The Good and The Bad of The Innate Immune Response In Necrotizing Enterocolitis
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Necrotizing Enterocolitis
Pathogenesis
Enterocolitis
Cronobacter sakazakii
Necrotizing Enterocolitis
Pathogenesis
Enterocolitis
Cronobacter sakazakii
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Necortizing enterocolitis(NEC)is a common neonatal gastrointestinal disease in new-born infants, especially in lower gestational age and lower birth weight groups.While the exact pathogenesis remains unclear, risk factors including prematurity, bacteria colonization, blood transfusion are confirmed.As recently revealed, ultrasonography and bio-markers can facilitate early diagnosis, whereas reasonable use of probiotics, lactoferrin, nitric oxide, amniotic fluids can effectively reduce the incidence of NEC.This paper is a review on pathogenesis and advances in diagnostic and therapeutic approaches of NEC.
Key words:
Necrotizing enterocolitis; Pathogenesis; Early diagnosis; Therapy
Necrotizing Enterocolitis
Pathogenesis
Lactoferrin
Enterocolitis
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<i>Background:</i> Neonatal necrotizing enterocolitis (NEC) is the most common gastrointestinal emergency in premature infants. The mortality rate associated with NEC is quite high and in most reports ranges from 20 to 30%. Despite extensive studies, the pathogenesis of NEC remains poorly understood. <i>Objectives:</i> To investigate the mechanisms of NEC in terms of inflammatory signaling in the intestine. <i>Methods:</i> A new enterocolitis model was established and examined the expression of inflammatory and anti-inflammatory signals in the intestines of rat pups. The premature rat pups, delivered by abdominal incision on day 20 of gestation (day 21 is considered as full term), were divided into three groups, and they were given a single administration of 0.05, 0.1, and 0.15 ml of formula milk via an orogastric catheter. After 24 h, the development of enterocolitis was evaluated by the presence of hemorrhagic enterocolitis, and the expression of signaling molecules, inhibitor of nuclear factor-ĸB (IĸB)-α/β and peroxisome proliferator-activated receptor (PPAR)-γ mRNA was examined by reverse transcription-polymerase chain reaction from inflamed and non-inflamed intestinal samples. <i>Results:</i> The incidence of enterocolitis increased with the volume of milk, and 50% of rat pups showed enterocolitis with a volume of 0.15 ml of milk. Expression of IĸB-α/β and PPAR-γ mRNA increased in inflamed intestine. <i>Conclusions:</i> Increased expression of IĸB-α/β suggested that the inflammatory mediator nuclear factor-ĸB is deeply involved in the pathogenesis of enterocolitis that can be easily introduced by overfeeding of milk ingestion in premature rat pups which mimic those seen in NEC. Increased expression of PPAR-γ may possibly regulate further development of enterocolitis in this system.
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Introduction. Neonatal infection with Cronobacter sakazakii can cause severe intestinal damage and necrotizing enterocolitis (NEC). The inflammasome and Toll-like receptors mediate intestinal damage caused by other intestinal pathogens causing NEC, but the exact mechanism is unclear.Aim. We evaluated the molecular mechanisms underlying C. sakazakii-induced NEC.Methodology. The effects of C. sakazakii treatment on two cell lines and a Sprague-Dawley rat model of NEC were evaluated by a cell death assay, western blot and real-time PCR analyses of the NLRP3 inflammasome and downstream factors, and observation of cell and intestinal damage.Results.C. sakazakii caused cellular damage in vitro, as well as intestinal damage in an animal model. NLRP3, caspase-1, TLR4 and MyD88, as well as the downstream factor IL-1β, were upregulated in C. sakazakii-infected J774A.1 and HT-29 cells. Western blotting showed that C. sakazakii-infected J774A.1 and HT-29 cells and the NEC rat model had higher expression levels of N-terminal gasdermin D (GSDMD) compared with those in the control groups. C. sakazakii and its components promote NF-κB expression via the TLR4/MyD88 signalling pathway, thereby regulating the NLRP3 inflammasome and mediating GSDMD cleavage, resulting in pyroptosis-induced intestinal damage.Conclusion. We found that C. sakazakii upregulates NF-κB via TLR4/MyD88 to promote activation of the NLRP3 inflammasome, leading to the up-regulation of downstream caspase-1, release of IL-1β, GSDMD-mediated pyroptosis and development of NEC. These findings clarify the mechanisms by which C. sakazakii contributes to NEC.
