Alterations of SP-A, SP-D and KL-6 in serum and bronchoalveolar lavage fluid in children with Mycoplasma pneumoniae pneumonia / 中华儿科杂志

<p><b>OBJECTIVE</b>To study the alterations and relationship of surfactant protein (SP)-A, SP-D and KL-6 in serum and bronchoalveolar lavage fluids (BALF) in children with Mycoplasma pneumoniae pneumonia (MPP).</p><p><b>METHOD</b>Self-control method was used for the study on SP-A, SP-D and KL-6 in serum, infected and non-infected BALFs in 32 MMP children with only one side of MPP.</p><p><b>RESULT</b>The contents of SP-A, SP-D and KL-6 in infected BALF were [mg/L;M (IQR) ]: 243 (90-468) , 187 (43-333) , 148 (47-426) ;104 (37-257) , 56 (25-131) , 35 (12-147) in non-infected BALF; 35 (25-69) , 33 (9-149) and 24 (15-62) in serum. The correlation coefficient of KL-6 between serum and infected BALF were -0.534 and -0.378 (P < 0.05).</p><p><b>CONCLUSION</b>There were significant correlation between the alterations of SP-A, SP-D and KL-6 in serum and lung infection in children with CAP. KL-6 in serum may be more sensitive than SP-A and SP-D.</p>

Expression of RANTES in the lung tissue of asthmatic rats, and the intervention effect of vitamin D on RANTES expression / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To investigate the effect of vitamin D on the expression of chemokine regulated on activation, normal T cells expressed and secreted (RANTES) in the lung tissue of asthmatic rats, and the role of vitamin D in the control of asthmatic airway inflammation and the synergistic action of hormones.</p><p><b>METHODS</b>Forty female Wistar rats were randomly and equally divided into normal control, asthma, vitamin D intervention, budesonide intervention, and budesonide+vitamin D intervention groups. Hematoxylin and eosin staining was used to observe pathological changes in the lung tissue. Immunohistochemistry was used to measure the protein expression of RANTES in lung tissue. Enzyme-linked immunosorbent assay was used to measure the level of RANTES in bronchoalveolar lavage fluid (BALF). Real-time quantitative PCR was used to measure the mRNA expression of RANTES.</p><p><b>RESULTS</b>The asthma group showed the most significant pathological changes in the lung tissue, including inflammatory cell infiltration, bronchial stenosis and distortion and smooth muscle rupture, while the intervention groups showed fewer pathological changes. Of the intervention groups, the budesonide intervention group showed fewer pathological changes than the vitamin D intervention group, and the budesonide+vitamin D intervention group showed the mildest pathological changes, which were similar to those observed in the normal control group. Protein expression of RANTES in the lung tissue and BALF was significantly higher in the asthma group than in the normal control group (P<0.05), while it was lower in the intervention groups than in the asthma group, exhibiting significant differences between each intervention group and the asthma group (P<0.05) (except the difference in protein expression of RANTES in BALF between the vitamin D intervention and asthma groups). The budesonide+vitamin D intervention group showed less protein expression of RANTES in the lung tissue and BALF than both the budesonide intervention and vitamin D intervention groups (P<0.05). The mRNA expression of RANTES was significantly higher in the asthma group than in the normal control group (P<0.05), while it was significantly lower in three intervention groups than in the asthma group (P<0.05), however no significant difference was found between the intervention groups in this regard. The budesonide+vitamin D intervention group showed the lowest level of RANTES mRNA, with no significant difference from the normal control group.</p><p><b>CONCLUSIONS</b>The mRNA and protein expression of RANTES in BALF and lung tissue increases significantly in asthmatic rats. Vitamin D intervention can decrease the expression of RANTES, suggesting that vitamin D can reduce airway inflammation by regulating the expression of RANTES. Vitamin D can be used together with budesonide to further decrease the mRNA and protein expression of RANTES.</p>

