Pulmonary Surfactant Phosphatidylglycerol Inhibits Mycoplasma pneumoniae-stimulated Eicosanoid Production from Human and Mouse Macrophages.
Summary of "Pulmonary Surfactant Phosphatidylglycerol Inhibits Mycoplasma pneumoniae-stimulated Eicosanoid Production from Human and Mouse Macrophages."
Mycoplasma pneumoniae is a human pathogen causing respiratory infections that are also associated with serious exacerbations of chronic lung diseases. Membranes and lipoproteins from M. pneumoniae induced a 4-fold increase in arachidonic acid (AA) release from RAW264.7 and a 2-fold increase in AA release from primary human alveolar macrophages. The bacterial lipoprotein mimic and TLR2/1 agonist Pam3Cys and the TLR2/6 agonist MALP-2 produced effects similar to those elicited by M. pneumoniae in macrophages by inducing the phosphorylation of p38(MAPK) and p44/42(ERK1/2) MAP kinases and cyclooxygenase-2 (COX-2) expression. M. pneumoniae induced the generation of prostaglandins PGD(2) and PGE(2) from RAW264.7 cells and thromboxane B(2) (TXB(2)) from human alveolar macrophages. Anti-TLR2 antibody completely abolished M. pneumoniae-induced AA release and TNFα secretion from RAW264.7 cells and human alveolar macrophages. Disruption of the phosphorylation of p44/42(ERK1/2) or inactivation of cytosolic phospholipase A(2)α (cPLA(2)α) completely inhibited M. pneumoniae-induced AA release from macrophages. The minor pulmonary surfactant phospholipid, palmitoyl-oleoyl-phosphatidylglycerol (POPG), antagonized the proinflammatory actions of M. pneumoniae, Pam3Cys, and MALP-2 by reducing the production of AA metabolites from macrophages. The effect of POPG was specific, insofar as saturated PG, and saturated and unsaturated phosphatidylcholines did not have significant effect on M. pneumoniae-induced AA release. Collectively, these data demonstrate that M. pneumoniae stimulates the production of eicosanoids from macrophages through TLR2, and POPG suppresses this pathogen-induced response.
From the Departments of Medicine and.
This article was published in the following journal.
Name: The Journal of biological chemistry
- PubMed Source: http://www.ncbi.nlm.nih.gov/pubmed/21205826
- DOI: http://dx.doi.org/10.1074/jbc.M110.170241
The appropriate choice of antibiotics against Mycoplasma pneumoniae infection has become difficult, as the prevalence of macrolide-resistant M. pneumoniae has increased.
To explore the features of pulmonary dysfunction in children with Mycoplasma pneumoniae pneumonia (MPP) with different chest imaging findings.
The associations of radiological features with clinical and laboratory findings in Mycoplasma pneumoniae infection are poorly understood. The purpose of this study was to assess the associations.
Mycoplasma pneumoniae is one of the causative organisms of community-acquired pneumonia which is found commonly in younger patients. Extrapulmonary complications similar to autoimmune disease are caus...
Mycoplasma pneumoniae (MP) pneumonia is a self-limiting disease, but some patients complain of progressive pneumonia, despite of appropriate antibiotic treatment. We aimed to introduce the role of imm...
Several case report showed that the co-infection of Mycoplasma pneumoniae in patients with pulmonary tuberculosis. The aim of this study is to elucidate the prevalence and its clinical sig...
Inherited deficiencies in any one of 3 genes (surfactant protein B, surfactant protein C, and ATP-binding cassette transporter A3) can cause neonatal respiratory distress syndrome by disru...
The objective of this pilot study is to examine the feasibility and safety of performing a larger trial to assess outcomes following treatment of meconium aspiration syndrome with surfacta...
The proposed study aims to provide current information, etiology and outcome of community-acquired pneumonia (CAP), risk factors for for CAP in isolates of Streptococcus pneumoniae and Ha...
To determine if surfactant administration at birth in infants at high risk for respiratory distress syndrome (RDS) modified the clinical course of the syndrome.
Medical and Biotech [MESH] Definitions
A pulmonary surfactant associated protein that plays a role in alveolar stability by lowering the surface tension at the air-liquid interface. It is a membrane-bound protein that constitutes 1-2% of the pulmonary surfactant mass. Pulmonary surfactant-associated protein C is one of the most hydrophobic peptides yet isolated and contains an alpha-helical domain with a central poly-valine segment that binds to phospholipid bilayers.
A pulmonary surfactant associated-protein that plays an essential role in alveolar stability by lowering the surface tension at the air-liquid interface. Inherited deficiency of pulmonary surfactant-associated protein B is one cause of RESPIRATORY DISTRESS SYNDROME, NEWBORN.
An abundant pulmonary surfactant-associated protein that binds to a variety of lung pathogens and enhances their opsinization and killing by phagocytic cells. Surfactant protein D contains a N-terminal collagen-like domain and a C-terminal lectin domain that are characteristic of members of the collectin family of proteins.
Interstitial pneumonia caused by extensive infection of the lungs (LUNG) and BRONCHI, particularly the lower lobes of the lungs, by MYCOPLASMA PNEUMONIAE in humans. In SHEEP, it is caused by MYCOPLASMA OVIPNEUMONIAE. In CATTLE, it may be caused by MYCOPLASMA DISPAR.
An abundant pulmonary surfactant-associated protein that binds to a variety of lung pathogens, resulting in their opsinization. It also stimulates MACROPHAGES to undergo PHAGOCYTOSIS of microorganisms. Surfactant protein A contains a N-terminal collagen-like domain and a C-terminal lectin domain that are characteristic of members of the collectin family of proteins.