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1.
Benef Microbes ; 11(4): 305-318, 2020 Aug 12.
Artigo em Inglês | MEDLINE | ID: mdl-32486899

RESUMO

Gastrointestinal mucositis (GIM) is an inflammation caused by antitumor therapy, especially after chemotherapy and radiotherapy. Currently in the clinical practice, only palliative measures are taken to treat GIM, representing the main clinical limitation in the management of this condition. Several studies have highlighted the potential benefits of probiotics for the management of GIM, but the actual role of these microorganisms in the maintenance of intestinal homeostasis remains elusive. In this context, here we aimed to realise a systematic review with meta-analysis to evaluate the effect of probiotics on experimental GIM. The meta-analysis showed that probiotics significantly suppressed the body weight loss related to GIM in rodents (95% confidence interval (CI): -2.67 to -0.70; I2=98%, P<0.00). Subgroup analysis showed that pre-treatment (≥7 days before chemotherapy) (95% CI: -8.84 to -0.17; I2=98%, P<0.04) with a high dose of probiotics (≥ 109 cfu/day) (95% CI: -2.58 to -0.28; I2=98%, P<0.00) comprising two or more microorganism species (95% CI: -6.49 to -0.28; I2=96%, P=0.03) remedied GIM more effectively. It was also revealed that fungi (specifically Saccharomyces boullardii) are more effective in remedying GIM than bacteria (P=0.03 vs P<0.00), and the mouse models are more receptive than rats to the enteroprotective effects of probiotics (95% CI: -4.76, -0.69; I2=97%, P=0.01). Qualitative analyses highlighted that probiotics suppress GIM through several mechanisms; they reduce the intestinal permeability, suppress the pro-inflammatory cytokine production while stimulating production and secretion of anti-inflammatory cytokines, inhibit the signalling pathways coupled to inflammation and apoptosis, accelerate the proliferation of enterocytes, reduce the levels of reactive oxygen species, and help maintain the protective mucus layer. In conclusion, this review highlights the therapeutic benefits of probiotics in experimental GIM.


Assuntos
Mucosite/terapia , Probióticos/uso terapêutico , Animais , Apoptose , Proliferação de Células , Citocinas/metabolismo , Modelos Animais de Doenças , Efeitos Colaterais e Reações Adversas Relacionados a Medicamentos , Microbioma Gastrointestinal , Inflamação , Mucosa Intestinal/metabolismo , Mucosa Intestinal/microbiologia , Mucosa Intestinal/patologia , Mucosite/induzido quimicamente , Mucosite/prevenção & controle , Redução de Peso
2.
Phytopathology ; 101(7): 887-93, 2011 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-21323466

RESUMO

Molecular fingerprinting techniques that have the potential to identify or subtype bacteria at the strain level are needed for improving diagnosis and understanding of the epidemiology of pathogens such as Xanthomonas citri pv. mangiferaeindicae, which causes mango bacterial canker disease. We developed a ligation-mediated polymerase chain reaction targeting the IS1595 insertion sequence as a means to differentiate pv. mangiferaeindicae from the closely related pv. anacardii (responsible for cashew bacterial spot), which has the potential to infect mango but not to cause significant disease. This technique produced weakly polymorphic fingerprints composed of ≈70 amplified fragments per strain for a worldwide collection of X. citri pv. mangiferaeindicae but produced no or very weak amplification for pv. anacardii strains. Together, 12 tandem repeat markers were able to subtype X. citri pv. mangiferaeindicae at the strain level, distinguishing 231 haplotypes from a worldwide collection of 299 strains. Multilocus variable number of tandem repeats analysis (MLVA), IS1595-ligation-mediated polymerase chain reaction, and amplified fragment length polymorphism showed differences in discriminatory power and were congruent in describing the diversity of this strain collection, suggesting low levels of recombination. The potential of the MLVA scheme for molecular epidemiology studies of X. citri pv. mangiferaeindicae is discussed.