Changes to surfactant proteins in the bronchoalveolar lavage fluid and serum of children with Mycoplasma pneumoniae pneumonia / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To study the changes to surfactant proteins in the serum and bronchoalveolar lavage fluids (BALF) of children with Mycoplasma pneumoniae pneumonia (MPP) and their significance.</p><p><b>METHODS</b>Self-control method was used in the study. Forty-seven MPP children were divided into single lung infected (n=32) and bilateral lung infected groups (n=15) according to lung CT results. Surfactant proteins SP-A, B, C and D were measured using ELISA in the serum and BALF in the two groups. The correlations between SP-A, B, C and D content in the serum and BALF were evaluated by Spearman correlation analysis.</p><p><b>RESULTS</b>SP-A, B, C and D content in BALF from the majorly infected or infected lung were significantly higher than from the opposite lung and serum (P<0.01). SP-A, B and C content in serum was significantly lower than in BALF from the non-infected lung in the single-side infected lung group (P<0.01 or 0.05), but there was no significant difference between serum SP-D content and BALF SP-D content from the non-infected lung. There were no significant differences in SP-A, B, C and D content in serum and BALF from the minorly infected lung in the bilateral lung infected group. Serum SP-D content was positively correlated with BALF SP-D content from the majorly infected lung in the bilateral lung infected group (P<0.01).</p><p><b>CONCLUSIONS</b>Serum SP-D content may serve as a biomarker for evaluating the severity of pulmonary infection in children with community-acquired pneumonia.</p>

Relationship between alveolar epithelial type II cells and pulmonary surfactant protein A levels in young rats with acute lung injury / 中国当代儿科杂志

<p><b>OBJECTIVE</b>This study examined the relationship between the ultrastructural alterations of alveolar epithelial cells type II (AEC-II) and pulmonary surfactant protein A (SP-A) levels in the lung tissue of young rats with acute lung injury (ALI) in order to explore the possible mechanism of ALI.</p><p><b>METHODS</b>Forty-eight young Sprague-Dawley rats were randomly divided into control and ALI groups. The rats in the ALI group were intraperitoneally injected with 4 mg/kg of lipopolysaccharide (LPS) in order to induce ALI. The control subjects were injected with the same volume of normal saline. Rats were sacrificed at 24, 48 and 72 hrs after LPS or NS injection. Lung samples were obtained from the lower parts of the left lung and fixed with 2.5% glutaraldehyde for transmission electron microscope examination and for Western blot test of SP-A.</p><p><b>RESULTS</b>The microvilli of AEC-II disappeared 24 hrs after LPS injection. After 24 and 48 hrs of LPS injection, lamellar body (Lb) increased in number, enlarged in size and reduced in density, and the ring-like arrangement of Lb was present. By 48 hrs after LPS injection, giant Lb with vacuole-like deformity appeared. The contents of lung SP-A in the ALI group 24 hrs (6.52+/-0.62 vs 5.02+/-0.35; P<0.01) and 48 hrs (6.65+/-0.62 vs 5.01+/-0.36; P<0.01) after LPS injection were significantly higher than those in the control group. By 72 hrs after LPS injection, Lbs ruptured and were reduced in number. The shape of the nuclei was irregular and the border was blurred. The content of lung SP-A was greatly reduced in the ALI group 72 hrs after LPS injection compared with that in the control group (3.87+/-0.50 vs 5.22+/-0.36; P<0.01).</p><p><b>CONCLUSIONS</b>The alterations of AEC-II and lung SP-A were time-dependent in young rats with ALI induced by LPS. In the early stage of ALI, the lung SP-A content showed a compensatory increase. With the increasing injury of AEC-II cells, the secretion of SP-A presented with a decompensation and the lung SP-A content decreased. This may be one possible mechanism for the development of ARD.</p>

Changes of pulmonary surfactant protein A in young rats with acute lung injury induced by lipopolysaccharide / 中国当代儿科杂志

