title: Lung function and bacterial proliferation in experimental neonatal pneumonia in ventilated rabbits exposed to monoclonal antibody to surfactant protein A.
abstract: Surfactant protein A (SP-A) increases the resistance of surfactant to inhibition by plasma and other proteins. In a previous study we found that a monoclonal anti-SP-A antibody (R 5) increased the sensitivity of surfactant to inhibition by fibrinogen in vivo and in vitro. SP-A has been shown to stimulate microbial phagocytosis and killing by alveolar macrophages. We hypothesized that using R 5 to inactivate SP-A in an animal model mimicking congenital group B streptococcal (GBS) pneumonia might result in increased bacterial proliferation and a deterioration in lung function. Newborn near term rabbits were delivered by Cesarean section, anesthetized, tracheotomized, and ventilated for 5 h in a plethysmograph system allowing measurement of dynamic lung-thorax compliance. Postnatally the animals received one intratracheal injection (5 ml/kg) of R 5, nonspecific IgG, or normal saline. At 30 min all animals received a standard dose of an encapsulated GBS strain by intratracheal injection. The number of bacteria (mean log10 CFU/g lung +/- S.D.; CFU = colony forming unit) was evaluated in lung homogenates. Histologic lung sections were judged by light microscopy. Bacterial proliferation was similar in rabbits treated with the monoclonal antibody (9.33 +/- 0.39; n = 14) and in control animals receiving saline (9.16 +/- 0.35; n = 14) or nonspecific IgG (9.26 +/- 0.31; n = 11). No significant differences were noted on the histologic analysis or in measurements of lung function. We conclude that intratracheal instillation of a monoclonal anti-SP-A antibody did not increase bacterial proliferation in GBS-infected newborn rabbits. These findings suggest that SP-A does not play an important role in protection against encapsulated GBS strains in the neonatal period.
authors.affiliation: Department of Pediatrics, University of Göttingen, Germany.
authors.forename: E
authors.initials: E
authors.lastname: Herting
authors.forename: D S
authors.initials: DS
authors.lastname: Strayer
authors.forename: C
authors.initials: C
authors.lastname: Jarstrand
authors.forename: B
authors.initials: B
authors.lastname: Sun
authors.forename: B
authors.initials: B
authors.lastname: Robertson
mesh_terms: D000818:Animals; D000831:Animals, Newborn / Q000276:immunology / Q000382:microbiology*; D000911:Antibodies, Monoclonal / Q000494:pharmacology*; D018410:Pneumonia, Bacterial / Q000276:immunology / Q000382:microbiology / Q000473:pathology / Q000503:physiopathology*; D011510:Proteolipids / Q000276:immunology*; D037662:Pulmonary Surfactant-Associated Protein A; D037661:Pulmonary Surfactant-Associated Proteins; D011663:Pulmonary Surfactants / Q000276:immunology*; D011817:Rabbits; D011897:Random Allocation; D051381:Rats; D012121:Respiration, Artificial; D012129:Respiratory Function Tests; D013290:Streptococcal Infections / Q000276:immunology / Q000382:microbiology / Q000473:pathology / Q000503:physiopathology*; D013292:Streptococcus agalactiae / Q000254:growth & development*
chemical_list: D000911:Antibodies, Monoclonal; D011510:Proteolipids; D037662:Pulmonary Surfactant-Associated Protein A; D037661:Pulmonary Surfactant-Associated Proteins; D011663:Pulmonary Surfactants