónica (EPOC) es una patología respiratoria con una alta morbi-mortalidad tanto en Venezuela como a nivel mundial. Esta enfermedad se caracteriza por una obstrucción progresiva, generalmente poco reversible, del flujo aéreo asociado a una disminución de la función pulmonar, comorbilidades sistémicas y en consecuencia un deterioro significativo en la calidad de vida. El factor de riesgo más importante es la exposición crónica a partículas tóxicas y gases particularmente el humo del cigarrillo. Las alteraciones anatómicas pulmonares en el paciente con EPOC son consecuencia de una respuesta inflamatoria que persiste a pesar de la cesación tabáquica. Las causas del mantenimiento de esta respuesta inflamatoria no están completamente esclarecidas. En esta revisión seactualizan conceptos relacionados con lamicrobiota pulmonar, un nuevo factor potencialmente involucrado en el desarrollo y evolución de la EPOC.

REVIEW ARTICLE

LUNG MICROBIOTA AND COPD: A CAUSAL RELATIONSHIP?

KEY WORDS: COPD. Microbiota. Microbiome. Lung. ABSTRACT

Chronic Obstructive Pulmonary Disease (COPD) is a respiratory illness with high morbidity and mortality both in Venezuela and worldwide. This disease is characterized byprogressive, not fully reversible, airway obstruction, decrease lung function, systemic comorbidities and consequently significant deterioration in quality of life. The most important risk factor is chronic exposure to particulates and toxic gases, especially cigarette smoking. The anatomic pulmonary alterations in patients with COPD are consequence of an inflammatory response that persists despite smoking cessation. The causes responsible for the persistence of this inflammatory response are not fully clarified. In this review we update concepts about lung microbiota, a new factor potentially involved in the development and evolution of COPD

