Pulmonary Surfactant Protein A Enhances the Host-defense Mechanism of Rat Alveolar Macrophages

Iwaarden, Freek van; Welmers, Berris; Verhoef, J.; Haagsman, Henk P.; Golde, L.M.G. Van

doi:10.1165/ajrcmb/2.1.91

Cited by 357 publications

(242 citation statements)

References 25 publications

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“…Both of these proteins are important stimulants of macrophage function (38,39). In addition, SP-A plays a key role in regulating surfactant secretion and recycling (40), and it increases resistance to inhibition by serum proteins.…”

Section: Herting Etalmentioning

confidence: 99%

Experimental Neonatal Group B Streptococcal Pneumonia: Effect of a Modified Porcine Surfactant on Bacterial Proliferation in Ventilated Near-Term Rabbits

et al. 1994

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jWe studied bacterial proliferation in relation to surfac-bacterial numbers in both groups ventilated for 5 h, but tant treatment in a model of neonatal group B streptococcal values for surfactant-treated animals (8.96 + 0.38) were (GBS) pneumonia. Surfactant (Curosurf) was isolated from lower than those for animals receiving saline (9.46 + 0.50; pig lungs with a method preserving only polar lipids and p < 0.05). After 5 h, 96% of GBS-infected animals had hydrophobic proteins. Near-term rabbit fetuses were ven-positive blood cultures. Light microscopic examination of tilated in a body plethysmograph system. At 15 min, a the right lung of GBS-infected animals revealed inflammasuspension of GBS strain 090 Ia LD (5 mL/kg, concentra-tory changes that tended to be less prominent in surfactanttion -109/mL) was instilled intratracheally. At 30 min, treated rabbits. We conclude that intratracheal inoculation surfactant (n = 12) or sterile saline (n = 13) was adminis-of near-term rabbits with GBS resulted in a significant tered via the airways (2.5 mL/kg). A control group (n = 12) bacterial proliferation during 5 h of ventilation and that received the same volumes of saline. After 5 h the animals bacterial growth was mitigated by treatment with surfacwere killed, and samples for blood cultures and blood gases tant. (Pediatr Res 36: [784][785][786][787][788][789][790][791] 1994) were taken from the heart. The left lung was aseptically removed, weighed, homogenized, serially diluted, and cultured on blood agar plates. The results were expressed as Abbreviations mean log,, colony forming units/g lung + SD. Compared CFU, colony forming unit with animals (n = 12) killed immediately after GBS instil-GBS, group B streptococcus lation (8.13 2 0.54), there was a significant increase in RDS, respiratory distress syndrome GBS is a frequently encountered pathogen in the neonatal period (1). Vaginal colonization with GBS is commonly found in pregnant women. Vertical transmission occurs in approximately 40% of deliveries, but only approximately 1% of neonates born to these mothers develop clinical signs of GBS infection (2). If diagnosis and treatment are delayed, the condition has a substantial mortality, especially in premature infants (2). Susceptibility to GBS infections depends on host defense factors (e-g. lack of type-specific opsonizing antibodies) and Received January 26, 1994; accepted June 21, 1994. virulence factors (e-g. polysaccharide capsule) of the infecting microorganism (3-6).Animal models using rabbits, mice, and rats have been used for studies of experimental neonatal GBS infections (7)(8)(9). In these studies, the animals were either infected b y injection (7, 9) o r a bacterial suspension was nebulized via the airways in spontaneously breathing animals (8,9). Our intention was t o develop a model of GBS pneumonia in ventilated newborn rabbits infected b y intratracheal injection of a bacterial suspension.RDS and GBS pneumonia are difficult to differentiate o n clinical grounds (lo), and therefore neonates with ...

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Section: Herting Etalmentioning

confidence: 99%

Experimental Neonatal Group B Streptococcal Pneumonia: Effect of a Modified Porcine Surfactant on Bacterial Proliferation in Ventilated Near-Term Rabbits

et al. 1994

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“…However, the carbohydrate recognition domain of SP-A is more generic, having a wider spectrum of microbial ligands that include lipid and protein moieties (12)(13)(14). Previous studies determined that SP-A is an opsonin for the Gram-positive S. aureus-enhancing phagocytosis of this pathogen by macrophages (15)(16)(17). On the other hand, binding of SP-A to S. aureus does not appear to involve lipoteichoic acid (LTA) or peptidoglycan, the major cell wall glycoconjugates of Gram-positive bacteria (18).…”

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confidence: 99%

Surfactant Protein A (SP-A)-mediated Clearance of Staphylococcus aureus Involves Binding of SP-A to the Staphylococcal Adhesin Eap and the Macrophage Receptors SP-A Receptor 210 and Scavenger Receptor Class A

