| Objectives: Neonatal respiratory distress syndrome (NRDS) is a critical disease in preterm infants. Due to the mechanical ventilation and surfactant replacement therapy adopted in treatment of NRDS, more and more preterm infants with NRDS have survived, but many of them frequently develop lung inflammation and injury. A growing body of literature suggests that persistent lung inflammation may play an important role in the pathogenesis of NRDS. In preterm infants, one of the predominantly inflammatory cells in the airway is alveolar macrophage (AM), which exhibits both phagocytotic and secretory function after being activated. AM activation is an initial event in the pathogenesis of lung inflammatory reactions. Neonates are vulnerable to be infected by Gram-negative(G-) bacteria. Lipopolysaccharide(LPS) is part of the outer structure of the cell wall of G-bacteria. CD11b/CD18 and mCD14 are both recognition receptors for LPS on the surface of AM, and they can mediate the activation of AM by LPS. At the same time, many cytokines, such as interleukin-1 β(IL-1 β) and interleukin-8(IL-8), are also involved in the course of pulmonary infection and injury. Increasing evidence suggests an important role for mCD14 and CD11b/CD18 expression on AM in the pathogenesis of various inflammatory diseases in mature hosts, such as adult RDS and sepsis. However, our knowledge about the mechanism of mCD14 and CD11b/CD18 expression on AM in the pathogenesis of NRDS in preterm infants is not yet fully understood, therefore we investigated this mechanism in mechanically ventilated neonates with respiratory distress syndrome. Methods: For the study, the preterm infants were divided into 2 groups, and all of them were admitted to the neonatal intensive care unit of Hebei Provincial Children's Hospital from Mar 1st, 2003 to Dec 30th, 2003. The experimental group consisted of 15 preterm infants with the diagnosis of acute respiratory failure and radiologic findings consistent with NRDS, and without systemic infectious diseases [ male/female= 9/6 ; gestational age of ( 30.53 ±1.55 ) weeks; postnatal age of ( 3.27 ±0.46 ) days; body weight: ( 1.51 ±0.07 ) kg; cesarotomy/eutocia=10/5 ] . The control group included 15 preterm infants with acute respiratory failure due to diseases of the central nervous system, such as critical HIE, and without respiratory disorders and other systemic infectious diseases [ male/female= 8/7 ; gestational age of ( 31.27 ±1.60 ) weeks; postnatal age of ( 3.47 ±0.52 ) days; body weight: ( 1.52 ±0.09 ) kg; cesarotomy/eutocia=9/6]. All of the infants were intubated and mechanically ventilated. Serial samples of airway aspiratesdisease and intubating. The expression of mCD14 or CD11b/CD18 on AM (the percentage of mCD14 or CD11b/CD18 positive AM) was analyzed with flow cytometry . Enzyme-linked immunosorbent assay (ELISA) was performed for detecting the concentrations of IL-1βand IL-8 in AA after inclusion of the last patient. SAS 6.12 statistical software was used to process the data. All of the values are expressed as mean±SD. t test, linear correlation and chi-square test (Fisher's exact test ) were used for statistical analysis. Differences were considered statistically significant when P value < 0.05. Results: 1. ①The percentage of mCD14 positive AM in experimental group ([54.772±17.341)%] was higher than that in control group [(14.023±10.713)%] , t=-7.7392,P<0.001; ②The expression of CD11b on AM in experimental group was [(72.920±14.968)%], which was significantly higher than that in control group [(13.792±9.024)%] , t=-13.1027,P<0.001; ③The expression of CD18 on AM in experimental group ([83.941±11.581)%] was higher than that in control group [(27.651±19.880)%] , t=-9.4754,P<0.001. 2. ①The concentration of IL-1βin the AA supernatant of experimental group [(263.220±69.015)pg/ml] was higher than that of control group [(73.979±40.850)pg/ml],t=-9.1389 , P<0.001 ;②The level of IL-8 in the AA supernatant of experimental group was [(377.564±165.867)pg/ml], which was higher than that of control gro...
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