Pulmonary Surfactant Protein A Augments the Phagocytosis of Streptococcus pneumoniae by Alveolar Macrophages through a Casein Kinase 2-dependent Increase of Cell Surface Localization of Scavenger Receptor A

Kuronuma, Koji; Sano, Hitomi; Kato, Kazunori; Kudo, Kazumi; Hyakushima, Naoki; Yokota, Shinichi; Takahashi, Hiroki; Fujii, Nobuhiro; Suzuki, Hiroshi; Kodama, Tatsuhiko; Abe, Shosaku; Kuroki, Yoshio

doi:10.1074/jbc.m312490200

Cited by 110 publications

(87 citation statements)

References 38 publications

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“…SP-A binds to bacteria, including Staphylococcus aureus, K. pneumoniae, Streptococcus pneumoniae, and Haemophilus influenzae and enhances their phagocytosis by macrophages (34 -37). The nonopsonic effect includes the direct interaction of the collectins with macrophages that results in the increased cell surface localization of phagocytic receptors, mannose receptor, and scavenger receptor A (24,38,39). In this study, we have shown macrophage-dependent and -independent activities of pulmonary collectins against L. pneumophila.…”

Section: Discussionmentioning

confidence: 63%

Pulmonary Collectins Protect Macrophages against Pore-forming Activity of Legionella pneumophila and Suppress Its Intracellular Growth

Sawada

Ariki

Kojima

et al. 2010

Journal of Biological Chemistry

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Section: Discussionmentioning

confidence: 63%

Pulmonary Collectins Protect Macrophages against Pore-forming Activity of Legionella pneumophila and Suppress Its Intracellular Growth

Sawada

Ariki

Kojima

et al. 2010

Journal of Biological Chemistry

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“…In this regard, SP-A can serve both as a microbial opsonin and as a direct activator of macrophage function. SP-A has been shown to up-regulate certain PRRs, such as SR-A and the MR, on macrophages (4,5,27). SP-A also regulates TNF-␣ production, either up or down, depending on which receptor it binds on the cell surface and the activation state of the cell (28).…”

mentioning

confidence: 99%

“…These include a greater phagocytic potential compared with other macrophages (2, 3) due to significant expression and activity of PRRs, such as the mannose receptor (MR) and scavenger receptor A (SR-A) (4,5); and immunoregulation through production of proinflammatory cytokines (e.g., such as TNF-␣ and/or anti-inflammatory cytokines (e.g., TGF-␤) (2,3). They also produce less IL-1␤ (TNF-␣), have a reduced oxidative response to pathogens compared with blood monocytes (6 -8), and serve as poor APCs (9), all of which are mechanisms that serve to control alveolar inflammation.…”

mentioning

confidence: 99%

Pulmonary Surfactant Protein A Regulates TLR Expression and Activity in Human Macrophages

Henning

Azad²,

Parsa

et al. 2008

The Journal of Immunology

133

115

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The pulmonary innate immune system responds to various airborne microbes. Although its specificity is broad and based on the recognition of pathogen-associated molecular patterns, it is uniquely regulated to limit inflammation and thereby prevent damage to the gas-exchanging alveoli. Macrophages, critical cell determinants of this system, recognize microbes through pattern recognition receptors such as TLRs, which typically mediate proinflammatory responses. The lung collectin, surfactant protein A (SP-A), has emerged as an important innate immune determinant that regulates microbe-macrophage interactions in this environment. In this study, we report the basal and SP-A-induced transcriptional and posttranslational regulation of TLR2 and TLR4 expression during the differentiation of primary human monocytes into macrophages. Despite SP-A’s ability to up-regulate TLR2 expression on human macrophages, it dampens TLR2 and TLR4 signaling in these cells. SP-A decreases the phosphorylation of IκBα, a key regulator of NF-κB activity, and nuclear translocation of p65 which result in diminished TNF-α secretion in response to TLR ligands. SP-A also reduces the phosphorylation of TLR signaling proteins upstream of NF-κB, including members of the MAPK family. Finally, we report for the first time that SP-A decreases the phosphorylation of Akt, a major cell regulator of NF-κB and potentially MAPKs. These data identify a critical role for SP-A in modulating the lung inflammatory response by regulating macrophage TLR activity.

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“…Both of them can bind to mycobacterial lipoarabinomannans but only SP-A can interact additionally with exposed glycoproteins in the cell wall of the pathogens [100][101][102]. It also can stimulate the expression of the other receptors involved in immunity response like complement receptor 3 and scavenger receptor [103,104]. Moreover, they can modulate the inflammatory response by regulating the cytokine production, the oxygen and nitrogen reactive species formation and functioning as chemo attractants for alveolar neutrophils and monocytes [105].…”

Section: Collectin Familymentioning

confidence: 99%

Macrophage Infection by Mycobacteria

Saleh¹

2016

Mycobact Dis

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Mycobacterium tuberculosis is the etiological agent of tuberculosis. It is a pathogen that continues to draw international concerns particularly due to the emergence of multi-drug resistance and to the difficulties associated with the diagnosis and treatment of latent tuberculosis. A key process in the pathogenesis of this disease is the interaction between this pathogen and host macrophages. Invasion of the macrophages protects the pathogen from attack by the immune system, allows it to multiply while protected within the macrophages, and alters the immune response as it influences the profiles of the cytokine and chemokine responses. Key to the intracellular survival of the pathogen within the macrophages is the specific interaction between the pathogen and its virulence factors with the host. This review provides an a summary of pertinent literature on the topic of macrophage receptors utilized by the pathogen, its survival strategies within the macrophage, and the general profile of immune signalling upon exposure to the pathogen. The importance of specific macrophage receptors and certain components of the pathogen to the direction of the immune response are also discussed.

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Pulmonary Surfactant Protein A Augments the Phagocytosis of Streptococcus pneumoniae by Alveolar Macrophages through a Casein Kinase 2-dependent Increase of Cell Surface Localization of Scavenger Receptor A

Abstract: Pulmonary surfactant proteins A (SP-A

Cited by 110 publications

References 38 publications

Pulmonary Collectins Protect Macrophages against Pore-forming Activity of Legionella pneumophila and Suppress Its Intracellular Growth

Pulmonary Collectins Protect Macrophages against Pore-forming Activity of Legionella pneumophila and Suppress Its Intracellular Growth

Pulmonary Surfactant Protein A Regulates TLR Expression and Activity in Human Macrophages

Macrophage Infection by Mycobacteria

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