Intestinal Bacterial Colonization Research Articles

Protein-based vaccine candidate MecVax broadly protects against enterotoxigenic Escherichia coli intestinal colonization in a rabbit model.

There are no vaccines licensed against enterotoxigenic Escherichia coli (ETEC), a leading cause of children's diarrhea and the most common cause of travelers' diarrhea. Multivalent vaccine candidate MecVax unprecedentedly targets two ETEC enterotoxins (heat-stable toxin, STa; heat-labile toxin, LT) and the seven most prevalent ETEC adhesins (colonization factor antigen, CFA/I, coli surface antigens, CS1-CS6) and has been demonstrated preclinically to protect against STa- and LT-mediated ETEC clinical diarrhea and prevent intestinal colonization from ETEC strain H10407 (CFA/I, STa, LT). However, it is unattested whether MecVax broadly protects against intestinal colonization from ETEC strains producing the other six adhesins (CS1-CS6) also targeted by this product. In this study, we immunized rabbits with MecVax and challenged them with heterogeneous ETEC strains that express CS1-CS6 adhesins to evaluate MecVax's efficacy against bacterial intestinal colonization, thus providing broad vaccine protection against ETEC infection. Data revealed that rabbits intramuscularly immunized with MecVax developed robust responses to both ETEC enterotoxins (STa, LT) and seven adhesins (CFA/I, CS1-CS6), and when challenged with ETEC isolates expressing CS1/CS3, CS2/CS3, CS4/CS6, CS5/CS6, or CS6 adhesin, the immunized rabbits prevented over two logs (>99%) of bacteria from colonization in small intestines. Additionally, compared to a CFA-toxoid fusion protein, which is another potential ETEC vaccine antigen to target two ETEC enterotoxins and the seven adhesins, MecVax exhibited better protection against ETEC intestinal colonization. These results, in conjunction with the protection data from early studies, evidenced that MecVax is broadly protective, validating MecVax's candidacy as an effective vaccine against ETEC-associated diarrhea and accelerating ETEC vaccine development.

Transcriptomic analysis identifies lactoferrin-induced quiescent circuits in neonatal macrophages.

Upon birth, a hitherto naïve immune system is confronted with a plethora of microbial antigens due to intestinal bacterial colonization. To prevent excessive inflammation and disruption of the epithelial barrier, physiological mechanisms must promote immune-anergy within the neonatal gut. As high concentrations of human lactoferrin (hLF), a transferrin glycoprotein shown to modulate macrophage function, are frequently encountered in colostrum, its direct interaction with intestinal macrophages may satisfy this physiological need. Thus, the primary objective of this study was to investigate transcriptional changes induced by human lactoferrin in neonatal monocyte-derived macrophages. Cord blood-derived monocytes were differentiated with M-CSF in presence or absence of 500 µg/mL hLF for 7 days and afterwards stimulated with 1 ng/mL LPS or left untreated. RNA was then isolated and subjected to microarray analysis. Differentiation of cord blood-derived monocytes in presence of hLF induced a distinct transcriptional program defined by cell cycle arrest in the G2/M phase, induction of IL-4/IL-13-like signaling, altered extracellular matrix interaction, and enhanced propensity for cell-cell interaction. Moreover, near-complete abrogation of transcriptional changes induced by TLR4 engagement with LPS was observed in hLF-treated samples. The global transition towards an M2-like homeostatic phenotype and the acquisition of quiescence elegantly demonstrate the ontogenetical relevance of hLF in attenuating pro-inflammatory signaling within the developing neonatal intestine. The marked anergy towards proinflammatory stimuli such as LPS further underlines the glycoprotein's potential therapeutic relevance.

The Novel Role of Phage Particles in Chronic Liver Diseases.

The gut microbiome is made up of bacteria, fungi, viruses and archaea, all of which are closely related with human health. As the main component of enterovirus, the role of bacteriophages (phages) in chronic liver disease has been gradually recognized. Chronic liver diseases, including alcohol-related liver disease and nonalcoholic fatty liver disease, exhibit alterations of the enteric phages. Phages shape intestinal bacterial colonization and regulate bacterial metabolism. Phages adjoining to intestinal epithelial cells prevent bacteria from invading the intestinal barrier, and mediate intestinal inflammatory response. Phages are also observed increasing intestinal permeability and migrating to peripheral blood and organs, likely contributing to inflammatory injury in chronic liver diseases. By preying on harmful bacteria, phages can improve the gut microbiome of patients with chronic liver disease and thus act as an effective treatment method.

