Surfactant Replacement Therapy in Premature Babies with Respiratory Distress Syndrome: Factors Affecting the Response to Surfactant and Comparison of Outcome from 1982–86 and 1987–91

Konishi, Mineo; Chida, Shoichi; Shimada, S.; Kasai, T; Murakami, Yoichi; Cho, Kazutoshi; Fujii, Yutaka; Maeta, Haruo; Fujiwara, Tetsuro

doi:10.1111/j.1442-200x.1992.tb01021.x

Cited by 22 publications

(20 citation statements)

References 27 publications

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“…Infection and asphyxia in neonates with respiratory distress syndrome are thought to worsen an already impaired surfactant system (35). Injury to the alveolar epithelial barrier, as seen in acute respiratory distress, will lead to increased permeability, allowing leakage of large amounts of plasma proteins into the alveolar space, and a considerable amount of alveolar surfactant components will permeate the circulation (36,37).…”

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confidence: 99%

Surfactant Protein D in Newborn Infants: Factors Influencing Surfactant Protein D Levels in Umbilical Cord Blood and Capillary Blood

et al. 2005

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Surfactant protein D (SP-D) is a collectin that plays an important role in the innate immune system. The role of SP-D in the metabolism of surfactant is as yet quite unclear. The aims of this study were to establish normal values of SP-D in the umbilical cord blood and capillary blood of mature newborn infants and to assess the influence of perinatal conditions on these levels. A total of 458 infants were enrolled in the present study. Umbilical cord blood was drawn at the time of birth and capillary blood at age 4 to 10 d. The concentration of SP-D in umbilical cord blood and capillary blood was measured by enzyme-linked immunosorbent assay. The median concentration of SP-D in umbilical cord blood was 392.1 ng/mL and was found to be influenced by maternal smoking and labor. The median concentration of SP-D in capillary blood was 777.5 ng/mL and was found to be influenced by the mode of delivery, the highest levels being observed in infants born by cesarean section. It was concluded that SP-D concentrations in umbilical cord blood and capillary blood are highly variable and depend on several perinatal conditions. Further studies are needed to elucidate the effect of respiratory distress and infection on SP-D concentrations. Collectins are oligomeric molecules consisting of carbohydrate recognition domains attached to collagen-like regions (5). In humans, three well-studied collectins are known at present (6). These are MBL, which is a serum protein, SP-A, and SP-D. SP-A and SP-D are mainly produced in the epithelial cells of the lungs, but SP-D is also found in epithelial cells and secretory glands in the gastrointestinal tract and in other tissues (7). SP-D plays an important role in the innate immune defense by binding to specific carbohydrate and lipid structures on the surface of microorganisms: bacteria, viral particles, fungi, and protozoa (8 -11). This binding mediates effector mechanisms like aggregation, chemotaxis, mediation of phagocytosis, and permeabilization (12). Pulmonary infections in adults have been shown to cause significant changes in SP-D levels (13). Whether SP-D has a role in avoiding infections in newborn babies has to our knowledge not been investigated.Both structural and promoter variants are known for the MBL gene, and several alleles correlate with low values of MBL in serum and lead to an increased risk of infectious diseases in otherwise healthy children (14,15). Three polymorphisms have been identified in the coding sequence of human SP-D: codons corresponding to amino acid residue 11 (Met11Thr), residue 160 (Ala160Thr), and residue 270 (Ser270Thr) in the mature protein. Two clinical studies have associated the SP-D variants of amino acid 11 with disease. The SP-D allele coding for methionine 11 has been associated with severe respiratory syncytial virus infection in infants, whereas threonine 11 has been suggested to increase susceptibility to tuberculosis (16,17). However, the connection between structural genetic variance and serum SP-D has not been investigated. We have perfo...

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confidence: 99%

Surfactant Protein D in Newborn Infants: Factors Influencing Surfactant Protein D Levels in Umbilical Cord Blood and Capillary Blood

et al. 2005

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“…We studied both the mucosal and systemic IgA Ab response, as well as the protective efficacy they conferred in comparison with a s.c. inoculation. Surfacten has been used in the treatment of respiratory distress syndrome in premature babies (20). To our surprise, intranasal administration of pulmonary surfactant and Surfacten as mucosal adjuvants complexed with IAV HA vaccine both induced mucosal neutralizing IgA against IAV in the airway as effectively as the most potent mucosal adjuvant, CT, though Surfacten (up to 0.2 g) did not induce systemic IgG or IgA.…”

