Previous reports provided recommendations for familial renal glucosuria diagnosis without complex view on differential diagnosis of glucosuria. The aim of this review was to provide an overview of the causes of glucosuria and to create an evidence-based diagnostic approach for children with glucosuria. We searched the current literature with a focus to identify the possible etiology of glucosuria, gaining insight into the pathophysiology of glucosuria. Urinary glucose is completely reabsorbed in the proximal tubule of kidneys. It only appears in the urine if the plasma glucose concentration exceeds the renal threshold for glucose or in the case of insufficient renal glucose reabsorption. The proteins that provide glucose reabsorption are SGLT2 and SGLT1 - sodium-dependent co-transporters that transport glucose from the lumen into epithelial cells - and GLUT2 - a passive transporter providing facilitative glucose transport from epithelial cells to plasma. Renal glucose reabsorption is affected in case of acquired or inherited complex dysfunction of proximal tubule called Fanconi Syndrome or due to pathogenic variants of genes encoding glucose transporters. Prior to diagnosing any of these, diabetes mellitus must be excluded together with other conditions leading to hyperglycemia. In conclusion, glucosuria is always an abnormal finding. The review provides a simple evidence-based diagnostic approach to navigate the differential diagnosis of glucosuria.
- MeSH
- Diagnosis, Differential MeSH
- Child MeSH
- Fanconi Syndrome diagnosis complications MeSH
- Glucose * metabolism MeSH
- Glycosuria * diagnosis etiology MeSH
- Humans MeSH
- Glucose Transporter Type 2 metabolism MeSH
- Kidney Tubules, Proximal metabolism MeSH
- Glycosuria, Renal * diagnosis etiology physiopathology MeSH
- Sodium-Glucose Transporter 1 metabolism MeSH
- Sodium-Glucose Transporter 2 metabolism MeSH
- Check Tag
- Child MeSH
- Humans MeSH
- Publication type
- Journal Article MeSH
- Review MeSH
Escherichia coli (E. coli) is a rod-shaped gram-negative bacterium that includes the diarrheagenic strains, an identical group of intestinal pathogens.E. coli diarrhea is transmitted through the feco-oral route, through contaminated food and water. Enteropathogenic E. coli (EPEC) is one of the leading causes of diarrhea in the pediatric age group in developing and developed countries. Depending on the absence or presence of E. coli adherence factor plasmids, they are classified as typical or atypical isolates. The distinguishing feature of EPEC's pathology is the attaching and effacing lesions, which facilitate localized damage by tightly adhering to intestinal epithelial cells, disarranging their surfaces, and effacing microvilli. Typical EPEC possess the locus of enterocyte effacement (LEE), a pathogenicity island, encoding adherence factors, including the Type III Secretion System (T3SS), a needle-like structure injecting effector proteins into host cells. EPEC also have other effector genes like cif or nleC encoded by non-LEE pathogenicity islands, which enable destruction of tight junctions in the host cell. Another key virulence factor is bundle-forming pili (BFP), which aids in the first attachment to enterocytes. Methods like quantitative PCR exist to diagnose EPEC accurately. As of today, no licensed vaccine exists to prevent EPEC infections. Virulence factors for attachment, such as bfpA and intimin, and immunogenic carriers can be potential candidates for vaccine development. Moreover, studies are required to better understand the interaction of EPECwith the intestinal microbiome and immune evasion strategies. This article is aimed at providing a comprehensive review of the epidemiology, transmission, virulence factors, challenges in studying EPEC virulence factors, pathogenesis, host-pathogen interaction, mechanism of intestinal injury, diagnosis, treatment, antibiotic resistance, and vaccination strategy for EPEC, and future research implications. We conducted a comprehensive literature search using credible sources such as PubMed, Google Scholar, and Scopus. We refined our keywords, applied database filters, and assessed citations in the included studies. No meta-analysis, statistical aggregation, or formal evaluation of risk bias was carried out as this review consolidates the literature narratively. High-quality English articles published in reputable peer-reviewed journals from 2010 to 2025 were analyzed, and their findings have been summarized in this comprehensive review.
