ABSTRACT
Objective:To investigate the protective effects of bovine lactoferrin (bLF) supplementation on intestinal mucosal tissue and its influence on of inflammatory factors in the premature rats model of necrotizing enterocolitis(NEC), and to provide the theoretical basis for prevention of NEC by bLF supplementation.Methods:Premature SD rats were randomly divided into 4 groups, 25 cases in each group.Control group: oral feeding; model group : oral feeding with lipopolysaccharides(LPS) gavage + hypoxic stimulation; high dose bLF intervention group: daily bLF (7 g/L) + oral feeding with LPS gavage + hypoxic stimulation; low dose bLF intervention group: daily bLF (2 g/L) + oral feeding with LPS gavage + hypoxic stimulation.Histopathological analysis was performed by HE staining.The expression levels of interleukin-1β(IL-1β)and interleukin-6(IL-6)in intestinal mucosa were detected by enzyme linked immunosorbent assay (ELISA).Results:(1) Morphological observation: the intestinal wall of model group was thin, and there were different degrees of pneumoconiosis and effusion in intestinal cavity.Under the microscopy, it could be observed that the intestinal tissue necrosis was serious, the intestinal villi fell off, glands arranged disorderly, epithelial edema was significant, the lamina propria and submucosa had severely edema and were separated, and there were a large number of inflammatory cells infiltrated.The above-mentioned manifestations were alleviated in the high-dose and low-dose bLF intervention groups, and no significant abnormalities were found in the control group.(2) The expression of IL-1β and IL-6 in intestinal tissue: the tissue concentration of IL-1β and IL-6 in the model group rats [(380.89±20.25) ng/L, (485.12±31.44) ng/L]were significantly higher than those in the control group[(270.69±45.58) ng/L, (212.62±89.46) ng/L]( q =9.785, 14.030, all P<0.01). The expression of IL-1β and IL-6 in mucosal tissue of ileum was significantly inhibited in hypoxic and LPS-stimulated rats fed with bLF(IL-1β: q=9.105, 8.761, all P<0.01; IL-6: q=8.175, 8.996, all P<0.01). There was no significant difference in the expression of IL-1β and IL-6 between high dose bLF(7 g/L) and low dose bLF (2 g/L) inter vention groups (IL-1β: q=-0.084, P>0.05; IL-6: q=-1.140, P>0.05). Conclusion:Enteral bLF supplementation can alleviate the damage of intestinal tissue in NEC model of premature SD rats, inhibit the expression of IL-1β and IL-6 inflammatory factors in intestinal tissue, and have a protective effect on intestinal tissue.
ABSTRACT
Trillions of microbes reside in the human body and participate in multiple physiological and pathophysiological processes that affect host health throughout the life cycle. The microbiome is hallmarked by distinctive compositional and functional features across different life periods. Accumulating evidence has shown that microbes residing in the human body may play fundamental roles in infant development and the maturation of the immune system. Gut microbes are thought to be essential for the facilitation of infantile and childhood development and immunity by assisting in breaking down food substances to liberate nutrients, protecting against pathogens, stimulating or modulating the immune system, and exerting control over the hypothalamic-pituitary-adrenal axis. This review aims to summarize the current understanding of the colonization and development of the gut microbiota in early life, highlighting the recent findings regarding the role of intestinal microbes in pediatric diseases. Furthermore, we also discuss the microbiota-mediated therapeutics that can reconfigure bacterial communities to treat dysbiosis.
Subject(s)
Child , Child, Preschool , Humans , Infant , Infant, Newborn , Disease , Dysbiosis , Therapeutics , Gastrointestinal MicrobiomeABSTRACT
Objective To explore a simplified and economical method to isolate the murine primary pancreatic acinar cells.Methods The collagenase and trypsin inhibitor dissolving in DMEM solution were used to digest the murine pancreas,and 4％ BSA dissolving in DMEM solution was used to purify and isolate primary pancreatic acinar cells from pancreas.CCK-8 method was applied to check the ability of pancreatic acinar cells to secret amylase.Results After digestion,shaking in the water bath,resuspension,filtration and precipitation,murine primary pancreatic acinar cells could be obtained within 2 hours.Pancreatic acinar cells in good conditions appeared in clusters,and their basolateral domains were round and devoid of blebs,and the cytoplasm appeared clear.Their apical domain were surrounded by hundreds of zymogen granules which looked darker.The nucleus was located in the basal area of the vesicular region.The basal level of amylase release as a percent of total release from pancreatic acinar cells was around 2.5％ in CCK8-unstimulated group.This rate started to increase after CCK-8 stimulation and reached its peak [(12.83 ± 1.04) ％] at a concentration of 50 pmol/L of CCK-8,but the ratio of the amylase level secreted by the pancreatic acinar cells to the total amylase level displayed a decreasing trend with the increase of CCK-8 concentration.Conclusions This optimized method had the advantage of being fast and simple,low technical difficulty and good repetition.It was a new simplified and cheap method for isolating murine pancreatic acinar cells.