Sever-Chroneos

Krupa

Davis

et al. 2011

Journal of Biological Chemistry

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There is limited knowledge about host factors that facilitate eradication of Staphylococcus aureus infection in the lung. Methicillin-resistant S. aureus has remained a major cause of hospital-and health care-associated pneumonia since its appearance over 40 years ago and has recently become a more prominent etiology in community acquired pneumonia. Colonization of nasal epithelium with S. aureus, a normal occurrence in over 20% of the population, increases the risk for the development of staphylococcal pneumonia (1). Furthermore, S. aureus co-infections are a major complication contributing to high morbidity and mortality during both pandemic and seasonal influenza virus pneumonia (2). S. aureus deploys a combination of virulence factors, including adhesins, toxins, and immunomodulatory molecules, that facilitate infection of different host tissues (3, 4).Surfactant protein A (SP-A) 3 is a crucial component of the pulmonary innate immune system in the alveolar spaces (5, 6). SP-A is the major protein constituent of pulmonary surfactant; it is involved in organization of large aggregate surfactant phospholipids lining the alveolar surface and acts as an opsonin for pathogens (7). SP-A is incorporated in the tubular myelin fraction of pulmonary surfactant that covers the alveolar lining fluid of the distal airway epithelium. The presence of pathogen-derived molecules may trigger reorganization of surfactant lipids (8 -11) and exposure of SP-A to bind pathogens at points of entry on the surfactant interface. Alveolar macrophages in the aqueous hypophase may then patrol areas of disturbance on the surfactant layer binding SP-A-opsonized bacteria. SP-A binds pathogens via a carboxyl-terminal carbohydrate recognition domain in a calcium-dependent manner. Amino-terminal collagen-like and coiled-coil do-

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“…Surfactant protein A (SP-A), a 34-to 36-kDa glycoprotein, plays a major role in the modulation of innate host defense in the lung (7,16,21,41,48,52). SP-A has been shown to stimulate chemotaxis of macrophages (70), enhance phagocytosis (11,34,44,46,47,50,63), induce generation of reactive oxidants (61), regulate the nitric oxide production (1,23), and influence the proliferation of immune cells (2,38) and the production of proinflammatory cytokines (3,27,37,39,68,69). SP-A can bind to receptors on the macrophage membrane (35).…”

mentioning

confidence: 99%

SP-A1 and SP-A2 variants differentially enhance association ofPseudomonas aeruginosawith rat alveolar macrophages

Mikerov¹,

Umstead²,

Huang³

et al. 2005

American Journal of Physiology-Lung Cellular and Molecular Phys

125

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aeruginosa. Two genes, SP-A1 and SP-A2, encode human SP-A. We hypothesized that genetically determined differences in the activity of SP-A1 and SP-A2 gene products exist. To test this, we studied association of a nonmucoid P. aeruginosa strain (ATCC 39018) with rat alveolar macrophages in the presence or absence of insect cellexpressed human SP-A variants. We used two trios, each consisting of SP-A1, SP-A2, and their coexpressed SP-A1/SP-A2 variants. We tested the 6A 2 and 6A 4 alleles (for SP-A1), the 1A 0 and 1A alleles (for SP-A2), and their respective coexpressed SP-A1/SP-A2 gene products. After incubation of alveolar macrophages with P. aeruginosa in the presence of the SP-A variants at 37°C for 1 h, the cell association of bacteria was assessed by light microscopy analysis. We found 1) depending on SP-A concentration and variant, SP-A2 variants significantly increased the cell association more than the SP-A1 variants (the phagocytic index for SP-A1 was ϳ52-95% of the SP-A2 activity); 2) coexpressed variants at certain concentrations were more active than single gene products; and 3) the phagocytic index for SP-A variants was ϳ18 -41% of the human SP-A from bronchoalveolar lavage. We conclude that human SP-A variants in vitro enhance association of P. aeruginosa with rat alveolar macrophages differentially and in a concentration-dependent manner, with SP-A2 variants having a higher activity compared with SP-A1 variants.

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Pulmonary Surfactant Protein A Enhances the Host-defense Mechanism of Rat Alveolar Macrophages

Cited by 357 publications

References 25 publications

Experimental Neonatal Group B Streptococcal Pneumonia: Effect of a Modified Porcine Surfactant on Bacterial Proliferation in Ventilated Near-Term Rabbits

Experimental Neonatal Group B Streptococcal Pneumonia: Effect of a Modified Porcine Surfactant on Bacterial Proliferation in Ventilated Near-Term Rabbits

Surfactant Protein A (SP-A)-mediated Clearance of Staphylococcus aureus Involves Binding of SP-A to the Staphylococcal Adhesin Eap and the Macrophage Receptors SP-A Receptor 210 and Scavenger Receptor Class A

SP-A1 and SP-A2 variants differentially enhance association ofPseudomonas aeruginosawith rat alveolar macrophages

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