- Publication type
- Journal Article MeSH
- Review MeSH
PURPOSE OF REVIEW: The immunological processes that lead to multiple sclerosis (MS) and occur during the progressive phase of the disease are manifold and still not well understood. This review summarizes new insights on this topic that were gained through recent studies with diverse scientific approaches. RECENT FINDINGS: While genetic risk clearly contributes to MS, external factors play a key role in its pathogenesis as well. Epstein-Barr virus infection correlates significantly with MS risk and seems to be a major causal factor. Even though our knowledge on the human gut microbiome and its connection to the central nervous system is far from being complete, several studies have proven that the gut-brain axis influences neuroinflammation and disease progression in MS. It has become much clearer that MS is not solely a T cell-mediated disease but is also strongly driven by B cells and pathogenic antibodies. Beyond the peripheral immune cells, glial cells and their interactions with neurons are important players contributing to disease activity and progression in MS. SUMMARY: Taken together, recent publications on immunological processes in the context of MS implicate a multitude of noncanonical mechanisms that need to be further explored regarding their interplay and contribution to the degenerative course of the disease.
Narušení mikrobiálního ekosystému člověka představuje významný patogenetický faktor řady onemocnění. Již několik desetiletí je známa úloha alterace střevní mikrobioty v patogenezi rekurentní klostridiové kolitidy. Závažné narušení ve složení nebo funkci mikrobioty (mluvíme o tzv. dysbióze) je dnes nicméně popisováno i v patogenezi dalších chorobných stavů. V tomto smyslu jsou nejčastěji uváděny idiopatické střevní záněty, syndrom dráždivého tračníku, diabetes mellitus 2. typu, roztroušená skleróza, Parkinsonova nemoc, dále také např. jaterní encefalopatie u pacientů s cirhózou jater. Terapeuticky zasáhnout na úrovni poškozené střevní mikrobioty se snažíme různými způsoby. Velmi nadějně se jeví metoda mající za cíl dosáhnout obnovy přirozené mikrobiální homeostázy v tlustém střevě pomocí stolice od zdravého dárce, která je přenesena do zažívacího traktu nemocného. Pro tuto metodu se u nás vžil název "fekální bakterioterapie". V zahraniční literatuře se nejčastěji setkáváme s označením "Fecal Microbiota Transplantation" či se zkratkou FMT.
Disruption of the human microbial ecosystem represents a significant pathogenic factor of many diseases. The role of altered intestinal microbiota in the pathogenesis of recurrent Clostridium difficile colitis has been known for decades. Still, severe disruptions in the composition or function of the microbiota (we are speaking about dysbiosis) is nowadays also described in the pathogenesis of other pathological conditions. In this sense, the most commonly listed are idiopathic inflammatory bowel diseases, irritable bowel syndrome, type 2 diabetes mellitus, multiple sclerosis, Parkinson's disease, furthermore, for example, hepatic encephalopathy in patients with liver cirrhosis. We try to therapeutically intervene on the level of damaged intestinal microbiota in various ways. One very promising method seeks to restore natural microbial homeostasis in the colon using stool from a healthy donor, which is transferred into the digestive tract of the patient. For us, this method became commonly known as "fecal bacteriotherapy". The international literature typically uses the term "Fecal Microbiota Transplantation" or by the abbreviation FMT.
- MeSH
- Drug Resistance, Bacterial MeSH
- Dysbiosis * therapy MeSH
- Fecal Microbiota Transplantation * statistics & numerical data trends MeSH
- Inflammatory Bowel Diseases therapy MeSH
- Humans MeSH
- Central Nervous System Diseases therapy MeSH
- Enterocolitis, Pseudomembranous prevention & control therapy MeSH
- Gastrointestinal Microbiome physiology MeSH
- Check Tag
- Humans MeSH
- Publication type
- Research Support, Non-U.S. Gov't MeSH
- Review MeSH
Mikrobiom střeva hraje klíčovou roli v dlouhodobém fyzickém i psychickém zdraví člověka. Jeho vhodné složení během počáteční kolonizace gastrointestinálního traktu novorozenců s dostatečným zastoupením taxonů s komenzálním či probiotickým potenciálem je zásadní pro obranu před infekcemi a správný vývoj imunitního systému. Enterobakterie tvoří nedílnou součást střevní mikrobioty a mají klíčovou úlohu v počáteční kolonizaci střeva novorozence. Zároveň se jedná o potenciální patogeny, které mohou způsobovat závažné infekce. V článku jsou popsány funkce enterobakterií v mikrobiotě kojenců, rizika spojená s jejich nadměrnou přítomností a strategie prevence infekcí. Dále jsou diskutovány faktory ovlivňující formování mikrobioty u dětí, včetně způsobu porodu a vlivu antibiotik. Výzkumy ukazují, že podpora přirozeného porodu, kojení a použití probiotik mohou pozitivně ovlivnit střevní mikrobiotu a eliminovat potenciální rizika spojená s enterobakteriemi. Článek poskytuje přehled současných poznatků o enterobakteriích v mikrobiotě kojenců a zdůrazňuje potřebu dalšího výzkumu a sdílení nových poznatků v klinické praxi, aby byl zajištěn zdravý vývoj dětí.