In vivo immunomodulatory alleviating effects of animal milk oligosaccharides on murine NEC: A study

Human milk oligosaccharides may mediate prebiotic and anti-inflammatory effects on newborns. It is essential for preterm infants susceptible to intestinal dysfunction and necrotizing enterocolitis (NEC). However, the infant breastfeeding rate remains low, and there is still a great demand for suitable substitutes for HMOs prebiotic effect. In this paper, we study the new molecular insights of the protective mechanism of four animal milk oligosaccharides against developing experimental NEC from the perspective of intestinal flora balance and immunomodulatory mechanism. Studies have found that milk oligosaccharides (MOs), especially yak milk oligosaccharides, can directly affect the intestinal barrier by inhibiting the expression of inflammatory factors, restoring the abundance of Bifidobacteria, Bacteroidetes and Lactobacilli, improving the intestinal function, bacterial colonization and NEC resistance of premature infants after birth. These results emphasize that MOs, a substitute for breastfeeding, have specific preventive and alleviating effects on neonatal NEC.

A polyvalent multiepitope protein cross-protects against Vibrio cholerae infection in rabbit colonization and passive protection models

Using epitope- and structure-based multiepitope fusion antigen vaccinology platform, we constructed a polyvalent protein immunogen that presents antigenic domains (epitopes) of Vibrio cholerae toxin-coregulated pilus A, cholera toxin (CT), sialidase, hemolysin A, flagellins (B, C, and D), and peptides mimicking lipopolysaccharide O-antigen on a flagellin B backbone. Mice and rabbits immunized intramuscularly with this polyvalent protein immunogen developed antibodies to all of the virulence factors targeted by the immunogen except lipopolysaccharide. Mouse and rabbit antibodies exhibited functional activities against CT enterotoxicity, CT binding to GM1 ganglioside, bacterial motility, and in vitro adherence of V. cholerae O1, O139, and non-O1/non-O139 serogroup strains. When challenged orogastrically with V. cholerae O1 El Tor N16961 or a non-O1/non-O139 strain, rabbits IM immunized with the immunogen showed a 2-log (99%) reduction in V. cholerae colonization of small intestines. Moreover, infant rabbits born to the mother immunized with the protein immunogen acquired antibodies passively and were protected from bacterial intestinal colonization (>2-log reduction), severe diarrhea (100%), and mild diarrhea (88%) after infection with V. cholerae O1 El Tor (N16961), O1 classical (O395), O139 (Bengal), or a non-O1/non-O139 strain. This study demonstrated that this polyvalent cholera protein is broadly immunogenic and cross-protective, and an adult rabbit colonization model and an infant rabbit passive protection model fill a gap in preclinical efficacy assessment in cholera vaccine development.

MlrA, a MerR family regulator in Vibrio cholerae, senses the anaerobic signal in the small intestine of the host to promote bacterial intestinal colonization

ABSTRACT Vibrio cholerae (V. cholerae), one of the most important bacterial pathogens in history, is a gram-negative motile bacterium that causes fatal pandemic disease in humans via oral ingestion of contaminated water or food. This process involves the coordinated actions of numerous regulatory factors. The MerR family regulators, which are widespread in prokaryotes, have been reported to be associated with pathogenicity. However, the role of the MerR family regulators in V. cholerae virulence remains unknown. Our study systematically investigated the influence of MerR family regulators on intestinal colonization of V. cholerae within the host. Among the five MerR family regulators, MlrA was found to significantly promote the colonization capacity of V. cholerae in infant mice. Furthermore, we revealed that MlrA increases bacterial intestinal colonization by directly enhancing the expression of tcpA, which encodes one of the most important virulence factors in V. cholerae, by binding to its promoter region. In addition, we revealed that during infection, mlrA is activated by anaerobic signals in the small intestine of the host through Fnr. In summary, our findings reveal a MlrA-mediated virulence regulation pathway that enables V. cholerae to sense environmental signals at the infection site to precisely activate virulence gene expression, thus providing useful insights into the pathogenic mechanisms of V. cholerae.

