Escherichia coli enterotoxigénica y enteroagregativa: prevalencia, patogénesis y modelos múridos / Enterotoxigenic and enteroaggregative Escherichia coli: prevalence, pathogenesis and murine models

Resumen Los patotipos de Escherichia coli enterotoxigénica (ETEC) y enteroagregativa (EAEC) son importantes agentes etiológicos causantes de diarrea en niños menores de cinco años de México y países en desarrollo, en quienes causan numerosas muertes. Ambos se han asociado con retraso en el crecimiento infantil y son los principales agentes causales de la "diarrea del viajero". La patogénesis de ambas bacterias se inicia cuando estas se adhieren al epitelio intestinal mediante fimbrias, denominadas factores de colonización en las cepas ETEC aisladas de humano y fimbrias de adherencia agregativa en las cepas de EAEC. Una vez que ETEC se adhiere al enterocito produce una o ambas de sus toxinas e induce la secreción de iones de cloruro, sodio y agua al lumen intestinal, produciendo su característica diarrea acusa. EAEC se une al epitelio intestinal formando una biopelícula, induce la producción de moco, libera sus toxinas y promueve inflamación. Modelos de infección de EAEC y ETEC con ratones C57BL/6 silvestres y deficientes del ligando de CD40 (con microbiotas intactas), respectivamente, revelaron que la desnutrición y la dieta baja en cinc incrementan la infección de EAEC causando retraso en el crecimiento y que ETEC coloniza, persiste e induce respuesta inmune humoral local y sistémica.

Abstract Enterotoxigenic (ETEC) and enteroaggregative Escherichia coli (EAEC) pathotypes are important etiological agents causative of diarrhea in children younger than 5 years of age in Mexico and in developing countries, where they cause numerous deaths. Both have been associated with delayed growth in children and are the main causative agents of traveler's diarrhea. The pathogenesis of both bacteria starts by adhering to the intestinal epithelium by means of fimbriae, called colonization factors in human ETEC isolates and aggregative adherence fimbriae in EAEC isolates. Once ETEC adheres to the enterocyte, it produces one or both of its toxins and induces the secretion of chloride and sodium ions and water into the intestinal lumen, producing its characteristic watery diarrhea. EAEC binds to the intestinal epithelium forming a biofilm, induces the production of mucus, releases its toxins and promotes inflammation. EAEC and ETEC infection models with wild-type C57BL/6 and CD40 ligand-deficient mice (with intact microbiota), respectively, revealed that undernutrition and low-zinc diet increases EAEC infection, causing growth retardation, and that ETEC colonizes, persists and induces local and systemic humoral immune response.

Murine models of infectious exacerbation of respiratory disease / 中国药理学通报

Asthma, chronic obstructive pulmonary disease (COPD), cystic fibrosis(CF) lung disease are common chronic respiratory diseases. There has been evidence that respiratory in-fections with bacteria and viruses underpin the pathogenesis of the respiratory diseases. It is now well-recognized that early life infections may induce more severe asthma by inducing permanent alterations in immunity and lung structure, and even induce ster-oid-resistant severe asthma in adulthood. Respiratory infections will exacerbate the inflammation and remodeling in lung of COPD. P. aeruginosa infection in lung will induce CF. There are no effective therapies preventing or reversing the exacerbation of respiratory diseases. The development and use of mouse mod-els are proved to be valuable in understanding the role of infec-tion in disease pathogenesis. This article reviews the progresses in murine models of infectious exacerbation of respiratory disea-ses, emphasizes on the pathological changes of the three respira-tory diseases found with the application of murine models, and explores the therapeutic method which can be developed and tested by the application of murine models, in order to offer ref-erence for clinical research and treatment.