The gut microbiome plays a key role in a person's long-term physical and psychological health. Its appropriate composition during the initial colonization of the gastrointestinal tract of newborns with the sufficient representation of the taxa with commensal or probiotic potential is essential for defence against infections and proper development of the immune system. Enterobacteria form an integral part of the intestinal microbiota and play a vital role in the initial colonization of the newborn gut. At the same time, these are potential pathogens that can cause serious infections. This article describes the functions of enterobacteria in the microbiota of infants, the risks associated with their excessive presence, and strategies for preventing infections. Furthermore, factors affecting microbiota formation in children are discussed, including the delivery method and the effect of antibiotics. Research shows that promoting natural childbirth, breastfeeding, and probiotic use can positively influence the gut microbiota and eliminate potential risks associated with enterobacteria. The article provides an overview of current knowledge about enterobacteria in the microbiota of infants and highlights the need for further research and the sharing of new knowledge in clinical practice to ensure the healthy development of children.
- MeSH
- Enterobacteriaceae * immunology MeSH
- Enterovirus Infections immunology microbiology MeSH
- Hygiene MeSH
- Breast Feeding MeSH
- Humans MeSH
- Microbiota * immunology MeSH
- Infant, Newborn, Diseases immunology metabolism MeSH
- Infant, Newborn MeSH
- Natural Childbirth MeSH
- Probiotics MeSH
- Check Tag
- Humans MeSH
- Infant, Newborn MeSH
Super- and low-shedding phenomena have been observed in genetically homogeneous hosts infected by a single bacterial strain. To decipher the mechanisms underlying these phenotypes, we conducted an experiment with chicks infected with Salmonella Enteritidis in a non-sterile isolator, which prevents bacterial transmission between animals while allowing the development of the gut microbiota. We investigated the impact of four commensal bacteria called Mix4, inoculated at hatching, on chicken systemic immune response and intestinal microbiota composition and functions, before and after Salmonella infection. Our results revealed that these phenotypes were not linked to changes in cell invasion capacity of bacteria during infection. Mix4 inoculation had both short- and long-term effects on immune response and microbiota and promoted the low-shedder phenotype. Kinetic analysis revealed that Mix4 activated immune response from day 4, which modified the microbiota on day 6. This change promotes a more fermentative microbiota, using the aromatic compounds degradation pathway, which inhibited Salmonella colonization by day 11 and beyond. In contrast, control animals exhibited a delayed TNF-driven pro-inflammatory response and developed a microbiota using anaerobic respiration, which facilitates Salmonella colonization and growth. This strategy offers promising opportunities to strengthen the barrier effect against Salmonella and possibly other pathogens.
- MeSH
- Bacteria * classification genetics isolation & purification MeSH
- Chickens * microbiology immunology MeSH
- Poultry Diseases * microbiology immunology prevention & control MeSH
- Salmonella enteritidis * immunology growth & development MeSH
- Salmonella Infections, Animal * microbiology immunology prevention & control MeSH
- Gastrointestinal Microbiome * MeSH
- Symbiosis MeSH
- Animals MeSH
- Check Tag
- Animals MeSH
- Publication type
- Journal Article MeSH
Kyselina močová (UA) se převážně tvoří v játrech, střevech a cévním endotelu jako konečný produkt metabolismu purinů získaných exogenně z potravy a endogenně z poškozených nebo mrtvých buněk. Ledviny hrají hlavní roli ve vylučování UA, eliminují asi 70 % denní produkce. Zbytek (přibližně 30 %) je vylučován střevem. Pokud tvorba UA překračuje její vylučování, vzniká hyperurikemie. Hyperurikemie je silně spojena s rozvojem a závažností metabolického syndromu. Nadměrná exprese urátového transportéru 1 (URAT1) a glukózového transportéru 9 (GLUT9) a narušení glykolýzy kvůli inzulinové rezistenci mohou souviset s rozvojem hyperurikemie u metabolického syndromu. Dříve se hyperurikemie po- važovala pouze za hlavní příčinu dny a dnavé artritidy. Také se předpokládalo, že hyperurikemie u pacientů s renálními onemocněními je důsledkem nedostatečného vylučování UA kvůli ledvinnému selhání, a proto nebyla cílem intenzivní léčby. Základní vědecké poznatky nyní naznačují, že hyperurikemie hraje patogenní roli při vzniku chronického onemocnění ledvin a kardiovaskulárních onemocnění, protože způsobuje endoteliální dysfunkci, proliferaci cévních hladkých svalových buněk a aktivaci renin-angiotenzinového systému. Další nashromážděné údaje naznačují, že léčba snižující hladinu UA zpomaluje progresi těchto onemocnění. Snížení hladiny UA je účinnou metodou pro zlepšení stavu, ale ne všechny látky snižující hladinu UA fungují stejně. V klinické praxi je třeba tyto látky používat s opatrností.