<p><b>OBJECTIVE</b>Pulmonary surfactant protein A (SP-A) plays an important role in the maintenance of pulmonary surfactant function and innative immune defence. This study aimed to explore the changes of SP-A concentration in the lungs of young rats with acute lung injury.</p><p><b>METHODS</b>Sprague-Dawley rats were randomly assigned to control and lung injury groups. Acute lung injury was induced by intraperitoneal injection of lipopolysaccharide (LPS) (4 mg/kg) in the lung injury group. The same amount of normal saline was given for the control group. The two groups were subdivided into 6 groups sacrificed at 6, 12, 24, 36, 48 and 72 hrs of injection (n=8 each). Western blot was employed to detect SP-A concentration in the lung tissues.</p><p><b>RESULTS</b>SP-A concentration in the lung injury group was not different from the the control group within 12 hrs after LPS injection. SP-A concentration in the lung injury group was elevated significantly during 24-48 hrs after LPS injection, peaking at 36 hrs (6.94+/-0.80 vs 5.01+/-0.36; P< 0.01), compared with the controls. However, SP-A concentration in the lung injury group was significantly reduced 72 hrs after LPS injection compared with the controls (P< 0.01).</p><p><b>CONCLUSIONS</b>The changes of lung SP-A concentration in rats following acute lung injury were time-dependent. The transient elevation of SP-A concentration in the lungs indicated a strong compensation ability of SP-A in the host defence against acute lung injury.</p>

Effects of dexamethasone on the ultrastructure of alveolar type II cells in young rats with lipopolysaccharide-induced acute lung injury / 中国当代儿科杂志

<p><b>OBJECTIVE</b>Alveolar type II (AT II) cells play a crucial role in the maintenance of pulmonary surfactant homeostasis and pulmonary immunity. The effects of dexamethasone (Dex) on the ultrastructure of AT II cells after acute lung injury remain unknown. This study focused on the ultrastructural changes caused by acute lung injury and on the effects of Dex administration on these ultrastructural changes in young rats.</p><p><b>METHODS</b>Seventy-two 21-day-old Sprague-Dawley rats were randomly divided into control, acute lung injury and Dex-treated groups. Rats in the lung injury group were intraperitoneally injected with 4 mg/kg lipopolysaccharide (LPS) in order to induce acute lung injury, while the control rats were injected with the same amount of normal saline (NS). The Dex-treated group was injected first with LPS followed 1 hr later by Dex (5 mg/kg) injection. Eight rats in each group were sacrificed 24, 48 and 72 hrs after LPS or NS injection. Lung samples were obtained from the lower parts of left lungs and fixed with 2.5% glutaraldehyde for transmission electron microscope examination.</p><p><b>RESULTS</b>Microvilli of AT II cells disappeared and the number of lamellar bodies (LBs) increased in the lung injury group 24 hrs after LPS injection. The ring-like arrangement of LBs around nuclei was present until 48 hrs after LPS injection. By 48 hrs after LPS injection, giant LBs with vacuole-like abnormalities appeared. The shape of nuclei became irregular and the border of the nuclei became blurred. By 72 hrs after LPS injection, the number of LBs was obviously reduced; nucleoli disappeared; and karyolysis occurred in some of the nuclei. In contrast, in the Dex-treated group, LBs crowded on one side of AT II cells and exocytosis appeared on the same side by 24 hrs after LPS injection. By 48 hrs, the number of LBs was reduced. The number of mitochondria increased, and some of them became swollen and enlarged. However, by 72 hrs, the number of LBs increased and the ring-like arrangement of LBs around the nucleus again appeared.</p><p><b>CONCLUSIONS</b>Ultrastructural changes of AT II cells following lung injury induced by LPS were time-dependent in young rats. Dex may ameliorate AT II cell injury and promote functional restoration of AT II cells in LPS-induced acute lung injury.</p>

Effect of dexamethasone on the content of pulmonary surfactant protein D in young rats with acute lung injury induced by lipopolysaccharide / 中国当代儿科杂志