Ефективність застосування пробіотиків у дітей з синдромом подразненого кишечника: питання оптимальної тривалості лікування

Following the biopsychosocial model of medicine, irritable bowel syndrome (IBS) is a heterogeneous disorder, which is caused by multiple factors in different combinations. However, in most clinical cases probiotics are included in the treatment of IBS due to their influence on intestinal bacterial colonization, and immune, metabolic and motoric activity of the gut. The purpose - to evaluate the efficiency of probiotics (Lactobacillus reuteri DSM 17938) in children with IBS and to determine the optimal duration of the treatment. Materials and methods. We examined 108 children aged 6-12 years with a verified diagnosis of IBS, according to Rome criteria IV. Assessment of the main clinical symptoms was obtained by 4-point Likert scale. Enzyme immunoassay RIDASCREEN Calprotectin (R-Biopharm AG, Germany) was used for the quantitative determination of calprotectin in stool samples. Data were processed using Microsoft Excel 2016 and analysed with GraphPad (Prism 5.0). Results. Our study revealed the heterogenety of IBS in children not only according to clinical subtype, but also due to the trigger factor of the disorder. Patients with stress-related IBS were characterized by the higher level of asthenic syndrome and autonomic dysfunction (р=0.0003). In contrast, children with post-infectious IBS had higher concentration of fecal calprotectin, which is a result of low-grade intestinal inflammation (р=0.0003). After 10 days and 1 month since the beginning of treatment, we have observed a significant decrease in the severity of clinical syndromes, but the level of fecal calprotectin remained elevated. Conclusions. The efficiency of probiotics was confirmed by positive dynamics of clinical signs and the level of fecal calprotectin in children with various clinical subtypes of IBS. Even in the absence of any symptoms, the optimal duration of the use of Lactobacillus reuteri DSM 17938 in children with IBS should be 1-3 months. The research was carried out in accordance with the principles of the Helsinki Declaration. The study protocol was approved by the Local Ethics Committee of all participating institutions. The informed consent of the patient was obtained for conducting the studies. No conflict of interests was declared by the authors.

Neonatal Feeding Intolerance and Its Characteristics: A Descriptive Study.

Background: Feeding intolerance (FI) is common in preterm infants leading to feeding and gastrointestinal disruptions. FI in newborns can be a sign of a variety of problems, ranging from minor, self-limiting illnesses to serious ones. Many causes are found to cause FI such as low intestinal motility, bacterial colonization, hormonal response, and local immunity response. We aim to find out the characteristics of full-term neonates with FI during the neonatal hospitalization period.Methods: This is a descriptive study that was conducted at King Hamad University Hospital in Bahrain. Our targeted population included neonates with FI. Full-term neonates (gestational age, GA >36 weeks) with lower than 1 week of age were included. Data were investigated and compared with the mode of delivery.Results: In this study, 46 neonates were included and their characteristics of FI were evaluated. The most common symptoms observed in neonates with FI were vomiting (91.3%) and abdominal distension (8.7%). Of the total cases, 52.2% of neonates were born through Cesarean section (C-section), while 47.8% had a vaginal delivery. All the neonates had normal APGAR (Appearance, Pulse, Grimace, Activity, and Respiration) scores. C-section cases had more vomiting problems than vaginal delivery cases. Abdominal distention was noted more in neonates born via vaginal delivery when compared to C-section.Conclusion: During hospitalization after birth, refusal to feed with frequent vomiting or abdominal distension is a common characteristic of FI in neonates. Newborns with this condition require constant monitoring and supportive care from competent nurses.

Dominant bacteria and influencing factors of early intestinal colonization in very low birth weight infants: A prospective cohort study.

