Programmed cell death induced by Klebsiella pneumoniae infection / 中华微生物学和免疫学杂志

Klebsiella pneumoniae can cause a variety of infectious diseases, especially in immunocompromised population. The emergence of multidrug-resistant hypervirulent Klebsiella pneumoniae has greatly limited the choice of treatment for Klebsiella pneumoniae infection, and the exploration of new treatment strategies is imminent. In the process of infection, there is a complex interaction between the programmed cell death of host cells and the invasion of Klebsiella pneumoniae. This paper mainly reviewed the research progress in several mechanisms of programmed cell death such as pyroptosis, apoptosis, necroptosis and autophagy caused by Klebsiella pneumoniae.

Challenges and perspectives in research and teaching of host pathogen interaction topics: new post-pandemic times to Brazil and other South American countries

Here is our proposal to improve learning in biomedical sciences for graduate and undergraduate courses with a broad vision integrating disciplines such as molecular cell biology, biochemistry, and biophysics around concepts of pathogen interaction within vertebrate and invertebrate hosts. Our paradigm is based on the possibility offered by the pandemic to have remote activities that give access to students and researchers from different places in Brazil and Latin American countries to discuss science. A multidisciplinary view of host-pathogen interaction allows us to understand better the mechanisms involved in the pathology of diseases, as well as to formulate broad strategies for the diagnosis, treatment, and control of thereof. The approach to integrating heterogeneous groups in science involves the critical analysis of national scientific resource distribution, where only some have the possibilities to conduct competitive scientific research. Solid theoretical training, contact, collaboration with groups of excellence, and training within a multidisciplinary network are our proposals for a permanent platform of scientific strengthening and dissemination for Latin America. Here we will review the concept of host-pathogen interaction, the type of institutions where it is taught and researched, new trends in active teaching methodologies, and the current political context in science.

La modulación de la expresión de IL-10 por el polimorfismo IL-10-592C/A (rs1800872) es independiente de la presencia y carga bacteriana de los periodontopatógenos clásicos / Modulation of IL-10 mRNA levels in periodontal lesions by IL-10-592C/A polymorphism (rs1800872) is independent of the frequency and load of classic periodontopathic bacteria

Objetivo: Reportamos la asociación entre el polimorfismo de nucleótido simple de IL-10-592C/A (rs1800872) y la detección/abundancia relativa de los periodontopatógenos Porfiromonas gingivalis, Tenerella forsythia, Treponema denticola y Aggregatibacter actinomycetemcomitans. Además investigamos la influencia de los determinantes genéticos y microbiológicos en los niveles de expresión de IL-10 en lesiones periodontales. Metodología Fueron reclutados 117 pacientes con periodontitis crónica y 58 controles. Luego del examen clínico fueron obtenidas muestras microbiológicas y la presencia/carga bacteriana de especies de periodontopatógenos fue cuantificada por RT-PCR. El genotipo para IL-10-592C/A fue determinado mediante restriction fragment length polymorphism. Resultados La distribución alélica del SNP rs1800872 en la población investigada cumplió con el equilibrio de Hardy-Weinberg (p = 0,64). Como ya ha sido reportado, los sujetos polimórficos demostraron menor expresión de IL-10 y riesgo aumentado de sufrir periodontitis crónica. El polimorfismo IL-10-592C/A no demostró relación con la detección o carga bacteriana de ninguna de las bacterias investigadas, además los niveles de expresión de IL-10 no fueron influenciados por el perfil microbiológico, sino que se correlacionaron directamente con el genotipo para el polimorfismo IL-10-592C/A.

Objective: A study was conducted to investigate the possible influence of the single nucleotide polymorphism (SNP) IL-10-592 C/A on the occurrence and load of the periodontal pathogens: P. gingivalis, T. forsythia, T. denticolaand A. Actinomycetemcomitans; as well to investigate the influence of microbial and genetic factors on the modulation of local IL-10 mRNA levels. Methodology The study included 117 cases and 58 controls. After clinical examination microbiological samples were obtained and the detection/quantification of the target bacterial species was performed by RT-PCR. SNP rs1800872 was assayed by restriction fragment length polymorphism (RFLP). Results Allele distribution of rs1800872 was in Hardy-Weinberg equilibrium (P = 64). As previously reported, polymorphic subjects demonstrated decreased IL-10 expression and increased risk of suffering chronic periodontitis. IL-10-592C/A rs1800872 SNP was not associated with the detection or the bacterial load of the investigated pathogens. Moreover, the presence/load of bacteria at periodontal sites did not influence IL-10 expression, which was determined by the genetic background of the study subjects. IL-10-592C/A SNP was not associated with detection/bacterial load of pathogenic bacteria. IL-10 expression levels were determined by the genetic background and were independent of the bacterial microenvironment.

Role of Intestinal Microbiota in Inflammatory Bowel Diseases

A vast number of micro-organisms within the human gut play a crucial role in maintaining human health. Intestinal microbiota maintains the intestinal homeostasis and function by mutually interacting with the host's epithelial cells and mucosal immune system; and the immune tolerance towards intestinal commensals should be permitted for such interactions to occur. In recent years, the prevalence of inflammatory bowel diseases has greatly increased, and the pathogenic pathway behind is considered to be related to an aggressive immune response which is a subset of commensal enteric bacteria in a genetically susceptible host. The abnormal host-microbial interactions play an important role in the pathophysiology of inflammatory bowel diseases, which have been proved through numerous studies in the field of genetics, molecular microbiology, immunology, and experimental rodent models, as well as various translational researches and clinical trials. This review briefly summarizes the composition and function of intestinal microbiota, interactions between the microbiota and the immune system, and the possible roles of the intestinal microbiota in the pathogenesis of inflammatory bowel diseases.