Childhood Mycoplasma pneumoniae: epidemiology and manifestation in Northeast and Inner Mongolia, China.

Mycoplasma pneumoniae (MP) is commonly detected in children. However, the epidemiological trends of MP in Northeast (NE) China are unclear. This retrospective study aimed to investigate the prevalence of MP infections in this understudied region. The clinical manifestations and bronchoscopic findings observed in hospitalized patients with severe Mycoplasma pneumoniae pneumonia (SMPP) were collected from comprehensive data obtained from six tertiary hospitals in NE and Inner Mongolian (IM) China, from 1 January 2017 to 31 December 2023. A total of 5,593,530 children who visited the outpatient and emergency departments, and 412,480 inpatient hospitalized children were included in the study. The positivity rate of MP immunoglobulin M (IgM) in the children who visited the outpatient and emergency departments varied from 7.80% to 10.12%, whereas that of MP infection in hospitalized children ranged from 27.18% to 30.10%. Children hospitalized for MP infection were mainly concentrated in the 1- to 4-year (41.39%) and 4- to 7-year (24.25%) age groups. Before 2020, the season with the highest incidence of MP was winter. After the implementation of non-pharmaceutical interventions (NPIs), the MP epidemic season changed, and the number of children with MP infections decreased; however, the proportion of MP infections in hospitalized children did not change significantly. Starting from August 2023, the MP infection rate in outpatient, emergency, and hospitalized children increased sharply, with SMPP and its complications (e.g., plastic bronchitis and pleural effusion) increasing significantly. MP is prevalent in NE and IM, China. When the NPIs ended, MP infection showed a delayed outbreak trend, and the number of children with severe infection increased significantly. IMPORTANCE: In Northeastern (NE) and Inner Mongolia (IM), the incidence of Mycoplasma pneumoniae (MP) infections, including severe Mycoplasma pneumoniae pneumonia (SMPP), is high, posing health risks and imposing substantial economic burdens on the local population. Therefore, it is imperative to prioritize the study of MP prevalence and address the research gaps in MP epidemiology in these areas of China. We obtained a comprehensive collection of pediatric outpatient, emergency, and inpatient data from six public Grade III hospitals. We believe that our study makes a significant contribution to the literature because understanding regional variations in MP infections can help healthcare professionals tailor prevention and treatment strategies, and studying bronchoscopic manifestations can provide insights into the impact of the disease on the respiratory system, potentially leading to a more effective clinical management.

Clinical features and risk factors analysis of bronchitis obliterans due to refractory Mycoplasma pneumoniae pneumonia in children: a nomogram prediction model.

BACKGROUND: Early prediction of bronchitis obliterans (BO) is of great significance to the improvement of the long-term prognosis of children caused by refractory Mycoplasma pneumoniae pneumonia (RMPP). This study aimed to establish a nomogram model to predict the risk of BO in children due to RMPP. METHODS: A retrospective observation was conducted to study the clinical data of children with RMPP (1-14 years old) during acute infection. According to whether there is BO observed in the bronchoscope, children were divided into BO and the non-BO groups. The multivariate logistic regression model was used to construct the nomogram model. RESULTS: One hundred and forty-one children with RMPP were finally included, of which 65 (46.0%) children with RMPP were complicated by BO. According to the multivariate logistic regression analysis, WBC count, ALB level, consolidation range exceeding 2/3 of lung lobes, timing of macrolides, glucocorticoids or fiber bronchoscopy and plastic bronchitis were independent influencing factors for the occurrence of BO and were incorporated into the nomogram. The area under the receiver operating characteristic curve (AUC-ROC) value of nomogram was 0.899 (95% confidence interval [CI] 0.848-0.950). The Hosmer-Lemeshow test showed good calibration of the nomogram (p = 0.692). CONCLUSION: A nomogram model found by seven risk factor was successfully constructed and can use to early prediction of children with BO due to RMPP.

Long noncoding RNA PTTG3P/miR-192-3p/CCNB1 axis is a potential biomarker of childhood asthma.