BackgroundThe intestine of newborns is colonized by bacteria immediately after birth. This study explored dominant bacteria and influencing factors of early intestinal colonization in the early life of very low birth weight infants (VLBWI).MethodsWe enrolled 81 VLBWI and collected anal swabs at 24 h, 7th, 14th and 21st day after birth. We conducted bacterial culture for anal swabs, then selected the colony with obvious growth advantages in the plate for further culture and identification. Afterward, we analyzed the distribution and influencing factors of intestinal dominant microbiota combined with clinical data.ResultsA total of 300 specimens were collected, of which 62.67% (188/300) had obvious dominant bacteria, including 29.26% (55/188) Gram‐positive bacteria and 70.74% (133/188) Gram‐negative bacteria. The top five bacteria with the highest detection rates were Klebsiella pneumoniae, Escherichia coli, Enterococcus faecium, Enterococcus faecalis and Serratia marcescens. Meconium‐stained amniotic fluid and chorioamnionitis were correlated with intestinal bacterial colonization within 24 h of birth. Mechanical ventilation and antibiotics were independent risk factors affecting colonization. Nosocomial infection of K. pneumoniae and S. marcescens were associated with intestinal colonization. The colonization rates of K. pneumoniae, E. coli, E. faecium, and E. faecalis increased with the birth time.ConclusionsThe colonization rate in the early life of VLBWI increased over time and the predominant bacteria were Gram‐negative bacteria. Meconium‐stained amniotic fluid and chorioamnionitis affect intestinal colonization in early life. Mechanical ventilation and antibiotics were independent risk factors for intestinal bacterial colonization. The nosocomial infection of some bacteria was significantly related to intestinal colonization.

Rewiring of the ubiquitinated proteome determines ageing in C. elegans

Ageing is driven by a loss of cellular integrity1. Given the major role of ubiquitin modifications in cell function2, here we assess the link between ubiquitination and ageing by quantifying whole-proteome ubiquitin signatures in Caenorhabditis elegans. We find a remodelling of the ubiquitinated proteome during ageing, which is ameliorated by longevity paradigms such as dietary restriction and reduced insulin signalling. Notably, ageing causes a global loss of ubiquitination that is triggered by increased deubiquitinase activity. Because ubiquitination can tag proteins for recognition by the proteasome3, a fundamental question is whether deficits in targeted degradation influence longevity. By integrating data from worms with a defective proteasome, we identify proteasomal targets that accumulate with age owing to decreased ubiquitination and subsequent degradation. Lowering the levels of age-dysregulated proteasome targets prolongs longevity, whereas preventing their degradation shortens lifespan. Among the proteasomal targets, we find the IFB-2 intermediate filament4 and the EPS-8 modulator of RAC signalling5. While increased levels of IFB-2 promote the loss of intestinal integrity and bacterial colonization, upregulation of EPS-8 hyperactivates RAC in muscle and neurons, and leads to alterations in the actin cytoskeleton and protein kinase JNK. In summary, age-related changes in targeted degradation of structural and regulatory proteins across tissues determine longevity.

Acceptive Immunity: The Role of Fucosylated Glycans in Human Host-Microbiome Interactions.

The growth in the number of chronic non-communicable diseases in the second half of the past century and in the first two decades of the new century is largely due to the disruption of the relationship between the human body and its symbiotic microbiota, and not pathogens. The interaction of the human immune system with symbionts is not accompanied by inflammation, but is a physiological norm. This is achieved via microbiota control by the immune system through a complex balance of pro-inflammatory and suppressive responses, and only a disturbance of this balance can trigger pathophysiological mechanisms. This review discusses the establishment of homeostatic relationships during immune system development and intestinal bacterial colonization through the interaction of milk glycans, mucins, and secretory immunoglobulins. In particular, the role of fucose and fucosylated glycans in the mechanism of interactions between host epithelial and immune cells is discussed.

Investigation of Commensal Escherichia coli Populations of Cormorant Hatchlings in the Absence of Anthropogenic Impacts in Remote Areas of West Mongolia.