REFERENCIAS BIBLIOGRAFICAS
1. WHO.int [Internet]. Suiza: WHO; [actualizado 20 de Julio de 2016; citado 16 de Agosto de 2016]. Disponible en: http://www.who.int/respiratory/copd/burden/en/
2. CELLI B, DECRAMER M, WEDZICHA J, WILSON K, AGUSTÍ A, CRINER G, et al. An Official American Thoracic Society/European Respiratory Society Statement: Research Questions in Chronic Obstructive Pulmonary Disease. Am J RespirCrit Care Med 2015: 191(7): e4 - e27.
3. LEDERBERG J, MCCRAY A. OmeSweet'Omics-a genealogical treasuryof words. The Scientist 2001; 15: 8.
4. The Human Microbiome Project Consortium. Structure, function and diversity of the healthy human microbiome. Nature 2012; 486: 207 - 214.
5. SIBLEY C, GRINWIS M, FIELD T, ESHAGHURSHAN C, FARÍA M, DOWD S, et al. Culture enriched molecular profiling of thecystic fibrosis airway microbiome. PLoS One 2011; 6:e22702.
6. BAUGHMAN R, THORPE J, STANECK J, RASHKIN M, FRAME P. Use of the protected specimen brush in patients with endotracheal or tracheostomy tubes. Chest 1987; 91(2): 233 - 236.
7. MIRA A. Análisis taxonómico y funcional del microbioma humano mediante aproximaciones clásicas, moleculares y metagenómicas [Tesis doctoral]. Valencia: Universidad de Valencia. Fundación para el Fomento de la Investigación Sanitaria yBiomédica de la Comunidad Valenciana (FISABIO), 2014.
8. TURNBAUGH P, LEY R, HAMADY M, FRASER-LIGGETT C, KNIGHT R, GORDON J. The human microbiome project. Nature 2007; 449: 804 - 810.
9. HAN M, HUANG Y, LIPUMA J, BOUSHEY H, BOUCHER R, COOKSON W, et al. Significance of the microbiome in obstructive lung disease. Thorax 2012; 67: 456 - 463.
10. SEGAL L, ROM W, WEIDEN M. Lung microbiome for clinicians. Ann Am ThoracSoc 2014; 11 (1): 108 - 116.
11. MORRIS A, BECK J, SCHLOSS P, CAMPBELL T, CROTHERS K, CURTIS J, et al. Comparison of the respiratory microbiome in healthy nonsmokers and smokers. Am J RespirCrit Care Med 2013; 187(10): 1067 - 1075.
12. WEINREICH U, KORSGAARD J. Bacterial colonization of lower airways in health and chronic lung disease. ClinRespir J 2008; 2: 116 - 122.
13. BAGDONAS E, RAUDONIUTE J, BRUZAUSKAITE I, ALDONYTE R. Novel aspects of pathogenesis and regeneration mechanisms in COPD. Int J COPD 2015; 10: 995 - 1013.
14. BASSIS C, ERB-DOWNWARD J, DICKSON R, FREEMAN C, SCHMIDT T, YOUNG V, et al. Analysis of the upper respiratory tract microbiotas as the source of the lung and gastric microbiotas in healthy individuals. MBio 2015; 6(2): e00037.
15. YU G, GAIL M, CONSONNI D, CARUGNO M, HUMPHRYS M, PESATORI A, et al. Characterizing human lung tissue microbiota and its relationship to epidemiological and clinical features. Genome Biol 2016; 17: 163.
16. WARNER B, HAMVAS A. Lung, microbes and the developing neonate. Neonatology 2015; 107(4): 337 - 343.
17. SETHI S, MALONEY J, GROVE L, WRONA C, BERENSON C. Airway inflammation and bronchial bacterial colonization in chronicobstructive pulmonary disease. Am JRespirCritCareMed 2006; 173: 991 - 998. 18. WU D, HOU C, LI Y, ZHAO Z, LIU J, LUX, et al. Analysis of the bacterial community in chronic obstructive pulmonary disease sputum samples by denaturing gradient gel electrophoresis and real-time PCR. BMC Pulm Med 2014; 14: 179.
19. HILTY M, BURKE C, PEDRO H, CARDENAS P, BUSH A, BOSSLEY C, et al. Disordered microbial communitiesin asthmatic airways. PLoS One2010; 5: 1 - 9.
20. EINARSSON G, COMER D, MCLLEAVEY, PARKHILL J, ENNIS M, TUNNEY M, et al. Community dynamics and the lower airway microbiota in stable chronic obstructive pulmonarydisease, smokers and healthy non-smokers. Thorax 2016; 71: 795 - 803.
21. SZE M, DIMITRIU P, HAYASHI S, ELLIOTT M, MCDONOUGH J, GOSSELINK J. The lung tissue microbiome in chronic obstructive pulmonary disease. Am J RespirCrit Care Med 2012; 185(10): 1073 - 1080.
22. ANGRILL J, AGUSTI C, DE CELIS R, RANO A, GONZALEZ J, SOLE T, et al. Bacterial colonization in patients with bronchiectasis: microbiological pattern and risk factors. Thorax 2002; 57: 15 - 19.
23. ERB-DOWNWARD J, THOMPSON D, HAN M, FREEMAN C, MCCLOSKEY L, SCHMIDT L, et al. Analysis of the lung microbiome in the “healthy” smoker and in COPD. PLoS One 2011; 6(2): e16384.
24. ZAKHARKINA T, HEINZEL E, KOCZULLA R, GREULICH T, RENTZ K, PAULING J, et al. Analysis of the airway microbiota of healthy Individuals and patients with chronic obstructive pulmonary disease by T-RFLP and clone Sequencing. PLoS One 2013; 8(7): e68302.
25. CABRERA-RUBIO R, GARCÍA-NUÑEZ M, SETÓ L, ANTÓ J, MOYA A, MONSÓ E, et al. Microbiome diversity in the bronchial tracts of patients with chronic obstructive pulmonary disease. J ClinMicrobiol 2012; 50(11): 3562 - 3568.
26. MOLYNEAUX P, MALLIA P, COX M, FOOTITT J, WILLIS-OWEN S, HOMOLA D, et al. Outgrowth of the bacterial airway microbiome after rhinovirus exacerbation of chronic obstructive pulmonary disease. Am J RespirCrit Care Med 2013; 188(10): 1224 - 1231.
27. PRAGMAN A, KIM H, REILLY C, WENDT C, ISAACSON R. The lung microbiome in moderate and severe chronic obstructive pulmonary disease. PLoS One 2012; 7(10): e47305.
28. HUANG Y, KIM E, COX M, BRODIE E, BROWN R, WIENER-KRONISH J, et al. A persistent and diverse airway microbiota present during chronic obstructive pulmonary disease exacerbations. OMICS 2010; 14(1): 9 - 59.
29. WELTE T. Inhaled corticosteroids in COPD and the risk of pneumonia. Lancet 2009; 374: 668 - 670.
30. GARCÍA-NUÑEZ M, MILLARES L, POMARES X, FERRARI R, PÉREZ-BROCAL V, GALLEGO M. Severity-related changes of bronchial microbiome in chronic obstructive pulmonary disease. J ClinMicrobiol 2014; 52(12): 4217 - 4223.
31. MILLARES L, FERRARI R, GALLEGO M, GARCÍA-NUÑEZ M, PÉREZ-BROCAL V, ESPASA M, et al. Bronchial microbiome of severe COPD patients colonized by Pseudomonas aeruginosa. Eur J ClinMicrobiol Infect Dis 2014; 33: 1101 - 1111.
32. CAMERON S, LEWIS K, HUWS S, LIN W, HEGARTY M, LEWIS P, et al. Metagenomic sequencing of the chronic obstructive pulmonary disease upper bronchial tract microbiome reveals functional changes associated with disease severity. PLoS One 2016; 11(2): e0149095.
33. MIRAVITLLES M, ANZUETO A. Role of infection in exacerbations of chronic obstructive pulmonary disease. CurrOpinPulm Med 2015; 21(3): 278 - 283.
34. WANG Z, BAFADHEL M, HALDAR K, SPIVAK A, MAYHEW D, MILLER B, et al. Lung microbiome dynamics in COPD exacerbations. EurRespir J 2016; 47(4): 1082 - 109.
35. STEIN M, HRUSCH C, GOZDZ J, IGARTUA C, PIVNIOUK V, MURRAY S, et al.Innate immunity and asthma risk in Amish and Hutterite farm children. NEnglJMed 2016; 375(5): 411 - 421.
36. HOOPER L, LITTMAN D, MACPHERSON A. Interactions between the microbiota and the immune system. Science 2012; 336(6086): 1268 - 1273.
37. CRAIG J, CLIFFE A, GARNETT K, HIGH N. Survival of nontypeableHaemophilusinfluenzaein macrophages. FEMS MicrobiolLett2001; 203: 55 - 61.
38. BERENSON CS, MURPHY TF, WRONA CT, SETHI S. Outer membrane protein P6 of nontypeableHaemophilus influenza is a potent and selective inducer of human macrophage proinflammatory cytokines. Infect Immun 2005; 73: 2728 - 2735.
39. MARTINEZ F, HAN M, FLAHERTY K, CURTIS J. Role of infection and antimicrobial therapy in acute exacerbations of chronic obstructive pulmonary disease. Expert Rev Anti Infect There 2006; 4(1): 101 - 124.
40. SETHI S, MURPHY T. Infection in the pathogenesis and courseof chronic obstructive pulmonary disease. N Engl J Med 2008; 359: 2355 - 2365.
41. MATKOVIC Z, MIRAVITLLES M. Chronic bronchial infection in COPD. Is there an infective phenotype? Respir Med 2013; 107(1): 10 - 22.
42. TANTUCCI C, PINI L. COPD: it is time to change! Int J Chron Obstruct Pulmon Dis 2015; 10: 2451 - 2457.
43.SIMOENS S, LAEKEMAN G, DECRAMER M. Preventing COPD exacerbations with macrolides: a review and budget impact analysis. Respir Med 2013; 107: 637 - 648.