BACKGROUND: Increasing evidence suggests that long non-coding RNAs (lncRNAs) affect the regulation of immune responses, airway inflammation, and other pathological processes involved in asthma. LncRNA PTTG3P is associated with the development of various tumors, but its role in childhood asthma remains unknown. In this study, we investigated the functions of the lncRNA PTTG3P in the progression of childhood asthma. METHODS: Twenty-six healthy children and 26 asthmatic children were monitored for disease progression for 2 years. We obtained blood samples during the chronic phase of disease for lncRNA/mRNA expression microarray analysis. A competitive endogenous RNA network (PTTG3P/miR-192-3p/CCNB1) was identified using bioinformatics analyses. Real-time qPCR and western blot were used to quantify gene and protein expression levels, respectively. Cell counting kit­8 and transwell assays were used to evaluate the proliferation and migration of bronchial epithelial (16HBE) cells. Double luciferase reporter gene assay was used to validate the predictive targets in PTTG3P, miR-192-3p, and CCNB1. RESULTS: PTTG3P was highly expressed in the peripheral blood of asthmatic children. Knocking down PTTG3P inhibited epithelial-mesenchymal transition, proliferation, and migration of 16HBE cells. PTTG3P promoted progression of childhood asthma by targeting the miR-192-3p/CCNB1 axis. CONCLUSIONS: Childhood asthma was associated with the PTTG3P/miR-192-3p/CCNB1 axis. This study provides potential diagnostic and treatment biomarkers for childhood asthma.

Significance of RNA N6-Methyladenosine Regulators in the Diagnosis and Subtype Classification of Childhood Asthma Using the Gene Expression Omnibus Database.

RNA N6-methyladenosine (m6A) regulators play important roles in a variety of biological functions. Nonetheless, the roles of m6A regulators in childhood asthma remain unknown. In this study, 11 significant m6A regulators were selected using difference analysis between non-asthmatic and asthmatic patients from the Gene Expression Omnibus GSE40888 dataset. The random forest model was used to screen five candidate m6A regulators (fragile X mental retardation 1, KIAA1429, Wilm's tumor 1-associated protein, YTH domain-containing 2, and zinc finger CCCH domain-containing protein 13) to predict the risk of childhood asthma. A nomogram model was established based on the five candidate m6A regulators. Decision curve analysis indicated that patients could benefit from the nomogram model. The consensus clustering method was performed to differentiate children with asthma into two m6A patterns (clusterA and clusterB) based on the selected significant m6A regulators. Principal component analysis algorithms were constructed to calculate the m6A score for each sample to quantify the m6A patterns. The patients in clusterB had higher m6A scores than those in clusterA. Furthermore, we found that the patients in clusterA were linked to helper T cell type 1 (Th1)-dominant immunity while those in clusterB were linked to Th2-dominant immunity. In summary, m6A regulators play nonnegligible roles in the occurrence of childhood asthma. Our investigation of m6A patterns may be able to guide future immunotherapy strategies for childhood asthma.

Expression of vitamin D receptor in bronchial asthma and its bioinformatics prediction.

Vitamin D receptors (VDRs) are associated with the occurrence and development of asthma. The aim of the present study was to analyze the secondary structure and B­cell and T­cell epitopes of VDR using online prediction software and aid in the future development of a highly efficient epitope­based vaccine against asthma. Blood samples were collected from peripheral blood of asthmatic children. Reverse transcription quantitative­polymerase chain reaction (RT­qPCR) was performed to detect the expression of VDR in the peripheral blood. Mouse models of asthma were established. Hematoxylin and eosin staining was performed to observe the pathological alterations of the lungs of mice. Immunohistochemistry, western blot analysis and RT­qPCR were performed to detect the expression of VDR in the lungs of asthmatic mice. Online prediction software immune epitope database and analysis resource, SYFPEITHI and linear epitope prediction based on propensity scale and support vector machines were used to predict the B­cell and T­cell epitopes and the RasMol and 3DLigandSite were used to analyze the tertiary structure of VDR. RT­qPCR demonstrated that VDR expression in the peripheral blood of asthmatic children was decreased. Immunohistochemistry, western blotting and RT­qPCR demonstrated that VDR expression also decreased in the lungs of mouse models of asthma. VDR B­cell epitopes were identified at 37­45, 88­94, 123­131, 231­239, 286­294 and 342­350 positions of the amino acid sequence and VDR T­cell epitopes were identified at 125­130, 231­239 and 265­272 positions. A total of six B­cell epitopes and three T­cell epitopes for VDR were predicted by bioinformatics, which when validated, may in the future aid in immunological diagnosis and development of a targeted drug therapy for clinical asthma.