To increase our understanding of bacterial intestinal colonization in animal populations lacking substantial anthropogenic influence we studied the diversity of E. coli in cormorants from the pristine West-Mongolian steppe. E. coli were isolated from individual birds of two cormorant colonies located on small islands in lakes at least 100 km away from human settlements. Diversity of the isolates was studied using pulsed-field gel electrophoresis (PFGE). 137 isolates of cormorant colony-1 and 75 isolates of cormorant colony-2 resulted in 60 and 33 PFGE types, respectively. Representative strains of each PFGE type were analyzed via PCR in terms of phylogroups and extraintestinal virulence-associated genes (exVAGs). Bacterial adhesion to the chicken intestinal cell line CHIC-8E11 and antimicrobial resistance was also determined. Most isolates belonged to phylogroup B1 (68.3%) followed by B2 and E with B2 harboring the highest total number of exVAGs per isolate. Unexpectedly, a PFGE type with relatively few exVAGs displayed the highest isolation frequency, also showing a high adhesion rate. Comparative analysis of exVAGs to other E. coli populations of wildlife origin revealed that the secreted autotransporter toxin encoding sat gene was only present in cormorants. Overall, E. coli in cormorants maintained a high diversity under minimal anthropogenic influences, which likely enables intestinal colonization.

Intestinal microbiota drives cholestasis-induced specific hepatic gene expression patterns

ABSTRACT Intestinal microbiota regulates multiple host metabolic and immunological processes. Consequently, any difference in its qualitative and quantitative composition is susceptible to exert significant effects, in particular along the gut-liver axis. Indeed, recent findings suggest that such changes modulate the severity and the evolution of a wide spectrum of hepatobiliary disorders. However, the mechanisms linking intestinal microbiota and the pathogenesis of liver disease remain largely unknown. In this work, we investigated how a distinct composition of the intestinal microbiota, in comparison with germ-free conditions, may lead to different outcomes in an experimental model of acute cholestasis. Acute cholestasis was induced in germ-free (GF) and altered Schaedler’s flora (ASF) colonized mice by common bile duct ligation (BDL). Studies were performed 5 days after BDL and hepatic histology, gene expression, inflammation, lipids metabolism, and mitochondrial functioning were evaluated in normal and cholestatic mice. Differences in plasma concentration of bile acids (BA) were evaluated by UHPLC-HRMS. The absence of intestinal microbiota was associated with significant aggravation of hepatic bile infarcts after BDL. At baseline, we found the absence of gut microbiota induced altered expression of genes involved in the metabolism of fatty and amino acids. In contrast, acute cholestasis induced altered expression of genes associated with extracellular matrix, cell cycle, autophagy, activation of MAPK, inflammation, metabolism of lipids, and mitochondrial functioning pathways. Ductular reactions, cell proliferation, deposition of collagen 1 and autophagy were increased in the presence of microbiota after BDL whereas GF mice were more susceptible to hepatic inflammation as evidenced by increased gene expression levels of osteopontin, interleukin (IL)-1β and activation of the ERK/MAPK pathway as compared to ASF colonized mice. Additonally, we found that the presence of microbiota provided partial protection to the mitochondrial functioning and impairment in the fatty acid metabolism after BDL. The concentration of the majority of BA markedly increased after BDL in both groups without remarkable differences according to the hygiene status of the mice. In conclusion, acute cholestasis induced more severe liver injury in GF mice compared to mice with limited intestinal bacterial colonization. This protective effect was associated with different hepatic gene expression profiles mostly related to tissue repair, metabolic and immune functions. Our findings suggest that microbial-induced differences may impact the course of cholestasis and modulate liver injury, offering a background for novel therapies based on the modulation of the intestinal microbiota.

Immune development of children born from Caesarean section

Several studies results have shown that mode of delivery affects the health of children, and recent studies showed that elective cesarean section (CS) is associated with aberrant short-term immune responses in the newborn baby and an increased risk of developing immune disorders. This article focused on the effect and role of the C-section on the immune development in children. Begin at pregnancy, the infant's immune system is activated and develops years after birth. In this article we find that cesarean delivery mode will influence the offspring's immune system by disrupting the intestinal tract's bacterial colonization, different levels of birth adaptive stress, and altering gene expression epigenetic regulation. Some studies have found that gut microbiome composition plays a significant role in the development of immune system along with other factors such as diet/lifestyle, antibiotic use, formula feeding, vaccination with life vaccine, and pathogen exposure. In early life, disrupted colonization induced dysbiosis that was associated with lower Bifidobacteria and higher counts of C. difficile. These findings are related to infant immune disease and allergy. Dysbiosis following C-section has a huge effect of developing altered immune system, and this microbiome imbalance can be controlled by nutritional support such as maternal breast milk or the use of different combinations of prebiotics and probiotics (synbiotic) which could be beneficial for the immune and metabolic system.

