| Objective:To observe the effect of intranasal instillation lipopolysaccharide(LPS)on lung development and the variation of NF κB,MIP-1α and VEGFR2,and explore the role and possible mechanism of postnatal pulmonary inflammation in the pathogenesis of bronchopulmonary dysplasia.Methods:A total of 40 C57 BL /6 mice at 1 day postnatally were randomly divided into two groups:LPS group,receiving an intranasal dose(25mg/kg)of LPS from postnatal 1d to 13 d,the saline group,receiving an equal intranasal dose of saline from postnatal 1d to 13 d.The mice were randomly sacrificed at postnatal 14 for the collection of the lung tissue.HE staining was used for the morphological changes of mice lung,The expression of CD31 was dectected by immunohistochemical and microvessel density was calculated.The distribution and expression of P65 and IκBα were measured by immunohistochemical and western blot.The mRNA expression of VEGFR2 and MIP-1 α was detected byRT-PCR.Western blot determined the protein level of phosphorylated P65(Ser536),phosphorylated IκBα(Ser32),and VEGFR2.Results:Compared to the saline group,the HE staining of LPS group showed alveolar enlargement and inflammatory cell infiltration around vessel.CD31 Immunohistochemistry showed microvessel density was decreased(P=0.003).Immunohistochemistry of P65 showed increased and was mostly distributed in nucleus(P=0.015).Immunohistochemistry of IκBαshowed decreased and were mostly distributed in cytoplasm(P=0.021).RT-PCR showed the mRNA level of VEGFR2 was decreased(P=0.000)and the mRNA level of MIP-1 α was increased(P=0.002).Western blot showed the protein expression levels of P65,phosphorylated P65(Ser536)and phosphorylated I κ B α(Ser32)were increased.I κ B α and VEGFR2 protein expression levels were decreased(P=0.000).Conclusion:Intranasal instillation lipopolysaccharide inhitbit lung development in newborn mice,postnatal pulmonary inflammation may participate in the occurrence of bronchopulmonary dysplasia.The mechanism related to the inhibition of VEGFR2,activation of NFκB and upregulation of MIP-1α.Objective:Intestinal stricture is a severe and common complication of necrotizing enterocolitis(NEC),causing severe and prolonged morbidity.Our goal was to investigate the clinical predictors for strictures developing after NEC and evaluate the management outcome of the post-NEC strictures to better orient their medicosurgical care.Methods:A total of 188 patients diagnosed with NEC with identical treatment protocols throughout the period under study were retrospectively reviewed from 4 academic neonatal centers between from January 1,2011,and October 31,2016.Clinical predictive factors and clinical outcomes,including demographic information,clinical management,laboratory data,histopathology of resected bowel segment,and discharge summaries,were evaluated on the basis of with post-NEC strictures or not.Results:Of the involved variables examined,the late-onsetNEC[risk ratio(RR),0.56;95%confidence interval(95%CI),0.41 – 0.92;P<0.001],cesarean delivery(RR,1.42;95% CI,0.98–2.29;P=0.026),and first procalcitonin(PCT)(onset of symptoms)(RR,1.82;95% CI,0.98 –3.15;P=0.009)were the independent predictive factors for the post-NEC strictures.C-reactive protein(CRP),white blood cell(WBC),and plateletcrit levels were markedly higher on infants with stricture and elevated levels were maintained until the stricture was healed.Infantswith intestinal stricture had significantly longer timesto beginning enteral feeds,than infantswithout intestinal stricture(P=0.023).The median age at discharge was also significantly higher in the group with stricture(P=0.014).Conclusion:This retrospective and multicenter study demonstrates that the early-onset NEC and cesarean delivery conferred protection over the post-NEC stricture.Infants with post-NEC stricture need prolonged hospitalization. |
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