Epigallocatechin gallate improves airway inflammation through TGF­ß1 signaling pathway in asthmatic mice.

The present study aimed to investigate the effect of epigallocatechin gallate (EGCG) on airway inflammation in mice with bronchial asthma, and the regulatory mechanism of transforming growth factor (TGF)­ß1 signaling pathway, so as to provide theoretical basis for research and development of a novel drug for clinical treatment. Mouse models of bronchial asthma were established and injected with dexamethasone and EGCG via the caudal vein. 7 days later, bronchoalveolar tissue was collected for hematoxylin and eosin staining. Determination of airway resistance (AWR) and lung function in mice was detected. Serum was separated for cytometric bead array to detect the changes in inflammatory factors. Bronchoalveolar lavage fluid was collected for eosinophil and neutrophil counts. Fresh blood was obtained for flow cytometry to determine the percentages of Th17 and Treg cells. Bronchovesicular tissue was utilized for western blot assay and reverse transcription­quantitative polymerase chain reaction to determine the proteins and transcription factors in the TGF­ß1 pathway. EGCG 20 mg/kg significantly reduced asthmatic symptoms, lung inflammatory cell infiltration, and the inflammatory factor levels of interleukin (IL)­2, IL­6 and tumor necrosis factor (TNF)­α. In addition, it increased the levels of inflammatory factors, including IL­10, diminished the percentage of Th17 cells, increased the percentage of Treg cells, and decreased the expression of TGF­ß1 and phosphorylated (p)­Smad2/3 expression. Following the inhibition of the TGF­ß1 receptor, the anti­inflammatory effect of EGCG disappeared, and the expression of TGF­ß1 and p­Smad2/3 increased. EGCG attenuated airway inflammation in asthmatic mice, decreased the percentage of Th17 cells and increased the percentage of Treg cells. The anti­inflammatory effect of EGCG is achieved via the TGF­ß1 signaling pathway.

Vasoactive intestinal peptide inhibits airway smooth muscle cell proliferation in a mouse model of asthma via the ERK1/2 signaling pathway.

Asthma is a heterogeneous clinical syndrome characterized by airway inflammation, hyper-responsiveness and remodeling. Airway remodeling is irreversible by current antiasthmatic drugs, and it is the main cause of severe asthma. Airway smooth muscle cells (ASMCs) act as the main effector cells for airway remodeling; the proliferation and hypertrophy of which are involved in airway remodeling. Caveolin (Cav)- 1 is present on the surface of ASMCs, which is involved in cell cycle and signal transduction regulation, allowing ASMCs to change from proliferation to apoptosis. The extracellular signal-regulated kinase (ERK)1/2 signaling pathway is a common pathway regulated by various proliferative factors, which demonstrates a regulatory role in airway remodeling of asthma. There have been many studies on the correlation between vasoactive intestinal peptide (VIP) and airway reactivity and inflammation in asthma, but the functions and related mechanisms of ASMCs remain unclear. In this study, we established an airway remodeling model in asthmatic mice, and concluded that VIP inhibits airway remodeling in vivo. The in vitro effect of VIP on interleukin-13-induced proliferation of ASMCs was studied by examining the effects of VIP on expression of ERK1/2, phospho-ERK1/2 and Cav-1 in ASMCs, as well as changes in cell cycle distribution. VIP inhibited phosphorylation of the ERK1/2 signaling pathway and expression of Cav-1 on ASMCs and decreased the proportion of S phase cells in the cell cycle, thus inhibiting the proliferation of ASMCs. This study provides a novel therapeutic mechanism for the treatment of asthma.

Epigallocatechin-3-gallate inhibits inflammation and epithelial­mesenchymal transition through the PI3K/AKT pathway via upregulation of PTEN in asthma.