Microbiota composition and inflammatory immune responses upon peroral application of the commercial competitive exclusion product Aviguard® to microbiota-depleted wildtype mice.

Non-antibiotic feed additives including competitive exclusion products have been shown effective in reducing pathogen loads including multi-drug resistant strains from the vertebrate gut. In the present study we surveyed the intestinal bacterial colonization properties, potential macroscopic and microscopic inflammatory sequelae and immune responses upon peroral application of the commercial competitive exclusion product Aviguard® to wildtype mice in which the gut microbiota had been depleted by antibiotic pre-treatment. Until four weeks following Aviguard® challenge, bacterial strains abundant in the probiotic suspension stably established within the murine intestines. Aviguard® application did neither induce any clinical signs nor gross macroscopic intestinal inflammatory sequelae, which also held true when assessing apoptotic and proliferative cell responses in colonic epithelia until day 28 post-challenge. Whereas numbers of colonic innate immune cell subsets such as macrophages and monocytes remained unaffected, peroral Aviguard® application to microbiota depleted mice was accompanied by decreases in colonic mucosal counts of adaptive immune cells such as T and B lymphocytes. In conclusion, peroral Aviguard® application results i.) in effective intestinal colonization within microbiota depleted mice, ii.) neither in macroscopic nor in microscopic inflammatory sequelae and iii.) in lower colonic mucosal T and B cell responses.

Intestinal Pioneer Colonizers as Drivers of Ileal Microbial Composition and Diversity of Broiler Chickens.

Given that recent advances in metagenomics have highlighted the importance of intestinal microbes for poultry health, there has been a corresponding search for early manipulation strategies of intestinal microbiota in order to advance immune system development and optimize functional properties of growth. In this study, we used the in ovo technique as an experimental model to address how early bacterial intestinal colonization could affect the development and establishment of the mature ileal microbiota. Inoculations containing one of the following: 0.2 mL of 0.9% sterile saline (S), approximately 102 cells of Citrobacter freundii (CF), Citrobacter species (C2) or lactic acid bacteria mixture (L) were administered via in ovo into the amnion. Results showed that Enterobacteriaceae abundance was negatively correlated with aging, although its high population at day of hatch affected the microbiota composition, delaying mature microbiota establishment. L treatment increased colonization of butyrate-producing bacteria by 3 and 10 days, and segmented filamentous bacteria in the lower ileum by 10 days. On the other hand, L-probiotic decreased the population of Enterococcaceae. In addition, L and C2 microbial communities were less diverse at 10 than 3 days of age in the upper ileum. Importantly, these findings provide a valuable resource for a potential study model for interactions between microbial colonization and associated immune responses. In conclusion, our analysis demonstrates that intestinal pioneer colonizers play a critical role in driving the course of microbial community composition and diversity over time, in which early life exposure to L-based probiotic supported selection alongside greater colonization of symbiotic populations in the ileum of young broilers.

Effect of delaying colostrum feeding on passive transfer and intestinal bacterial colonization in neonatal male Holstein calves