<p><b>OBJECTIVE</b>Pulmonary surfactant protein-D (SP-D) is regarded as a valuable biomarker in acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). This study was to explore the changes of SP-D content in lung tissue following ALI and the effect of dexamethasone (Dex) on the SP-D content in young rats.</p><p><b>METHODS</b>One hundred and forty-four 21-day-old Sprague-Dawley rats were randomly assigned into control, ALI and Dex-treated groups. ALI was induced by intraperitoneal injection of lipopolysaccharide (LPS) (4 mg/kg) in the rats from the ALI and Dex-treated groups. Normal saline was given for the control group. Dex (5 mg/kg) was administered 1 hr after LPS injection in the Dex-treated group. At each time interval of 6, 12, 24, 36, 48 and 72 hrs after LPS injection, eight rats of each group were randomly chosen and sacrificed. Western blot was employed to detect the content of SP-D in lung tissues.</p><p><b>RESULTS</b>The pulmonary SP-D content decreased significantly at 36, 48 and 72 hrs after LPS administration in the ALI group, and reduced to a nadir (0.92 +/-0.11 vs 3.27 +/- 0.52) at 48 hrs compared with that of the control group (P < 0.01). The SP-D content in the Dex-treated group increased significantly at 36,48 and 72 hrs after LPS administration when compared with the ALI group (P < 0.01). A significant difference in the SP-D content between the Dex-treated and the control group was noted only at 72 hrs after LPS administration (P < 0.05).</p><p><b>CONCLUSIONS</b>The SP-D content in lung tissue was reduced following ALI in young rats at the early stage. Early administration of Dex can significantly increase the pulmonary SP-D content.</p>

Serum procalcitonin levels in children with bacterial or viral meningitis / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To investigate the ability of serum procalcitonin (PCT) to differentiate between bacterial and viral meningitis.</p><p><b>METHODS</b>The serum PCT levels were measured in 41 children with acute bacterial (n=18) or viral (n=23) meningitis by immunoluminometric assay. Meanwhile serum CRP levels and erythrocyte sedimentation rate (ESR) were measured.</p><p><b>RESULTS</b>The children with acute bacterial meningitis had higher levels of PCT (51.73 +/- 30.75 microg/L) and CRP(182.36 +/- 54.5 mg/L) and ESR (50.44 +/- 8.95 mm/h) than those with viral meningitis (0.84 +/- 0.99 microg/L, 8.90 +/- 10.66 mg/L and 16.75 +/- 13.23 mm/h respectively, P < 0.01). Both PCT and CRP had high predictive value for bacterial meningitis based on the area under curve of the receiver operating characteristics curves, 0.984 for PCT (95% confidence interval 0.953-1.013) and 0.983 for CRP (95% confidence interval 0.954-1.012) (P > 0.05). All of the children with bacterial meningitis had serum PCT levels above 0.5 microg/L, but only 2 patients with viral meningitis exceeded this value.</p><p><b>CONCLUSIONS</b>The measurement of serum PCT levels may be of value in the differential diagnosis of meningitis due to either bacterial or viruses.</p>

Changes of platelet endothelial cell adhesion molecule-1, tissue type plasminogen activator and plasminogen activator inhibitor-1 expression in the lung tissue of neonatal rats after intraperitoneal injection with lipopolysaccharide / 中华儿科杂志