Registro 2 de 2, Base de información BOLMED
Portada
Artículos de éste númeroArtículos de éste número
Autor: Santeliz Casavilca, Joanna V. jsanteliz@ucla.edu.ve
Oprima aquí para enviar un correo electrónico a esta dirección; López, William ; Mosquera, Elis ; Guerrero, Antonio ; Álvarez de Mora, Isabel ; López, William ; Mosquera, Elis ; Guerrero, Antonio ; Álvarez de Mora, Isabel
Título: NIVELES SÉRICOS DE IL-8, IL-10, IL-13, IFN? y TNFa EN PACIENTES PEDIÁTRICOS CON INFECCIÓN AGUDA POR DIFERENTES SEROTIPOS DE VIRUS DENGUE
SERUM LEVELS OF IL-8, IL-10, IL-13, IFN? AND TNFa IN PEDIATRIC PATIENTS WITH ACUTE INFECTION WITH DIFFERENT DENGUE VIRUS SEROTYPES
ISSN: 2342-5534
Fecha: 2016
Páginas/Colación: pp. 27-32
En:/ REVISTA VENEZOLANA DE SALUD PUBLICA Vol. 4 Nro. 1 Enero - Junio 2016
Información de existenciaInformación de existencia
Categoría Temática: Palabras: MED02 MED02
Palabras Claves del Autor: Palabras: DENGUE DENGUE, Palabras: ELISA ELISA, Palabras: INTERLEUCINAS INTERLEUCINAS, Palabras: TH1/TH2 TH1/TH2
Documentos asociados
Oprima aquí para visualizar el documento PDF:Documento en formato PDF Documento en formato PDF