Section: Modified Pulmonary Surfactant Is a Potent Adjuvant Thatmentioning

confidence: 91%

Modified Pulmonary Surfactant Is a Potent Adjuvant That Stimulates the Mucosal IgA Production in Response to the Influenza Virus Antigen

Mizuno

Ide-Kurihara

Ichinomiya

et al. 2006

The Journal of Immunology

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The intranasal administration of influenza hemagglutinin (HA) vaccine with Surfacten, a modified pulmonary surfactant free of antigenic c-type lectins, as a mucosal adjuvant induced the highest protective mucosal immunity in the airway. The intranasal immunization of mice with HA vaccine (0.2 μg)-Surfacten (0.2 μg) selectively induced the neutralizing anti-HA IgA, but not IgG, and conferred nearly maximal protection in the airway, without inducing a systemic response. In contrast, intranasal inoculation of vaccine with 0.2 μg of the potent mucosal adjuvant cholera toxin B* (CT-B*), prepared by adding 0.2% native CT to the B subunit of CT, induced both anti-HA IgA and IgG in the airway and in the serum. The intranasal administration of HA vaccine alone induced a limited amount of mucosal IgA against influenza virus. Although the s.c. administration of HA vaccine prominently induced serum IgG and IgA, Surfacten and CT-B* did not enhance their induction, and the concentrations of Abs leaking into the airways were insufficient to prevent viral multiplication. The intranasal administration of HA-Surfacten stimulated the expression of MHC class II, CD40, and CD86 molecules in the CD11c-positive cells isolated from the nasal mucosa, but not the expression of cells from the lungs or spleens. Lymphocytes isolated from the airway mucosa after intranasal HA-Surfacten immunization prominently induced TGF-β1 which, compared with inoculation without Surfacten, promoted an Ag-specific mucosal IgA response. Surfacten alone, however, did not induce TGF-β1. Our observations suggest that Surfacten, by mimicking the natural surfactant, is an effective mucosal adjuvant in the process of airway immunization.

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“…Infection and asphyxia in neonates with RDS are thought to worsen an already impaired surfactant system [2]. In permeable lung, a large amount of plasma proteins will leak into alveolar space on one side, and a considerable amount of alveolar surfactant components including SP-A will permeate to the circulation on the other side [18].…”

Section: Discussionmentioning

confidence: 99%

“…Clinical studies have clearly shown that surfactant replacement therapy for respiratory distress syndrome (RDS) of premature infants is effective, and that prophylactic administration of surfactant is superior to rescue treatment with surfactant for fully-developed RDS [1,2]. Prediction of developing RDS is essential for the optimization of surfactant replacement therapy.…”

Section: Introductionmentioning

confidence: 99%

Prediction of Respiratory Distress Syndrome by the Level of Pulmonary Surfactant Protein A in Cord Blood Sera

et al. 2000

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The purpose of this study was to determine the utility of measuring the level of pulmonary surfactant protein A (SP-A) in cord blood sera to predict for respiratory distress syndrome (RDS). SP-A levels in cord blood sera from 48 infants born at gestational ages < 32 weeks were measured by a sandwich ELISA system. Mean value of SP-A in cord blood was 5.8 ng/ml in cases with RDS and 15.1 ng/ml in those without RDS (p = 0.002). The best cut-off point of cord blood SP-A to predict RDS was determined as 10 ng/ml. The sensitivity and the specificity of the cut-off point for predicting RDS were 81 and 76%, respectively. Multivariate regression analysis showed that high SP-A level in cord blood, premature rupture of the membranes longer than 24 h and heavy birth weight were all significantly related to the non-RDS outcome.

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Surfactant Replacement Therapy in Premature Babies with Respiratory Distress Syndrome: Factors Affecting the Response to Surfactant and Comparison of Outcome from 1982–86 and 1987–91

Cited by 22 publications

References 27 publications

Surfactant Protein D in Newborn Infants: Factors Influencing Surfactant Protein D Levels in Umbilical Cord Blood and Capillary Blood

Surfactant Protein D in Newborn Infants: Factors Influencing Surfactant Protein D Levels in Umbilical Cord Blood and Capillary Blood

Modified Pulmonary Surfactant Is a Potent Adjuvant That Stimulates the Mucosal IgA Production in Response to the Influenza Virus Antigen

Prediction of Respiratory Distress Syndrome by the Level of Pulmonary Surfactant Protein A in Cord Blood Sera

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