Necrotizing Enterocolitis
Cronobacter sakazakii
Enterocolitis
Enterobacteriaceae Infections
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The effect of human colostrum in the prevention of diarrhea and necrotizing enterocolitis, as well as the advantages of its use in gastroenteritis, was studied in 71 premature newborns. The frequency of diarrhea and enterocolitis in 16 healthy newborns who were given human colostrum (group II), was less than in the 22 healthy newborns who received only cows milk (group I), but without statistical significance. In 25 infants with diarrhea who were given human colostrum, the frequency of enterocolitis and sepsis (group IV) was less than in the 8 infants with diarrhea who didn't receive human colostrum (group III). At the end we suggest that human colostrum should be given in high risk infants in order to decrease the frequency of diarrhea and enterocolitis and we also make some recommendation as to how to obtain and store human colostrum.
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Enterocolitis
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To study the occurrence of bacterial translocation and to assess the impact of breastfeeding on bacterial translocation in the animal model of necrotizing enterocolitis.A total of 20 neonate Sprague-Dawley rats were enrolled in the study. Rats were randomly allocated into either control or study group just after birth. Ten newborn rats in the control group were left with their mother to be breast-fed. In contrary, necrotizing enterocolitis group consisted of neonates that were separated from their mothers, housed in an incubator and were gavaged with a special rodent formula three times daily. Survival rates, weight changes, and morphologic scoring obtained after microscopic evaluation were determined as microbiologic evaluation criteria.All the rats in the control group survived, while 1 (10 %) rat died in the necrotizing enterocolitis group. Mortality rates of the two groups were similar. All the formula-fed animals in the necrotizing enterocolitis group had significant weight loss compared to the breast milk-fed rats in the control group (p<0.05). A total of 7 (70 %) and 2 (20 %) E. coli growths were identified in the bowel lumen, liver, and spleen of necrotizing enterocolitis and control groups, respectively. This difference was statistically significant. In peritoneal smear cultures, a total of 3 (30 %) growths were detected in the necrotizing enterocolitis group and 1 (10 %) growth in the control group.As the result of a disturbance in the intestinal flora and impairment of the intestinal barrier in necrotizing enterocolitis, microrganisms in the bowel pass through the intestinal barrier and reach the liver and the spleen via the hematogenous route. This condition is closely related to the impairment of physiological and functional features of the intestinal barrier and is independent from the degree of intestinal injury. Bacterial translocation should be remembered in cases suspected of necrotizing enterocolitis, and a rapid and effective treatment algorithm should be applied in such circumstances (Tab. 3, Fig. 3, Ref. 21). Full Text in PDF www.elis.sk.
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To summarize and differentiate abdominal ultrasound findings of necrotizing enterocolitis and food protein-induced enterocolitis syndrome.From January 2017 to December 2018, the abdominal ultrasound results of 304 cases diagnosed necrotizing enterocolitis or food protein-induced enterocolitis syndrome were retrospectively analyzed. The presence of pneumatosis intestinalis, portal venous gas, bowel wall thickening, intestinal motility, focal fluid collections and hypoechoic change of gallbladder wall were calculated, and the results were compared and analyzed.Pneumatosis intestinalis, portal venous gas, bowel wall thickening, intestinal motility weakened/absent, focal fluid collections and hypoechoic change of gallbladder wall can be found in both necrotizing enterocolitis and food protein-induced enterocolitis syndrome infants. However, in infants with necrotizing enterocolitis, intestinal motility was weakened/absent in whole abdomen, and in food protein-induced enterocolitis syndrome, it only involved isolated segment of bowel. The positive rates of above signs in necrotizing enterocolitis infants were significantly higher than those in food protein-induced enterocolitis syndrome (p<0.01). Moreover, it was observed that the rate of weakened intestinal motility besides the lesion segment of bowel in necrotizing enterocolitis infants was 100%, and in food protein-induced enterocolitis syndrome infants, it was 0%, which is supposed to be a main sign for identification.In the early stage, abdominal ultrasound can be used to differentiate necrotizing enterocolitis and food protein-induced enterocolitis syndrome.
Necrotizing Enterocolitis
Enterocolitis
Pneumatosis Intestinalis
Short Bowel Syndrome
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Necrotizing Enterocolitis
Enterocolitis
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Necrotizing enterocolitis is common in preterm and low birth weight infants but rare beyond the neonatal period. Various infectious agents including bacterial and viral organisms have been implicated in its pathogenesis. Rotavirus has recently been shown to be associated with necrotizing enterocolitis. In this report we describe two infants with congenital cardiac disease who developed fulminating necrotizing enterocolitis after cardiac catheterization. Both infants were beyond the newborn period and developed enterocolitis during an epidemic of rotaviral infection. We postulate a relationship between rotavirus infection and the development of necrotizing enterocolitis in older infants with congenital heart disease after cardiac catheterization.
Necrotizing Enterocolitis
Enterocolitis
Cardiac catheterization
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