The objective of this study was to investigate the effect of time of first colostrum feeding on the passive transfer of IgG and on bacterial colonization in the intestine of neonatal dairy calves. Twenty-seven male Holstein calves were randomly assigned to 1 of 3 treatments at birth: calves were fed colostrum at 45 min (0 h, n = 9), 6 h (n = 9), or 12 h after birth (n = 9). Calves were fed pooled, heat-treated colostrum (62 g of IgG/L) at their respective feeding times at 7.5% of birth body weight and fed milk replacer at 2.5% of birth body weight per meal every 6 h thereafter. Blood samples were taken every 3 h using a jugular catheter and were analyzed for determination of serum IgG by radial immunodiffusion. At 51 h after birth, calves were euthanized for collection of tissue and digesta of the distal jejunum, ileum, and colon. Quantitative real-time PCR was used to estimate the prevalence of Bifidobacterium spp., Lactobacillus spp., Fecalibacterium prausnitzii, Clostridium cluster XIVa, and total Escherichia coli. Delaying colostrum feeding by 6 h (35.6 ± 1.88%) and 12 h (35.1 ± 3.15%) decreased the maximum apparent efficiency of absorption of IgG compared with feeding colostrum immediately after birth (51.8 ± 4.18%) and delayed the time to maximum serum IgG concentration (24 h vs. 15 h, respectively). Moreover, 12-h calves tended to have a lower prevalence of Bifidobacterium spp. (0.12 ± 0.017%) and Lactobacillus spp. (0.07 ± 0.019%) associated with the colon mucosa compared with 0-h calves (1.24 ± 0.648% and 0.26 ± 0.075%, respectively). In addition, 6-h (0.26 ± 0.124%) and 12-h (0.49 ± 0.233%) calves had a lower prevalence of total E. coli associated with ileum mucosa compared with 0-h calves (1.20 ± 0.458%). These findings suggest that delaying colostrum feeding within 12 h of life decreases the passive transfer of IgG and may delay the colonization of bacteria in the intestine, possibly leaving the calf vulnerable to infections during the preweaning period.

Bifidobacterial strains in the intestines of newborns originate from their mothers.

The gastrointestinal tract is believed to be colonized rapidly with bacteria immediately from birth. The source of these intestinal microbes is an ongoing topic of interest because increasing evidence suggests that the composition of the initial intestinal bacterial colonization strongly affects health. In particular, the source of bifidobacteria has received marked attention because these bacteria are suggested to play a crucial role in protecting against susceptibility to diverse diseases later in life. However, the source of these microbes has remained unclear. Recently, it was confirmed that mothers transmit their unique bifidobacterial strains to their children shortly after birth. The transmitted strains predominate during early infancy, suggesting that maternal intestinal bifidobacteria are an important source of the infant gut microbiota. Accordingly, maintenance of a healthy, balanced gut microbiota during pregnancy has an important positive influence on the newborn gut microbiota.

Importance of functional diagnostics in gastroenterology

In this review article important and frequently used investigation methods for gastrointestinal functional diagnostics are presented. Some other rarely used special investigations are also explained. The hydrogen breath test is simple to carry out, ubiquitously available and enables the detection of lactose, fructose and sorbitol malabsorption. Furthermore, by the application of glucose, the test can be carried out when there is a suspicion of abnormal intestinal bacterial colonization and using lactulose for measuring small intestinal transit time. The 13C urea breath test is applied for non-invasive determination of Helicobacter pylori infections and assessment of gastrointestinal transit time, liver and exocrine pancreas functions. The secretin cholecystokinin test was the gold standard for the detection of exocrine pancreas insufficiency. However, measurement of pancreatic elastase in stool is less invasive but also less sensitive. Scintigraphy and capsule investigations with pH and temperature probes constitute important methods for determination of gastric emptying, intestinal and colon transit times. For evaluation of constipation panoramic abdominal images are taken after intake of radiologically opaque markers (Hinton test). For the diagnosis of functional esophageal diseases manometry is indispensable. In addition, manometry is only occasionally used for diagnosing a dysfunction of the sphincter of Oddi, due to the danger of inducing pancreatitis. A24 h pH-metry is applied for the detection of non-erosive gastroesophageal reflux disease and, if necessary, with impedance measurements. Recent investigation procedures, e. g. specific MRI sequences, sonographic determination of gall bladder ejection fraction, analysis of gastric accomodation or real-time lumen imaging, require further evaluation prior to clinical application.

Neonatal infection and neonatal necrotizing enterocolitis

Neonatal necrotizing enterocolitis(NEC) is a common critical disease of the digestive system in neonatal period.In severe case, it may even endanger the lives of newborn.The mechanism of NEC is complex and uncertain.Neonatal infection is one of the most important aspects of the mechanism.The immature digestive system, intestinal barrier structure and function in premature infants, the innate defects of intestinal immunity and the abnormal intestinal bacterial colonization can lead to a high incidence of NEC in premature infants.Currently, there is limited specific treatment.It will benefit for reducing incidence of NEC if prevention is targeted on the found of risk factors. Key words: Infection; Necrotizing enterocolitis; Neonates,