RESUMEN
El dengue es una enfermedad aguda febril causada por cuatro serotipos del virus dengue (DENV) cuya prevalencia en las Américas se ha quintuplicado entre 2003 y 2013. La respuesta inmune contra la infección del virus del dengue involucra la participación de factores celulares y humorales. Se realizó una investigación de corte transversal observacional para evaluar los niveles de interleucinas de la respuesta inmune innata (IL-8, TNFa), de respuesta TH1 (IFN?), TH2 (IL-13) y regulatoria (IL-10) en suero de pacientes durante la fase aguda de infección por los serotipos DENV1, DENV3 y DENV4. Se incluyeron cuarenta pacientes con una edad promedio de 8,74 ± 1,11 años. No hubo diferencias significativas en los niveles de las interleucinas evaluadas entre pacientes con infección por diferentes serotipos sin embargo se observa una tendencia a una mayor concentración de éstas en pacientes infectados con DENV1. Las concentraciones de IL-8, TNFa, IL-10 e IL-13 fueron descendiendo progresivamente a lo largo de la etapa aguda de la infección, no obstante, desde el inicio, los niveles de IFN? mostraron niveles comparativamente más bajos. Para evaluar la presencia de polarización TH1/TH2 se determinó el cociente IFN?/IL-13 no observándose diferencias estadísticamente significativas entre los grupos, a pesar de evidenciarse una tendencia a una respuesta tipo TH1 en pacientes infectados con DENV1. En conclusión, en pacientes infectados con el virus dengue, los niveles séricos de IL-8, IL-10, IL-13, IFN? y TNFa parecieran ser independientes del serotipo viral.

Palabras clave: Dengue, ELISA, Interleucinas, PCR-TR, TH1/TH2

SERUM LEVELS OF IL-8, IL-10, IL-13, IFN? AND TNFa IN PEDIATRIC PATIENTS WITH ACUTE INFECTION WITH DIFFERENT DENGUE VIRUS SEROTYPES

ABSTRACT

Dengue is an acute febrile disease caused by four dengue virus (DENV) serotypes whose prevalence in the Americas has quintupled between 2003 and 2013. The immune response against the infection with dengue virus involves cellular and humoral factors. We performed an observational and cross-sectional study to evaluate the levels of interleukins of the innate immune response (IL-8, TNFa), TH1 response (IFN?), TH2 (IL-13) and regulatory (IL-10) in serum of patients during the acute phase of infection with the DENV1, DENV3 and DENV4 serotypes. Forty patients with an average age of 8,74 ± 1,11 were included. There was no significant difference between the levels of interleukins among patients infected with different viral serotypes, however a tendency of higher concentrations of all interleukins in patients infected with the DENV1 serotype was observed. The concentrations of IL-8, TNFa, IL-10 and IL-13 descended during the acute phase of the infection, although from the beginning the levels of IFN? were comparatively lower. To evaluate the presence of polarization TH1/TH2 we determined the IFN?/IL-13 ratio not finding statistical differences between groups however a tendency towards a TH1 response was observed in patients infected with DENV1. In conclusion, in patients infected with dengue virus, serum levels of IL-8, IL-10, IL-13, IFN? and TNFa seem to be independent of viral serotype.

