SP-A enhances uptake of bacillus Calmette-Guerin by macrophages through a specific SP-A receptor

Weikert, Laura F.; Edwards, Kathryn M.; Chroneos, Zissis C.; Hager, Cynthia; Hoffman, Loren H.; Shepherd, Virginia L.

doi:10.1152/ajplung.1997.272.5.l989

Cited by 80 publications

(101 citation statements)

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“…However, the present ( Fig. 2A) and previous studies (23,26) showed that SP-A-opsonized bacteria induced secretion of TNF␣ in macrophages. TNF␣ is crucial for orchestrating recruitment of neutrophils and resolution of inflammation (59,60), whereas TNF␣ primes neutrophils to kill S. aureus infection in vivo (61).…”

Section: Sp-r210(dn) Macrophages Display Enhanced Non-opsoniccontrasting

confidence: 48%

“…SP-R210 Suppresses Growth of S. aureus Infection via Secretion of TNF␣-Earlier studies in rat bone marrow-derived macrophages demonstrated that SP-R210 mediates the phagocytosis of SP-A-opsonized Mycobacterium bovis BCG and killing of intracellular bacteria through secretion of TNF␣ (23,26). Previous studies determined that TNF␣ is crucial for clearance of S. aureus in vivo (43).…”

Section: Sp-r210 S Binds Sp-a-opsonized S Aureus-previouslymentioning

confidence: 99%

“…However, SP-R210 L is only expressed in mature macrophages (25). Earlier studies showed that SP-R210 mediates phagocytosis and killing of SP-A-opsonized Mycobacterium bovis BCG (SP-A-BCG) by bone marrowderived macrophages (23). These studies showed that ligation of SP-R210 with SP-A-BCG complexes enhanced expression of TNF␣ and nitric oxide that enabled macrophages to control mycobacterial growth (23,26).…”

mentioning

confidence: 99%

“…Earlier studies showed that SP-R210 mediates phagocytosis and killing of SP-A-opsonized Mycobacterium bovis BCG (SP-A-BCG) by bone marrowderived macrophages (23). These studies showed that ligation of SP-R210 with SP-A-BCG complexes enhanced expression of TNF␣ and nitric oxide that enabled macrophages to control mycobacterial growth (23,26). On the other hand, SP-R210 can control the level of inflammatory cells and mediators in the presence of mycobacterial extracts, suggesting a secondary role of SP-R210 in immune homeostasis (27).…”

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confidence: 99%

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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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Section: Sp-r210(dn) Macrophages Display Enhanced Non-opsoniccontrasting

confidence: 48%

Section: Sp-r210 S Binds Sp-a-opsonized S Aureus-previouslymentioning

confidence: 99%

mentioning

confidence: 99%

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confidence: 99%

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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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“…AMs bind, phagocytose, and kill pathogens by producing reactive oxygen/nitrogen intermediates (108), such as NO (109), and trigger specific immunity by presenting antigen to T lymphocytes (110). SP-A induces opsonization of pathogens by binding mannose and N-acetylglucosamine residues on microbial cell walls (111), which enhances their attachment and phagocytosis by AMs via specific and nonspecific receptors (112)(113)(114)(115)(116)(117)(118). SP-A also induces AM chemotaxis and killing that stimulate release of reactive oxygen intermediates, such as NO (107,118).…”

Section: Humoral Immunitymentioning

confidence: 99%

Lung Transplantation: Opportunities for Research and Clinical Advancement

Wilkes¹

2006

Am J Respir Crit Care Med

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Lung transplantation is the only definitive therapy for many forms of end-stage lung diseases. However, the success of lung transplantation is limited by many factors: (1 ) Too few lungs available for transplantation due to limited donors or injury to the donor lung; (2 ) current methods of preservation of excised lungs do not allow extended periods of time between procurement and implantation; (3 ) acute graft failure is more common with lungs than other solid organs, thus contributing to poorer short-term survival after lung transplant compared with that for recipients of other organs; (4 ) lung transplant recipients are particularly vulnerable to pulmonary infections; and (5 ) chronic allograft dysfunction, manifest by bronchiolitis obliterans syndrome, is frequent and limits long-term survival. Scientific advances may provide significant improvements in the outcome of lung transplantation. The National Heart, Lung, and Blood Institute convened a working group of investigators on June 14-15, 2004, in Bethesda, Maryland, to identify opportunities for scientific advancement in lung transplantation, including basic and clinical research. This workshop provides a framework to identify critical issues related to clinical lung transplantation, and to delineate important areas for productive scientific investigation. Keywords: allograft dysfunction; infection; ischemia-reperfusion injury; lung transplantation; obliterative bronchiolitis; rejectionThe transplantation of organs offers the promise of life-saving and life-enhancing therapy for a variety of ailments. Lung transplantation (LTx) has become an acceptable therapy to palliate patients with a variety of end-stage lung diseases. However, lung transplantation has not turned out to be a panacea for chronic lung disease because of significant limitations in the entire transplant process (Figure 1). First, there are not nearly enough suitable donor lungs to meet the needs of all patients with end-stage lung disease. As a result, more patients die waiting for transplants than from mortality associated with a lung transplant. Second, early graft survival after LTx is worse than for other types of organs transplanted (1). Finally, late survival after successful LTx is hampered by the development of chronic allograft dysfunction and by the life-limiting complications associated with conventional immunosuppressive medications. Two factors impede progress to address these problems: (1 ) lung transplant centers lack the infrastructure to facilitate prospective, multicenter clinical studies of sufficient power to address clinical questions and (2 ) there are too few investigators studying the biology of lung transplantation.The NHLBI convened a workshop on June 14-15, 2004, to better understand these complex problems and to identify strategies to address these and prioritize them. The topics addressed by participants were wide-ranging. They included the following: lung use rates from conventional brain-dead organ donors; safe limits for donor lung function; consideration o...

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