Uric acid (UA) is predominantly formed in the liver, intestine and vascular endothelium as an end product of the metabolism of purines derived from food and endogenously from damaged or dead cells. The kidneys play a major role in the excretion of UA, eliminating about 70 % of the daily production. The remainder (approximately 30 %) is excreted by the intestine. If the production of UA exceeds the capacity of its excretion, hyperuricaemia results. Overexpression of urate transporter 1 (URAT1), glucose transporter 9 (GLUT9) and impaired glycolysis due to insulin resistance may be related to the development of hyperuricaemia in metabolic syndrome. Hyperuricemia is associated with the development and severity of metabolic syndrome. Previously, hyperuricaemia was thought to be the main cause of gout and gouty arthritis only. It was also assumed that hyperuricemia in patients with renal disease was a consequence of inadequate UA excretion due to renal failure and therefore was not a target for intensive treatment. Basic scientific evidence now suggests that hyperuricemia plays a pathogenic role in the development of chronic kidney disease and cardiovascular disease by causing endothelial dysfunction, vascular smooth muscle cell proliferation, and activation of the renin- angiotensin system. Lowering UA levels is an effective method for improving the condition, but not all UA lowering agents work the same. In clinical practice, these agents should be used with caution. Further accumulating data suggest that UA-lowering therapy slows the progression of these diseases.
- MeSH
- Allopurinol administration & dosage therapeutic use MeSH
- Gout Suppressants antagonists & inhibitors pharmacology therapeutic use MeSH
- Febuxostat administration & dosage therapeutic use MeSH
- Hyperuricemia drug therapy complications MeSH
- Cardiovascular Diseases prevention & control MeSH
- Uric Acid blood MeSH
- Humans MeSH
- Metabolic Syndrome * diagnosis etiology therapy MeSH
- Check Tag
- Humans MeSH
BACKGROUND: Schistosoma mansoni was introduced from Africa to the Americas during the transatlantic slave trade and remains a major public health problem in parts of South America and the Caribbean. This study presents a comprehensive comparative analysis of three S. mansoni strains with different geographical origins-from Liberia, Belo Horizonte and Puerto Rico. We demonstrated significant variation in virulence and host-parasite interactions. METHODS: We investigated the phenotypic characteristics of the parasite and its eggs, as well as the immunopathologic effects on laboratory mouse organ systems. RESULTS: Our results show significant differences in worm morphology, worm burden, egg size, and pathologic organ changes between these strains. The Puerto Rican strain showed the highest virulence, as evidenced by marked liver and spleen changes and advanced liver fibrosis indicated by increased collagen content. In contrast, the strains from Liberia and Belo Horizonte had a less pathogenic profile with less liver fibrosis. We found further variations in granuloma formation, cytokine expression and T-cell dynamics, indicating different immune responses. CONCLUSION: Our study emphasizes the importance of considering intra-specific variations of S. mansoni for the development of targeted therapies and public health strategies. The different virulence patterns, host immune responses and organ pathologies observed in these strains provide important insights for future research and could inform region-specific interventions for schistosomiasis control.