Key words: Dengue, ELISA, Interleukins, RT-PCR, TH1/TH2

REFERENCIAS BIBLIOGRAFICAS
1. Dengue-PAHO/WHO, 2014. (Revisado el 08/03/2016 en http://www.paho.org/world-health day2014/wpcontent/uploads/2014/04/ Dengue-esp.pdf).
2. Tuiskunen A, Monteil V, Plumet S, et al. Phenotypic and genotypic characterization of dengue virus isolates differentiates dengue fever and dengue hemorrhagic fever from dengue shock syndrome. Arch Virol 2011; 20: 2023-2032.
3. Sudiro T, Zivny J, Ishiko H, et al. Analysis of plasma viral RNA levels during acute dengue virus infection using quantitative competitor reverse transcription-polymerase chain reaction. J Med Virol 2001; 20:29-34.
4. Halstead S. Neutralization and antibody-dependent enhancement of dengue viruses. Adv Virus Res 2003; 60:421-467.
5. Lin C, Lei H, Liu C, et al. Autoimmunity in Dengue Virus Infection. Dengue Bull 2004; 28: 51-57.
6. Lanciotti R, Calisher C, Gubler D, et al. Rapid Detection and Typing of Dengue Viruses from Clinical Samples by Using Reverse Transcriptase-Polymerase Chain Reaction. J Clin Microbiol 1992; 30(3): 545-551.
7. Yohan B , Kendarsari RI , Mutia K , et al. Growth characteristics and cytokine/chemokine induction profiles of dengue viruses in various cell lines. Acta Virol 2014; 58(1): 20-7.
8. Jain A , Pandey N , Garg R, et al. IL-17 level in patients with Dengue virus infection & its association with severity of illness. J Clin Immunol 2013; 33(3): 613-8.
9. Sierra B, Pérez A, Álvarez M, et al. Variation in Inflammatory/Regulatory Cytokines in Secondary, Tertiary, and Quaternary Challenges with Dengue Virus. Am J Trop Med Hyg 2012; 87(3): 538-547.
10. Kuno G, Bailey R. Cytokine responses among to dengue infection among Puerto Rican patients. Mem Inst Oswaldo Cruz 1994; 89(2): 179-82.
11. Raghupathy R, Chaturvedi U, Al-Sayer H, et al. Elevated levels of IL-8 in dengue hemorrhagic fever. J Med Virol 1998; 56(3): 280-285.
12. Lee Y, Liu M, Lei H, et al. MCP-1, a highly expressed chemokine in dengue hemorrhagic fever/dengue shock syndrome patients, may cause permeability change, possibly through reduced tight junctions of vascular endothelium cells. J Gen Virol 2006; 87:3623-3630.
13. Fink J, Gu F, Ling L, et al. Host gene expression profiling of dengue virus infection in cell lines and patients. PLoS Negl Trop Dis 2007; 1(2):e86.
14. Malavige G, Gomes L, Alles L, et al. Serum IL-10 as a marker of severe dengue infection. BMC Infect Dis 2013; 13: 341.
15. Chaturvedi U, Agarwal R, Elbishbishi E, et al. Cytokine cascade in dengue hemorrhagic fever: implications for pathogenesis. FEMS Immunol Med Microbiol 2000; 28:183-188.
16. Mustafa A, Elbishbishi E, Agarwal R, et al. Elevated levels of interleukin-13 and IL-18 in patients with dengue hemorrhagic fever. FEMS Immunol Med Microbiol 2001; 30(3): 229-33.
17. Pacsa A, Agarwal R, Elbishbishi E, et al. Role of interleukin-12 in patients with dengue hemorrhagic fever. FEMS Immunol Med Microbiol 2000; 28(2):151-5.
18. Chen R, Yang K, Wang L, et al. Different clinical and laboratory manifestations between dengue hemorrhagic fever and dengue fever with bleeding tendency. Trans R Soc Trop Med Hyg 2007; 101(11):1106-13.
19. Chaturvedi U, Elbishbishi E, Agarwal R, et al. Sequential production of cytokines by dengue virus-infected human peripheral blood leukocyte cultures. Med Virol 1999; 59(3):335-40.
20. Guy B , Nougarede N , Begue S , et al. Cell-mediated immunity induced by chimeric tetravalent dengue vaccine in naive or flavivirus-primed subjects.Vaccine 2008; 26(45): 5712-21.
21. Guy B. Immunogenicity of sanofi pasteur tetravalent dengue vaccine. J Clin Virol 2009; 46(2): S16-9.
22. Qiao M, Shaw D, Forrat R, et al. Priming Effect of Dengue and Yellow Fever Vaccination on the Immunogenicity, Infectivity, and Safety of a Tetravalent Dengue Vaccine in Humans. Am J Trop Med Hyg 2011; 85(4): 724-731.


 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 

** Back-end Alejandría BE 7.3.0b3 *