Surfactant Protein A Binds Flagellin Enhancing Phagocytosis and IL-1β Production

Ketko, Anastasia; Lin, Chinhong; Moore, Bethany B.; LeVine, Ann Marie

doi:10.1371/journal.pone.0082680

Cited by 14 publications

(10 citation statements)

References 40 publications

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“…In animal cell models, P. aeruginosa flagella can recognise the basolateral surface of polarized lung epithelial cells through heparan sulphate, a highly sulphated proteoglycan [ 46 ]. A recent study supports a new role for surfactant protein A in binding and enhancing the clearance of P. aeruginosa flagellin, mediated in part by enhanced IL-1β production [ 47 ]. Furthermore, the P. aeruginosa flagellum has been described to bind glycolipids monosialoganglioside (GM) or disialoganglioside (GD), playing a role in the pulmonary infection where flagellin binding to GM1 was greater than to asialoGM1 [ 48 ].…”

Section: Twist and Stick: Interactions With Host Tissuesmentioning

confidence: 91%

Bacterial Flagella: Twist and Stick, or Dodge across the Kingdoms

et al. 2015

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The flagellum organelle is an intricate multiprotein assembly best known for its rotational propulsion of bacteria. However, recent studies have expanded our knowledge of other functions in pathogenic contexts, particularly adherence and immune modulation, e.g., for Salmonella enterica, Campylobacter jejuni, Pseudomonas aeruginosa, and Escherichia coli. Flagella-mediated adherence is important in host colonisation for several plant and animal pathogens, but the specific interactions that promote flagella binding to such diverse host tissues has remained elusive. Recent work has shown that the organelles act like probes that find favourable surface topologies to initiate binding. An emerging theme is that more general properties, such as ionic charge of repetitive binding epitopes and rotational force, allow interactions with plasma membrane components. At the same time, flagellin monomers are important inducers of plant and animal innate immunity: variation in their recognition impacts the course and outcome of infections in hosts from both kingdoms. Bacteria have evolved different strategies to evade or even promote this specific recognition, with some important differences shown for phytopathogens. These studies have provided a wider appreciation of the functions of bacterial flagella in the context of both plant and animal reservoirs.

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Section: Twist and Stick: Interactions With Host Tissuesmentioning

confidence: 91%

Bacterial Flagella: Twist and Stick, or Dodge across the Kingdoms

et al. 2015

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“…Interestingly both flagellin and a motile flagellum are required to activate the NAIP-NLRC4-inflammasome ( 5 , 15 – 17 ), but how host cells sense flagellar motility remains unclear. Beyond its ability to activate host cell signaling pathways, the flagellum also promotes adherence and colonization of host surfaces, and various specific targets have been identified including MUC1 mucin ( 18 ), heparin sulfate ( 19 ), surfactant protein A ( 20 ), and asialoGM1 ( 21 ).…”

Section: Bacterial Factors Involved In Host Interactions and Recognitmentioning

confidence: 99%

Pseudomonas aeruginosa in Chronic Lung Infections: How to Adapt Within the Host?

2018

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Bacteria that readily adapt to different natural environments, can also exploit this versatility upon infection of the host to persist. Pseudomonas aeruginosa, a ubiquitous Gram-negative bacterium, is harmless to healthy individuals, and yet a formidable opportunistic pathogen in compromised hosts. When pathogenic, P. aeruginosa causes invasive and highly lethal disease in certain compromised hosts. In others, such as individuals with the genetic disease cystic fibrosis, this pathogen causes chronic lung infections which persist for decades. During chronic lung infections, P. aeruginosa adapts to the host environment by evolving toward a state of reduced bacterial invasiveness that favors bacterial persistence without causing overwhelming host injury. Host responses to chronic P. aeruginosa infections are complex and dynamic, ranging from vigorous activation of innate immune responses that are ineffective at eradicating the infecting bacteria, to relative host tolerance and dampened activation of host immunity. This review will examine how P. aeruginosa subverts host defenses and modulates immune and inflammatory responses during chronic infection. This dynamic interplay between host and pathogen is a major determinant in the pathogenesis of chronic P. aeruginosa lung infections.

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“…Thus, SP-A inhibits TNF-α and IL-6 production, which is unleashed as a response to LPS [ 25 ]. In Pseudomonas aeruginosa infection, SP-A knockout mice show lower levels of IL-1β than do wild-type mice, which suggest that SP-A induces IL-1β production through the inflammasome pathway [ 26 ].…”

Section: Reviewmentioning

confidence: 99%

Surfactant proteins, SP-A and SP-D, in respiratory fungal infections: their role in the inflammatory response

2016

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Pulmonary surfactant is a complex fluid that comprises phospholipids and four proteins (SP-A, SP-B, SP-C, and SP-D) with different biological functions. SP-B, SP-C, and SP-D are essential for the lungs’ surface tension function and for the organization, stability and metabolism of lung parenchyma. SP-A and SP-D, which are also known as pulmonary collectins, have an important function in the host’s lung immune response; they act as opsonins for different pathogens via a C-terminal carbohydrate recognition domain and enhance the attachment to phagocytic cells or show their own microbicidal activity by increasing the cellular membrane permeability. Interactions between the pulmonary collectins and bacteria or viruses have been extensively studied, but this is not the same for fungal pathogens. SP-A and SP-D bind glucan and mannose residues from fungal cell wall, but there is still a lack of information on their binding to other fungal carbohydrate residues. In addition, both their relation with immune cells for the clearance of these pathogens and the role of surfactant proteins’ regulation during respiratory fungal infections remain unknown. Here we highlight the relevant findings associated with SP-A and SP-D in those respiratory mycoses where the fungal infective propagules reach the lungs by the airways.

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Surfactant Protein A Binds Flagellin Enhancing Phagocytosis and IL-1β Production

Cited by 14 publications

References 40 publications

Bacterial Flagella: Twist and Stick, or Dodge across the Kingdoms

Bacterial Flagella: Twist and Stick, or Dodge across the Kingdoms

Pseudomonas aeruginosa in Chronic Lung Infections: How to Adapt Within the Host?

Surfactant proteins, SP-A and SP-D, in respiratory fungal infections: their role in the inflammatory response

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