Asthma is a chronic disease associated with hyperresponsiveness, obstruction and remodeling of the airways. Epithelial-mesenchymal transition (EMT) has an important role in these alterations and may account for the accumulation of subepithelial mesenchymal cells, thus contributing to airway hyperresponsiveness and remodeling. Epigallo-catechin­3­gallate (EGCG), which is a type of polyphenol, is the most potent ingredient in green tea, and exhibits antibacterial, antiviral, antioxidative, anticancer and chemopreventive activities. Recently, numerous studies have investigated the protective effects of EGCG against asthma and other lung diseases. In the present study, the role of EGCG in ovalbumin (OVA)­challenged asthmatic mice was determined. In addition, the inhibitory effects of EGCG against transforming growth factor (TGF)­ß1­induced EMT and migration of 16HBE cells, and the underlying mechanisms of the phosphatidylinositol 3­kinase/protein kinase B (PI3K/Akt) signaling pathway, were investigated by immunofluorescence, Transwell, wound healing assay and western blot analysis, respectively. The results indicated that EGCG may suppress inflammation and inflammatory cell infiltration into the lungs of OVA­challenged asthmatic mice, and may also inhibit EMT via the PI3K/Akt signaling pathway through upregulating the expression of phosphatase and tensin homolog (PTEN) in vivo and in vitro. The present study also revealed the anti­migratory effects of EGCG in TGF­ß1­induced 16HBE cells, thus suggesting it may reduce airway remodeling. The present study provides a novel insight into understanding the protective effects of EGCG on airway remodeling in asthma, and indicates that EGCG may be useful as an adjuvant therapy for bronchial asthma.

Gender and age affect the levels of exhaled nitric oxide in healthy children.

Asthma is a chronic inflammatory disorder of the lung and diagnosis is difficult in children. The measurement of fractional exhaled nitric oxide (FeNO) may be useful in the diagnosis and monitoring of treatments. A number of factors affect FeNO levels and their influence varies across countries and regions. This study included 300 healthy students, aged from 6 to 14 years, who participated voluntarily. A comprehensive medical survey was used and measurements of FeNO levels and spirometric parameters were recorded in Shenyang, China. We observed that the median FeNO was 11 ppb (range, 8-16 ppb) in children from the northern areas of China. For males, the median level was 13 ppb (range, 9-18 ppb) and the median level was 10 ppb (range, 8-14 ppb) for females. There was a significant difference between males and females (P= 0.007) and age was correlated with FeNO (R2= 0.6554), while weight, height, body mass index (BMI), forced vital capacity (FVC), forced expiratory volume (FEV1), FEV1/FVC and peak expiratory flow (PEF) had no correlation with FeNO. In conclusion, the median FeNO is 11 ppb (range, 8-16 ppb) in male and female healthy children from northern areas of China and is affected by gender and age.

[Alterations of SP-A, SP-D and KL-6 in serum and bronchoalveolar lavage fluid in children with Mycoplasma pneumoniae pneumonia].

OBJECTIVE: 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). METHOD: 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. RESULT: 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). CONCLUSION: 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.

[Changes to surfactant proteins in the bronchoalveolar lavage fluid and serum of children with Mycoplasma pneumoniae pneumonia].

OBJECTIVE: 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. METHODS: 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. RESULTS: 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). CONCLUSIONS: Serum SP-D content may serve as a biomarker for evaluating the severity of pulmonary infection in children with community-acquired pneumonia.

[Expression of RANTES in the lung tissue of asthmatic rats, and the intervention effect of vitamin D on RANTES expression].

OBJECTIVE: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.

[Relationship between alveolar epithelial type II cells and pulmonary surfactant protein A levels in young rats with acute lung injury].

OBJECTIVE: 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. METHODS: 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. RESULTS: 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). CONCLUSIONS: 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.

[Changes of pulmonary surfactant protein A in young rats with acute lung injury induced by lipopolysaccharide].

OBJECTIVE: 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. METHODS: 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. RESULTS: 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). CONCLUSIONS: 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.

Effects of dexamethasone on the ultrastructure of alveolar type II cells in young rats with lipopolysaccharide-induced acute lung injury.

OBJECTIVE: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.

Effect of dexamethasone on the content of pulmonary surfactant protein D in young rats with acute lung injury induced by lipopolysaccharide.

OBJECTIVE: 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. METHODS: 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. RESULTS: 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). CONCLUSIONS: 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.

[Serum procalcitonin levels in children with bacterial or viral meningitis].

OBJECTIVE: To investigate the ability of serum procalcitonin (PCT) to differentiate between bacterial and viral meningitis. METHODS: 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. RESULTS: 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. CONCLUSIONS: The measurement of serum PCT levels may be of value in the differential diagnosis of meningitis due to either bacterial or viruses.

[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].

OBJECTIVE: 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. METHODS: 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. RESULTS: 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). CONCLUSIONS: 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.