Assuntos
Elementos de DNA Transponíveis/genética , Mangifera/microbiologia , Doenças das Plantas/microbiologia , Sequências de Repetição em Tandem/genética , Xanthomonas/classificação , Análise do Polimorfismo de Comprimento de Fragmentos Amplificados , Ásia , Austrália , Técnicas de Tipagem Bacteriana/métodos , Brasil , Comores , Pegada de DNA , DNA Bacteriano/química , DNA Bacteriano/genética , França , Variação Genética , Genótipo , Mauritânia , Epidemiologia Molecular/métodos , Reação em Cadeia da Polimerase/métodos , África do Sul , Xanthomonas/genética , Xanthomonas/patogenicidade
3.
Plant Dis ; 95(10): 1311, 2011 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-30731685

RESUMO

In February 2010, grapefruit (Citrus paradisi) and Mexican lime (C. aurantifolia) leaves with erumpent callus-like lesions were collected in Senegal in the Sebikotane area between Dakar and Thies. Similar symptoms have been observed by local farmers since 2008, and lesions were morphologically similar to those of citrus canker caused by Xanthomonas citri pv. citri (Asiatic canker) and X. citri pv. aurantifolii (South American canker). Lesions were primarily reported from grapefruit (cv. Shambar), which is the most frequent citrus species produced in this area, and Mexican lime, which is also commonly grown. Both species are very susceptible to X. citri pv. citri pathotype A, and Mexican lime is susceptible to X. citri pv. citri pathotype A* and X. citri pv. aurantifolii (4). Fifteen Xanthomonas-like strains were isolated from disease samples using KC semiselective medium (3). PCR with primer pair 4/7 (2) revealed that all the Senegalese strains and the X. citri pv. citri strain CFBP 2525 from New Zealand, used as a positive control, generated the expected DNA fragment, whereas no fragment was observed for negative controls (distilled water instead of the template). Insertion sequence ligation-mediated (IS-LM)-PCR analysis (1) of X. citri pv. citri strains from Senegal and reference strains of X. citri pv. citri pathotypes A and A* (1), with MspI and four primer pairs (unlabelled MspI primer and four 5'-labelled insertion sequence-specific primers targeting three IS elements), indicated that the strains from Senegal were related to X. citri pv. citri but not to pv. aurantifolii. They were closely related to X. citri pv. citri pathotype A strains, with a broad host range, present in the Indian subcontinent and Mali (C. Vernière, unpublished data). Multilocus sequence analysis of four partial housekeeping gene sequences (atpD, dnaK, efp, and gyrB) confirmed that four Senegalese strains were not related to X. citri pv. aurantifolii and showed a full sequence identity to X. citri pv. citri sequence type ST3 (2), fully consistent with IS-LM-PCR. Using a detached leaf assay (4), Duncan grapefruit, Pineapple sweet orange, and Mexican lime leaves inoculated with all strains from Senegal developed typical erumpent, callus-like tissue at wound sites 2 weeks after the inoculations. Xanthomonas-like colonies were reisolated and PCR amplification with the primer pair 4/7 produced the same 468-nt DNA fragment. This represents the fourth outbreak of citrus canker reported from Africa within the last 5 years, the other documented reports were from Ethiopia (2007) and Mali and Somalia (2008). High disease prevalence was observed in Senegal with incidence exceeding 90% in the orchards where lime and grapefruit were infected for 3 years, indicating the suitability of environmental conditions in this region for the development of Asiatic citrus canker. The origin of the inoculum associated with the reported canker outbreak in Senegal is currently unknown and the precise distribution of the pathogen needs to be thoroughly assessed. To our knowledge, this is the first documented report of the presence of Asiatic citrus canker in Senegal and this occurrence increases the threat to citriculture in West Africa. References: (1) L. Bui Thi Ngoc et al. FEMS Microbiol. Lett. 288:33, 2008. (2) L. Bui Thi Ngoc et al. Int. J. Syst. Evol. Microbiol. 60:515, 2010. (3) O. Pruvost et al. J. Appl. Microbiol. 99:803, 2005. (4) C. Vernière et al. Eur. J. Plant Pathol. 104:477, 1998.

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