<p><b>OBJECTIVE</b>To further explore the pathogenesis of neonatal acute lung injury and neonatal pulmonary hemorrhage by establishing the animal model of neonatal acute lung injury (ALI) and by investigating the changes of platelet endothelial cell adhesion molecule-1 (PECAM-1), tissue type plasminogen activator (t-PA) and plasminogen activator inhibitor-1 (PAI-1) in ALI.</p><p><b>METHODS</b>Totally 88 neonatal rats which were divided into 8 groups randomly including one normal saline control group and 30 min, 1 h, 2 h, 4 h, 8 h, 16 h and 24 h post injection groups. The changes of lung pathology in newborn rats were observed at different time after LPS was injected intraperitoneally. The changes of PECAM-1 protein, t-PA and PAI-1 mRNA expression were measured by immunohistochemistry and RT-PCR.</p><p><b>RESULTS</b>The expression of PECAM-1 protein and mRNA was decreased and the lowest level was reached at 8 h and 16 h post injection, respectively. The average values were 95.1 +/- 9.76 and 0.861 +/- 0.016, respectively, which were significantly lower than those in the control group (129.5 +/- 6.15, 1.192 +/- 0.035, P < 0.01). The expression of t-PA and PAI-1 mRNA was increased after LPS was injected. The highest level of t-PA mRNA expression was observed at 2 h after injection. The average value was 1.195 +/- 0.036, which was significantly higher than that in the control group (0.781 +/- 0.017, P < 0.01). The highest level of PAI-1 mRNA expression was observed at 2 h, 4 h and 8 h post injection. The average values were 1.178 +/- 0.069, 1.153 +/- 0.036 and 1.176 +/- 0.044, respectively, which was significantly higher than those of the control group (0.681 +/- 0.019, P < 0.01).</p><p><b>CONCLUSIONS</b>The expression of PECAM-1 protein and mRNA was decreased after LPS injection, suggesting the disruption of the tissue protective mechanism; the expression of t-PA and PAI-1 mRNA was increased, indicating the presence of a hypercoagulability state. At the same time, the expression of t-PA mRNA was increased which caused the extra-cellular matrix degradation at the early phase after LPS injection. These three phenomena might be the contributory factors to pulmonary hemorrhage.</p>

Dynamic Changes of Th1/Th2 Cell Factor in Induced Sputum and Clinical Significance in Children with My-coplasma Pneumoniae Pneumonia / 实用儿科临床杂志

Objective To detect levels of IL - 4 and INF - ? in induced sputum dynamically in children with mycnplasma pneamo-niae pneumonia( MPP), and to analyze the function of Th1 /Th2 cell factor immune response in the genesis and development of MPP, so as to evaluate the clinical value of induced sputum method in MPP research. Methods There were 38 cases who were diagnoses as MPP using 3% high osmotic pressure of saline water to ultrasonic atomizing inhalation for inducing sputum. ELISA was used to detect IL-4 and INF-?. Results The content of IL-4 in acute stage was higher than that in convalescence stage in induced sputum of MPP children. Severe stage was higher than mild stage. However, the comparison between acute and convalescence stage didn't have statistics difference in the content of INF-?, neither did the comparison between severe and mild stage. IL- 4/INF- ? in acute stage was higher than that in convalescence stage. Severe stage was higher than mild stage. In convalescence stage, the comparison of INF - ?, IL - 4, IL - 4/INF - ? between the severe and the mild didn' t have statistic significance. Conclusions IL-4 and INF - ? have participated in the monogenesis of MPP. The disequilibria of Th1 /Fh2 is existed in MPP and Th2 reaction predominates. So induced sputum analysis can be a better way to judge the light or heavy press degree of MPP practically, conveniently and sensitively.

Effect of intrauterine acute ischemic-hypoxia on the expression of lung SP-A and SP-B in neonatal rats / 中华儿科杂志