ABSTRACT
Objective To explore the effects of ApoC3 gene on the severity of hypertriglyceridemiainduced acute pancreatitis (AP).Methods ApoC3 transgenetic mice and C57BL/6J mice AP model was induced by cerulein intraperitoneal injection,and ApoC3 transgenetic mice and C57BL/6J mice injected by normal saline solution in equal volume served as control group.Serum triglyceride and cholesterol were detected,and the pathological changes of the pancreas were observed.RT PCR method was used to examine the changes of the inflammatory factor including IL-1β,IL-6,α-SMA and TNF-α mRNA levels,which reflected the severity of the inflammation.Results Serum triglyceride and cholesterol were higher in ApoC3 transgenetic mice than in C57BL/6J mice [(3.434 ± 0.931) mmol/L vs (0.766 ± 0.120) mmol/L,(2.553 ±0.178) mmol/L vs (1.996 ± 0.080) mmol/L],and the differences were statistically different (P ＜ 0.05).The pathological changes of the pancreas were more severe in ApoC3 transgenetic AP mice than in C57BL/6J AP mice,and the IL-1β,IL-6 and α-SMA mRNA levels in the pancreatic tissue were obviously higher in ApoC3 transgenetic AP mice than in C57BL/6J mice (1.72 ± 0.07vs 0.78 ± 0.09,1.58 ± 0.09vs 0.87 ±0.04,0.83 ± 0.05vs 0.44 ± 0.04),and the differences were statistically significant (P ＜ 0.05),while there was no statistical difference on TNF-αmRNA level (0.70 ± 0.09vs 0.65 ± 0.08,P ＞ 0.05).Conclusions ApoC3 gene could aggravate the severity of the inflammation in hypertriglyceridemia-induced AP.
ABSTRACT
Objective To investigate the clinical distribution and antimicrobial resistance of Streptococcus agalactiae(S.agalactiae) in neonatal intensive care unit(NICU), and provide reference for antimicrobial use and intervention measures.Methods Specimens from neonates in the NICU of a hospital in 2010-2014 were collected, the department sources and antimicrobial susceptibility testing results of 62 strains of S.agalactiae isolated from children were analyzed.Results 62 strains of S.agalactiae were mainly distributed at full-term NICU, accounting for 64.52％;the main source of specimens was blood, accounting for 90.33％, followed, by cerebrospinal fluid (6.45％), sputum, and secretion(both were 1.61％).S.agalactiae had the highest resistance rate to tetracycline(79.03％);resistance rates to erythromycin and clindamycin were both 74.19％, resistance rate to levofloxacin was 40.32％, susceptibility rates to penicillin and ampicillin were both 100％.Conclusion S.agalactiae infection mainly occurred in neonates in full-term NICU, and has high resistance rate to multiple antimicrobial agents, penicillin and ampicillin can be used as the preferred antimicrobial agents for the treatment of S.agalactiae infection.
ABSTRACT
Objective To investigate the clinical characteristics and antimicrobial resistance of Acinetobacter baumannii(A.baumannii) in neonatal intensive care units (NICUs).Methods The clinical isolation and antimicrobial resistance of A.baumannii causing healthcare-associated infection(HAD in 4 NICUs of a hospital from October 2012 to October 2014 were analyzed statistically.Results A total of 11 640 neonates were admitted in 4 NICUs,500(4.3 ％) developed HAI,51 (10.2 ％) developed 52 cases of A.baumannii infection.Distribution of A.baumannii infection was as follows:NICU of extremely premature infants,premature infants,full-term infants,and surgical NICU were 42,1,4,and 5 cases respectively.Incidences of A.baumannii HAI in 4 seasons were compared,difference was statistically significant(x2 =16.05,P＜0.05),infection mainly occurred in the spring and summer.A.baumannii had high resistance rates to β-1actam antibiotics (such as piperacillin/sulbactam,cefepime,imipenem)and gentamycin(＞90 ％),resistance rate to amikacin was the lowest (51.9 ％).Among 52 strains of A.baumannii,46 were multidrug-resistant strains,and 3 were extensively drug-resistant strains.Conclusion A.baumannii HAI is most serious in NICU of extremely premature infants,resistance rates to commonly used antimicrobial agents are high.
ABSTRACT
Screening and diagnosis of early colorectal cancer(CRC)can reduce CRC mortality and improve overall survival. Currently,the major screening methods for early CRC include fecal occult blood test(FOBT)and colonoscopy. FOBT exhibits low sensitivity with high false positive rate,while the gold standard -- colonoscopy is invasive and with low compliance. Therefore,a convenient and effective screening and diagnostic method for early CRC is urgently needed. Plasma SEPT9 gene methylation assay is a new non-invasive screening and diagnostic method for early CRC used clinically in recent years,it exhibits high accuracy,and is convenient for mass screening and diagnosis of early CRC. This article reviewed the research progress and diagnostic value of plasma SEPT9 gene methylation assay for CRC.