Effect of different surfactants on pulmonary group B streptococcal infection in premature rabbits☆,☆☆,★,★★
Section snippets
Animals
The animal procedures used in this study were approved by the Chancellor's Animal Research Committee of the University of California, Los Angeles, and met the standards of the National Institutes of Health. Time-dated, pregnant New Zealand white rabbits (Irish Farms, Norco, Calif.) underwent cesarean section on day 28 or 29 of gestation. Immediately thereafter, preterm pups were placed in warmed (37° C), humidified (75% relative humidity) incubators. Sufficient inspired oxygen was provided to
Group B streptococcal clearance in premature versus term neonatal lung
Birth weights, infective doses of GBS in the left lung at 0 hour, and the numbers of GBS present in the left lung at 4 hours after surfactant therapy are shown in Table II. The different groups of preterm rabbits did not differ in birth weight or initial inoculum of GBS after aerosol infection. Untreated premature rabbits inhaled fewer streptococci than did rabbits born by cesarean section at term. Nevertheless, these premature rabbits had nearly a sixfold increase in intrapulmonary GBS after 4
DISCUSSION
Although group B streptococcal pneumonia is a common cause of congenital pulmonary infection,22 it is infrequently responsible for nosocomial lung infections in intensive care nurseries.23 The growth of GBS in the lungs of preterm rabbits versus the progressive inactivation of this bacterium in the lungs of term and postnatal rabbits offers a rationale for the relative absence of group B streptococcal pneumonia in human beings beyond 3 days of age. Several factors explain the timely maturation
References (40)
- et al.
Improved outcome at 28 days of age for very low birth weight infants treated with a single dose of a synthetic surfactant
J PEDIATR
(1990) - et al.
Prevention of pulmonary alveolar macrophage proliferation in newborn rabbits by hyperoxia
J PEDIATR
(1988) - et al.
Lactoferrin and lysozyme deficiency in airway secretions: association with the development of bronchopulmonary dysplasia
J PEDIATR
(1992) - et al.
Artificial surfactant and natural surfactant: comparative study of the effects on premature rabbit lungs
Arch Dis Child
(1980) - et al.
Tracheal aspiration and its clinical correlates in the diagnosis of congenital pneumonia
Pediatrics
(1980) - et al.
Gram's stains of tracheal secretions predict neonatal bacteremia
Am J Dis Child
(1984) - et al.
Early-onset sepsis and pneumonia observed as respiratory distress syndrome: assessment of lung maturity
Am J Dis Child
(1980) - et al.
Correlation of clinical and pathologic findings in early onset neonatal group B streptococcal infection with disease severity and prediction of outcome
Pediatr Infect Dis J
(1988) Ten Centre Trial of Artificial Surfactant (artificial lung expanding compound) in very premature babies
BMJ
(1987)- et al.
Surfactant replacement therapy at birth: final analysis of a clinical trial and comparisons with similar trials
Pediatrics
(1988)
Hyperoxia damages phagocytic defenses of neonatal rabbit lung
J Appl Physiol
Surfactant therapy of newborn rabbits impairs lung macro-phage bactericidal activity
J Appl Physiol
Isolation of human surfactant from amniotic fluid and a pilot study of its efficacy in respiratory distress syndrome
Pediatrics
Double-blind, randomized trial of a calf lung surfactant extract administered at birth to very premature infants for prevention of respiratory distress syndrome
Pediatrics
Lung function in prematurely delivered rabbits treated with a synthetic surfactant
Am Rev Respir Dis
Randomized, controlled trial of exogenous surfactant for the treatment of hyaline membrane disease
Pediatrics
Structural and functional characterization of porcine surfactant isolated by liquid-gel chromatography
Growth of neonatal bacterial pathogens in clinically relevant surfactants
Pediatr Res
Electrolyte composition of pulmonary alveolar subphase in anesthetized rabbits
J Appl Physiol
Mechanisms and regulation of ion transport in adult mammalian alveolar type II pneumocytes
Am J Physiol
Cited by (40)
Surfactant Therapy for Acute Lung Injury and Acute Respiratory Distress Syndrome
2011, Critical Care ClinicsCitation Excerpt :The ability of exogenous surfactant therapy to improve acute respiratory symptoms in animal models of ALI/ARDS in vivo is similarly well documented (Box 2). Examples of animal models found to display acute improvements in arterial oxygenation and/or lung mechanics following surfactant therapy are acid aspiration,80–82 meconium aspiration,83–86 antilung serum,87 bacterial or endotoxin injury,88–93 pulmonary contusion,78 bilateral vagotomy,94 hyperoxia,95–99 in vivo lavage,100–105 N-nitroso-N-methylurethane injury,106–108 and viral pneumonia.109,110 Animals studies of acute injury are typically not designed to assess efficacy based on long-term outcomes.
Surfactant for Pediatric Acute Lung Injury
2008, Pediatric Clinics of North AmericaCitation Excerpt :The ability of exogenous surfactant therapy to reverse or mitigate acute respiratory pathology in animal models of ALI/ARDS also has been documented extensively (Box 1). Examples of animal studies showing benefits in acute lung function or mechanics following surfactant therapy include acid aspiration [82–84], meconium aspiration [85–88], anti-lung serum [89], bacterial or endotoxin injury [90–95], bilateral vagotomy [96], hyperoxia [97–101], in vivo lavage [102–107], N-nitroso-N-methylurethane (NNNMU) injury [108–110], and viral pneumonia [111,112]. These acute animal model studies typically did not address long-term outcomes.
Differential effect of surfactant and its saturated phosphatidylcholines on human blood macrophages
2007, Journal of Lipid ResearchCitation Excerpt :Although the concept of macrophages as targets of surfactant components is well known, investigation of these PC species, which are subject to changes during lung development (2, 3), is new. Moreover, the use of peripheral blood monocyte-derived macrophages contrasts to other studies on macrophages from lung lavage fluid: besides limited access to the latter, our experimental system offers the advantage of studying “surfactant-naïve” cells that are not yet primed within the alveolar environment, and corresponds to inflammatory processes in vivo, when the number of resident alveolar macrophages is reduced and blood monocytes are recruited to the alveolar space (20). Although for physiological conditions, macrophages in the alveolar spaces are subject to regulation by the whole phospholipoprotein complex of surfactant, the isolated action of individual phospholipid molecular species is important to define their role in the whole environmental scenario, and for clinical situations in which patients are only treated with the hydrophobic components of surfactant, namely the phospholipids and SP-B and -C or their synthetic analogs.
Effect of surfactant and specific antibody on bacterial proliferation and lung function in experimental pneumococcal pneumonia
2001, International Journal of Infectious Diseases
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From the Department of Pediatrics, University of California, Los Angeles, Medical Center, the Department of Pediatrics, University of California, Davis, Medical Center, the Clinical Research Division, Burroughs Wellcome Co., Research Triangle Park, North Carolina, the Department of Pediatrics, University of North Carolina at Chapel Hill, Ross Laboratories, Division of Abbott Laboratories, Columbus, Ohio, the Department of Clinical Chemistry, Danderyd Hospital, Danderyd, Sweden, and the Research Unit for Experimental Pathology, Karolinska Hospital, Stockholm, Sweden.
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Supported by National Institutes of Health grants HL40675 and HL/H35036, American Lung Association of California grant R-S900425, Food and Drug Administration grant 00012, and the Swedish Medical Research Council (project No. 3351) and Oscar II:s Jubileumsfond.
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Reprint requests: Michael P. Sherman, MD, University of Kansas Medical Center, 3901 Rainbow Blvd., Kansas City, KS 66160-7330.
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