Background: The aim of the present study was to undertake a systematic review exploring the relationship between childhood obesity and fecal microorganisms, to answer the following question: “Are Firmicutes and Bacteroidetes a significant risk indicator/factor for obesity in children?” The main search terms were “child” and “obesity” together with “gut microbiota” (PubMed: 2005–2017). The minimal requirements for inclusion were the evaluation of gut microbiota composition and BMI in children between 0 and 13 years of age. Methods: Assessed articles were carefully classified according to a predetermined criterion, and the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) were considered. Seven articles were critically appraised and used as a basis for conclusions. Results: Three studies showed a positive association between Bacteroides fragilis and obesity. In addition, a high value of evidence indicated that a decrease in the Bacteroidetes phylum and in Bacteroides/Prevotella groups was related to high BMI. For the Firmicutes phylum, one high-quality study highlighted that it was positively correlated with weight gain. With regard to Firmicutes species, Clostridium leptum , Eubacterium hallii , and Lactobacillus spp. indicated adipose tissue storage, while Clostridium difficile and the Staphylococcus genus were correlated with low BMI. Despite the fact that only one study did not perform real-time polymerase chain reaction to quantify the microorganisms, its results corroborated those of the studies that did. Conclusions: Changes in Firmicutes and Bacteroidetes phyla/species levels might in fact be significant indicators/factors for childhood obesity. However, given the small number of articles appraising these entire phyla and the heterogeneity among the species assessed, further well-designed studies are required to improve the knowledge.

For reliable results, Reverse Transcription Quantitative real-time Polymerase Chain Reaction (RT-qPCR) analyses depend on stably expressed reference genes for data normalization purposes.Klebsiella pneumoniaeis an opportunistic Gram-negative bacterium that has become a serious threat worldwide. Unfortunately, there is no consensus for an ideal reference gene for RT-qPCR data normalization onK. pneumoniae. In this study, the expression profile of eleven candidate reference genes was assessed inK. pneumoniaecells submitted to various experimental conditions, and the expression stability of these candidate genes was evaluated using statistical algorithms BestKeeper, NormFinder, geNorm, Delta C_Tand RefFinder. The statistical analyses rankedrecA,rho,proCandrpoDas the most suitable reference genes for accurate RT-qPCR data normalization inK. pneumoniae. The reliability of the proposed reference genes was validated by normalizing the relative expression of iron-regulated genes inK. pneumoniaecells submitted to iron-replete and iron-limited conditions. This work emphasizes that the stable expression of any potential reference candidate gene must be validated in each physiological condition or experimental treatment under study.

Klebsiella pneumoniae is a Gram-negative pathogen that has become a worldwide concern due to the emergence of multidrug-resistant isolates responsible for various invasive infectious diseases. Biofilm formation constitutes a major virulence factor for K. pneumoniae and relies on the expression of fimbrial adhesins and aggregation of bacterial cells on biotic or abiotic surfaces in a coordinated manner. During biofilm aggregation, bacterial cells communicate with each other through inter- or intra-species interactions mediated by signallng molecules, called autoinducers, in a mechanism known as quorum sensing (QS). In most Gram-negative bacteria, intra-species communication typically involves the LuxI/LuxR system: LuxI synthase produces N-acyl homoserine lactones (AHLs) as autoinducers and the LuxR transcription factor is their cognate receptor. However, K. pneumoniae does not produce AHL but encodes SdiA, an orphan LuxR-type receptor that responds to exogenous AHL molecules produced by other bacterial species. While SdiA regulates several cellular processes and the expression of virulence factors in many pathogens, the role of this regulator in K. pneumoniae remains unknown. In this study, we describe the characterization of sdiA mutant strain of K. pneumoniae. The sdiA mutant strain has increased biofilm formation, which correlates with the increased expression of type 1 fimbriae, thus revealing a repressive role of SdiA in fimbriae expression and bacterial cell adherence and aggregation. On the other hand, SdiA acts as a transcriptional activator of cell division machinery assembly in the septum, since cells lacking SdiA regulator exhibited a filamentary shape rather than the typical rod shape. We also show that K. pneumoniae cells lacking SdiA regulator present constant production of QS autoinducers at maximum levels, suggesting a putative role for SdiA in the regulation of AI-2 production. Taken together, our results demonstrate that SdiA regulates cell division and the expression of virulence factors such as fimbriae expression, biofilm formation, and production of QS autoinducers in K. pneumoniae.

The complement system plays a central role in immune defense against Streptococcus pneumoniae. In order to evade complement attack, pneumococci have evolved a number of mechanisms that limit complement mediated opsonization and subsequent phagocytosis. This review focuses on the strategies employed by pneumococci to circumvent complement mediated immunity, both in vitro and in vivo. At last, since many of the proteins involved in interactions with complement components are vaccine candidates in different stages of validation, we explore the use of these antigens alone or in combination, as potential vaccine approaches that aim at elimination or drastic reduction in the ability of this bacterium to evade complement.

Although originally known as an opportunistic pathogen, Klebsiella pneumoniae has been considered a worldwide health threat nowadays due to the emergence of hypervirulent and antibiotic-resistant strains capable of causing severe infections not only on immunocompromised patients but also on healthy individuals. Fimbriae is an essential virulence factor for K. pneumoniae, especially in urinary tract infections (UTIs), because it allows the pathogen to adhere and invade urothelial cells and to form biofilms on biotic and abiotic surfaces. The importance of fimbriae for K. pneumoniae pathogenicity is highlighted by the large number of fimbrial gene clusters on the bacterium genome, which requires a coordinated and finely adjusted system to control the synthesis of these structures. In this work, we describe KpfR as a new transcriptional repressor of fimbrial expression in K. pneumoniae and discuss its role in the bacterium pathogenicity. K. pneumoniae with disrupted kpfR gene exhibited a hyperfimbriated phenotype with enhanced biofilm formation and greater adhesion to and replication within epithelial host cells. Nonetheless, the mutant strain was attenuated for colonization of the bladder in a murine model of urinary tract infection. These results indicate that KpfR is an important transcriptional repressor that, by negatively controlling the expression of fimbriae, prevents K. pneumoniae from having a hyperfimbriated phenotype and from being recognized and eliminated by the host immune system.