Helicobacter pylori (H. pylori) remains the most-researched etiological factor for gastric inflammation and malignancies. Its evolution towards gastric complications is dependent upon host immune response. Toll-like receptors (TLRs) recognize surface and molecular patterns of the bacterium, especially the lipopolysaccharide (LPS), and act upon pathways, which will finally lead to activation of the nuclear factor-kappa B (NF-kB), a transcription factor that stimulates release of inflammatory cytokines. MicroRNAs (MiRNAs) finely modulate TLR signaling, but their expression is also modulated by activation of NF-kB-dependent pathways. This review aims to focus upon several of the most researched miRNAs on this subject, with known implications in host immune responses caused by H. pylori, including let-7 family, miRNA-155, miRNA-146, miRNA-125, miRNA-21, and miRNA-221. TLR–LPS interactions and their afferent pathways are regulated by these miRNAs, which can be considered as a bridge, which connects gastric inflammation to pre-neoplastic and malignant lesions. Therefore, they could serve as potential non-invasive biomarkers, capable of discriminating H. pylori infection, as well as its associated complications. Given that data on this matter is limited in children, as well as for as significant number of miRNAs, future research has yet to clarify the exact involvement of these entities in the progression of H. pylori-associated gastric conditions.
The developmental origins of adult disease theory support the concept that undernourished fetuses are at risk of developing metabolic syndrome due to the energy-saving ‘Thrifty Phenotype’. This metabolic plasticity represents an evolutionary adaptation that allows individuals to resist the intense pressure caused by cyclically recurring periods of nutritional deprivation. A comprehensive review was conducted following an extensive literature search in the PubMed/Medline and EMBASE databases concerning reports on fetal/intrauterine growth restriction and its metabolic-related long-term outcomes. We only included articles written in English that were published before 1 July 2024. There are several underlying mechanisms and metabolic and endocrine adjustments shaped by the perinatal environment, and they all contribute to progression towards adult disease. From in utero malnutrition or other insults during the fetal period to fetal programing and postnatal catch-up growth, it is difficult to identify the exact moment when this adaptative phenomenon meant to assure fetal survival and to set children on their own physiological growth curves lose its beneficial effect, establishing the trajectory to obesity, insulin resistance, and other hallmarks of metabolic syndrome. With clinical correspondence to an altered body mass, composition, and eating behaviors, it is evident that the metabolic complications linked to FGR are intricate and arise from disturbances in several pathways and organs, but the underlying processes responsible for the long-term consequences are just starting to be understood. The lack of continuity in perinatal-to-pediatric FGR research sets the challenge of exploring new directions in future scientific opportunities. These will hopefully represent a cornerstone in the management of FGR-related metabolic disorders in children, preventing these disorders from evolving into adult disease.
Helicobacter pylori (H. pylori) is the most common bacterial infection worldwide, is usually acquired during childhood and is related to gastric carcinogenesis during adulthood. Therefore, its early proper diagnosis and subsequent successful eradication represent the cornerstones of gastric cancer prevention. The aim of this narrative review was to assess traditional and modern diagnostic methods in terms of H. pylori diagnosis. Several invasive and non-invasive methods were described, each with its pros and cons. The invasive diagnostic methods comprise endoscopy with biopsy, rapid urease tests, histopathological exams, cultures and biopsy-based molecular tests. Among these, probably the most available, accurate and cost-effective test remains histology, albeit molecular tests definitely remain the most accurate despite their high costs. The non-invasive tests consist of urea breath tests, serology, stool antigens and non-invasive molecular tests. Urea breath tests and stool antigens are the most useful in clinical practice both for the diagnosis of H. pylori infection and for monitoring the eradication of this infection after therapy. The challenges related to accurate diagnosis lead to a choice that must be based on H. pylori virulence, environmental factors and host peculiarities.
Considered to be of greater complexity than the human genome itself, the microbiome, the structure of the body made up of trillions of bacteria, viruses, and fungi, has proven to play a crucial role in the context of the development of pathological processes in the body, starting from various infections, autoimmune diseases, atopies, and culminating in its involvement in the development of some forms of cancer, a diagnosis that is considered the most disabling for the patient from a psychological point of view. Therefore, being a cornerstone in the understanding and optimal treatment of a multitude of ailments, the body’s microbiome has become an intensively studied subject in the scientific literature of the last decade. This review aims to bring the microbiome–asthma correlation up to date by classifying asthmatic patterns, emphasizing the development patterns of the microbiome starting from the perinatal period and the impact of pulmonary dysbiosis on asthmatic symptoms in children. Likewise, the effects of intestinal dysbiosis reflected at the level of homeostasis of the internal environment through the intestine–lung/vital organs axis, the circumstances in which it occurs, but also the main methods of studying bacterial variability used for diagnostic purposes and in research should not be omitted. In conclusion, we draw current and future therapeutic lines worthy of consideration both in obtaining and maintaining remission, as well as in delaying the development of primary acute episodes and preventing future relapses.
Helicobacter pylori (H. pylori), the most common infection of childhood, results in life-threatening complications during adulthood if left untreated. Most of these complications are related to H. pylori-induced chronic inflammation. The dysbiosis caused by H. pylori is not limited to the gastric microenvironment, but it affects the entire gastrointestinal tract. Eradication of H. pylori has recently become a real challenge for clinicians due to both the persistent increase in antibiotic resistance worldwide and the wide spectrum of side effects associated with the eradication regimens resulting; therefore, there is an urgent need for more effective and less noxious treatment options. Thus, probiotics might be a promising choice in both adults and children with H. pylori infection since their role in improving the eradication rate of this infection has been proved in multiple studies. The positive effects of probiotics might be explained by their abilities to produce antimicrobial compounds and antioxidants, alter local gastric pH, and subsequently decrease H. pylori colonization and adherence to gastric epithelial cells. Nevertheless, if used alone probiotics do not considerably increase the eradication rate.
Background: Pediatric obesity represents a multifactorial condition in which gut microbiota dysbiosis, low-grade systemic inflammation, and metabolic dysfunction are intricately connected. Objectives: This systematic review sought to evaluate and integrate current findings regarding the interactions between gut microbial composition, dietary influences, inflammatory status, and metabolic outcomes in obese pediatric populations. Methods: A comprehensive search of PubMed, Scopus, and Web of Science databases was conducted for studies published from January 2010 onward. Eligible studies comprised randomized controlled trials, and cohort, cross-sectional, and longitudinal designs involving individuals aged ≤18 years. Study quality was appraised using the NIH Study Quality Assessment Tool. Results: Sixteen studies fulfilled the inclusion criteria. Dysbiosis was consistently observed among obese children, characterized by alterations in microbial diversity and abundance associated with increased inflammation and adverse metabolic profiles. Dietary interventions, notably symbiotic supplementation and adherence to Mediterranean diet patterns, were associated with favorable modulation of gut microbiota and inflammatory parameters. The majority of studies demonstrated high methodological quality, although minor observational limitations were noted. Conclusions: Gut microbiota dysregulation plays a central role in the development of metabolic and inflammatory complications associated with pediatric obesity. Although dietary and microbiota-modifying strategies show therapeutic promise, their effectiveness must be substantiated through robust, long-term studies.