<p><b>OBJECTIVE</b>Neonatal asphyxia is one of the main causes for the acute respiratory distress syndrome (ARDS) in full-term newborns. Now it is believed that the reduced amount and abnormal function of pulmonary surfactant due to various causes is a major factor leading to acute lung injury. This study aimed at using an intrauterine acute ischemic-hypoxia rat model and investigating the effect of intrauterine acute ischemic-hypoxia on the expression of surfactant protein A (SP-A) and surfactant protein B (SP-B) in neonatal rat lungs.</p><p><b>METHODS</b>The rat model of acute intrauterine ischemic-hypoxia was established by ligating the unilateral uterine horn vessels of Wistar rats at the 21st gestational day. While the rat pups from the other side of the uterus, of which the uterine horn vessel was not ligated, were the sham-operation group. Rat pups were delivered by cesarean section at the 20, 30 and 40 min following the ischemic-hypoxia insult. The rat pups delivered by cesarean section from the gestation of 21 days were the normal control group. There were 42 rat pups and 6 pups in each group in this study. The distribution of SP-B protein in the neonatal rat lungs of different period of ischemia was examined by using SABC method. The average gray value of SP-B staining in type II alveolar epithelial cells were measured by Universal Imaging Porporation with Meta Morph software. The reverse transcription polymerase chain reaction (RT-PCR) was performed to quantitate the expression of SP-A and SP-B mRNA.</p><p><b>RESULTS</b>Following the intrauterine acute ischemic-hypoxia, the numbers of type II alveolar epithelial cells with the positive SP-B staining were markedly declined. The average gray values at the 20, 30 and 40 min after the ischemia were 78.89 +/- 1.08, 79.69 +/- 0.13 and 80.00 +/- 0.63, respectively, which increased significantly compared with the normal control group (76.13 +/- 0.43, P < 0.01). The expression of SP-A and SP-B mRNA was weak following the ischemic-hypoxia insult. The relative amounts of SP-A (1.16 +/- 0.06, 1.14 +/- 0.01 and 1.13 +/- 0.04, respectively) and SP-B (0.81 +/- 0.02, 0.78 +/- 0.02 and 0.79 +/- 0.04, respectively) at the 20, 30 and 40 min after the ischemia were reduced significantly compared with controls (1.27 +/- 0.09 and 0.89 +/- 0.06, respectively, P < 0.05 and < 0.01) and reduced gradually following the prolongation of the insult. There were no significant differences (P > 0.05) between the normal and sham operation control groups on the expressions of SP-B protein as well as the SP-A and SP-B mRNA.</p><p><b>CONCLUSION</b>The reduced synthesis of SP-B protein and the reduced expression of SP-A and SP-B mRNA might be caused by intrauterine acute ischemic-hypoxia, which may support theoretically the early application of pulmonary surfactant including SP-A and SP-B for treating the lung injuries of asphyxia in newborns.</p>

Change of neurokinin A plasma level in asthmatic children / 中华儿科杂志

<p><b>OBJECTIVE</b>Chronic inflammation of airway in bronchial asthma is caused by many complicated elements. Recently, a close attention has been paid to the neurogenic inflammation in airway which is mediated by sensory neuropeptides secreted by sensory nerve in the lung. Neurokinin A (NKA) is an important sensory neuropeptide leading to neurogenic inflammation in airway. Experimental studies showed that NKA has a close relation to asthma. The purpose of the present study was to investigate the changes of NKA in plasma of asthmatic children and possible relationship between sensory neuropeptides and asthma in children.</p><p><b>METHODS</b>Thirty-five children with bronchial asthma were studied; 16 of the cases were < 3 yrs and 19 were >or= 3 yrs. Eighteen of the cases had severe asthma and 16 had mild asthma. None of the subjects was treated with glucocorticoid within 3 days before the study started; 15 healthy children without history of asthma or family history of asthma were enrolled as control subjects. Plasma was collected from each case during acute attack of asthma and their clinical remission of the asthmatic children. After purifying with SEP-pak C(18), NKA content was detect by enzyme-linked immunosorbent assay (ELISA) as instructed by the manufacturer of the NKA Kit (NKA unit: ng/L).</p><p><b>RESULTS</b>(1) The content of plasma NKA of asthmatic children was significantly higher at the asthma attack (256 +/- 153) than that at their clinical remission stage (70 +/- 66; q = 9.497, P < 0.01) and than that of the normal control group (38 +/- 6; q = 8.599, P < 0.01); no significant difference in plasma NKA was found between the clinical remission stage and the normal control group (q = 1.245, P > 0.05). (2) There was a significant positive correlation between the asthmatic clinical state and the levels of plasma NKA; the contents of plasma NKA at the stage of acute attack in severe asthma (296 +/- 170) were significantly higher than those of the mild asthmatic children (190 +/- 99; q = 3.77, P < 0.05).</p><p><b>CONCLUSIONS</b>The contents of plasma NKA were significantly higher during the asthma attack stage of children, and the higher was the level of NKA, the more severe the attack.; with asthma remission, the contents of plasma NKA decreased to normal; the contents of plasma NKA has a close relation to the asthmatic children.</p>