- MeSH
- Cytokines metabolism MeSH
- Host-Parasite Interactions MeSH
- Liver * parasitology pathology MeSH
- Mice MeSH
- Schistosoma mansoni * pathogenicity genetics immunology MeSH
- Schistosomiasis mansoni * parasitology immunology pathology MeSH
- Spleen parasitology pathology immunology MeSH
- Virulence MeSH
- Animals MeSH
- Check Tag
- Male MeSH
- Mice MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Geographicals
- Liberia MeSH
- Puerto Rico MeSH
PURPOSE: The significance of dental status and oral hygiene on a range of medical conditions is well-recognised. However, the correlation between periodontitis, oral bacterial dysbiosis and visceral surgical outcomes is less well established. To this end, we study sought to determine the influence of dental health and oral hygiene on the rates of postoperative complications following major visceral and transplant surgery in an exploratory, single-center, retrospective, non-interventional study. METHODS: Our retrospective non-interventional study was conducted at the Department of General, Visceral, and Transplant Surgery, University Hospital Heidelberg, Germany. Patients operated on between January 2018 and December 2019 were retrospectively enrolled in the study based on inclusion (minimum age of 18 years, surgery at our Department, intensive care / IMC treatment after major surgery, availability of patient-specific preoperative dental status assessment, documentation of postoperative complications) and exclusion criteria (minor patients or legally incapacitated patients, lack of intensive care or intermediate care (IMC) monitoring, incomplete documentation of preoperative dental status, intestinal surgery with potential intraoperative contamination of the site by intestinal microbes, pre-existing preoperative infection, absence of data regarding the primary endpoints of the study). The primary study endpoint was the incidence of postoperative complications. Secondary study endpoints were: 30-day mortality, length of hospital stay, duration of intensive care stay, Incidence of infectious complications, the microbial spectrum of infectious complication. A bacteriology examination was added whenever possible (if and only if the examination was safe for the patient)for infectious complications. RESULTS: The final patient cohort consisted of 417 patients. While dental status did not show an influence (p = 0.73) on postoperative complications, BMI (p = 0.035), age (p = 0.049) and quick (p = 0.033) were shown to be significant prognostic factors. There was significant association between oral health and the rate of infectious complications for all surgical procedures (p = 0.034), excluding transplant surgery. However, this did not result in increased 30-day mortality rates, prolonged intensive care unit treatment or an increase in the length of hospital stay (LOS) for the cohort as a whole. In contrast there was a significant correlation between the presence of oral pathogens and postoperative complications for a group as a whole (p < 0.001) and the visceral surgery subgroup (p < 0.001). Whilst this was not the case in the cohort who underwent transplant surgery, there was a correlation between oral health and LOS in this subgroup (p = 0.040). Bacterial swabs supports the link between poor oral health and infectious morbidity. CONCLUSIONS: Dental status was a significant predictor of postoperative infectious complications in this visceral surgery cohort. This study highlights the importance preoperative dental assessment and treatment prior to major surgery, particularly in the case of elective surgical procedures. Further research is required to determine the effect of oral health on surgical outcomes in order to inform future practice. TRIAL REGISTRATION: Trial registered under the ethics-number S-082/2022 (Ethic Committee of the University Heidelberg).
- MeSH
- Length of Stay statistics & numerical data MeSH
- Adult MeSH
- Middle Aged MeSH
- Humans MeSH
- Oral Hygiene MeSH
- Oral Health MeSH
- Postoperative Complications * epidemiology etiology MeSH
- Retrospective Studies MeSH
- Aged MeSH
- Organ Transplantation adverse effects MeSH
- Check Tag
- Adult MeSH
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
- Aged MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Observational Study MeSH
- Geographicals
- Germany MeSH
Aging is generally regarded as an irreversible process, and its intricate relationship with the immune system has garnered significant attention due to its profound implications for the health and well-being of the aging population. As people age, a multitude of alterations occur within the immune system, affecting both innate and adaptive immunity. In the realm of innate immunity, aging brings about changes in the number and function of various immune cells, including neutrophils, monocytes, and macrophages. Additionally, certain immune pathways, like the cGAS-STING, become activated. These alterations can potentially result in telomere damage, the disruption of cytokine signaling, and impaired recognition of pathogens. The adaptive immune system, too, undergoes a myriad of changes as age advances. These include shifts in the number, frequency, subtype, and function of T cells and B cells. Furthermore, the human gut microbiota undergoes dynamic changes as a part of the aging process. Notably, the interplay between immune changes and gut microbiota highlights the gut's role in modulating immune responses and maintaining immune homeostasis. The gut microbiota of centenarians exhibits characteristics akin to those found in young individuals, setting it apart from the microbiota observed in typical elderly individuals. This review delves into the current understanding of how aging impacts the immune system and suggests potential strategies for reversing aging through interventions in immune factors.
- MeSH
- Adaptive Immunity * MeSH
- Humans MeSH
- Immunity, Innate * MeSH
- Aging * immunology MeSH
- Gastrointestinal Microbiome * immunology MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Review MeSH
