General Information:

Id: 2,123 (click here to show other Interactions for entry)
Diseases: Pseudomonas aeruginosa diseases
pathogen-host system
Pseudomonas aeruginosa/mammalia
review
Reference: Sadikot RT et al.(2005) Pathogen-host interactions in Pseudomonas aeruginosa pneumonia Am. J. Respir. Crit. Care Med. 171: 1209-1223 [PMID: 15695491]

Interaction Information:

Comment As a cause of ventilator-associated pneumonia (VAP), P. aeruginosa has a high mortality compared with other pathogens. P. aeruginosa is the second most common cause of nosocomial pneumonia after Staphylococcus aureus.
Formal Description
Interaction-ID: 17426

process

P. aeruginosa infection

increases_activity of

disease

Pneumonia

Comment P. aeruginosa encodes a type III secretion system that is a major determinant of virulence and allows the bacterium to inject toxins into the host cell.
Formal Description
Interaction-ID: 17527

process

P. aeruginosa infection

increases_activity of

process

T3SS

Comment P. aeruginosa has developed a mechanism to coordinate expression of genes important for adaptation to the environment. This response is controlled by quorum-sensing systems. Quorum-sensing signaling molecules are acyl homoserine lactones (AHL), which are freely diffusible. When a threshold AHL concentration is reached, AHL binds LasR/RhlR transcriptional activators to induce expression of certain genes. P. aeruginosa predominately makes two autoinducers: N-3-oxododecanoyl homoserine lactone (3-O-C12-HSL, also called PAI-1) and N-butyryl-L-homoserine lactone (C4-HSL, also called PAI-2).
Formal Description
Interaction-ID: 17553

process

P. aeruginosa infection

affects_activity of

process

Acyl-HSL quorum sensing

Comment The activation of the quorum-sensing cascade promotes the formation of biofilms, structured communities that coat mucosal surfaces and invasive devices. The formation of biofilms makes conditions more favorable for bacterial persistence in the lungs.
Formal Description
Interaction-ID: 17557

process

P. aeruginosa infection

increases_activity of

Comment P. aeruginosa produces two major siderophores: pyochelin and pyoverdin. These siderophores bind iron efficiently and are then taken up by the bacteria through specific cell-surface receptors. The siderophores are major virulence factors important not only for providing iron to support bacterial metabolic processes but also for controlling the expression of other P. aeruginosa virulence factors, such as exotoxin A, endoprotease, and pyoverdine itself.
Formal Description
Interaction-ID: 17584

process

P. aeruginosa infection

increases_quantity of

drug/chemical compound

Pyochelin

Comment P. aeruginosa produces two major siderophores: pyochelin and pyoverdin. These siderophores bind iron efficiently and are then taken up by the bacteria through specific cell-surface receptors. The siderophores are major virulence factors important not only for providing iron to support bacterial metabolic processes but also for controlling the expression of other P. aeruginosa virulence factors, such as exotoxin A, endoprotease, and pyoverdine itself.
Formal Description
Interaction-ID: 17585

process

P. aeruginosa infection

increases_quantity of

drug/chemical compound

Pyoverdine I

Comment Tissue invasion by P. aeruginosa is promoted by the production of elastase, alkaline proteases, hemolysins (phospholipase and lecithinase), cytotoxin (leukocidin), siderophores with their uptake systems, and diffusible pyocyanin pigment.
Formal Description
Interaction-ID: 17678

process

P. aeruginosa infection

increases_quantity of

drug/chemical compound

Pyocyanine

Comment Apoptosis induced by the CD95-CD95 ligand interaction requires clustering of the CD95 receptors, which involves the generation of ceramide by the action of acid sphingomyelinase on sphingolipids. P. aeruginosa infection can trigger activation of acid sphingomyelinase and induce the formation of lipid rafts containing CD95, which appear to regulate apoptosis and cytokine responses by infected cells.
Formal Description
Interaction-ID: 17724

process

P. aeruginosa infection

increases_activity of

gene/protein

SMPD1

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Comment The interaction of P. aeruginosa with macrophages occurs via multiple cell surface receptors and is accompanied by the formation of pseudopods.
Formal Description
Interaction-ID: 17732

process

P. aeruginosa infection

increases_activity of

Comment The type of T-cell response in the lung may contribute to the level of resistance to P. aeruginosa. A Th2-dominated pulmonary response is seen in susceptible strains, whereas mice that are resistant to P. aeruginosa infection show a Th1-dominated pulmonary response.
Formal Description
Interaction-ID: 17762

process

P. aeruginosa infection

increases_activity of

process

immune response

Comment P. aeruginosa has been shown to signal through TLR4 with its LPS moiety. Although TLR4 is expressed in airway epithelial cells, it does not appear to be prominently involved in signaling of P. aeruginosa presented at the apical surface of polarized epithelial cells.
Formal Description
Interaction-ID: 17775

process

P. aeruginosa infection

increases_activity of

gene/protein

TLR4

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Comment Both IL-1 and IL-18 activity impairs bacterial clearance in P. aeruginosa lung infections; however, the molecular mechanisms by which these cytokines impair host defense in this setting have not been elucidated.
Formal Description
Interaction-ID: 17784

gene/protein

IL18

increases_activity of

process

P. aeruginosa infection

Comment IL-10 is an antiinflammatory cytokine. Antiinflammatory cytokines are involved in regulating the potentially damaging effects of neutrophilic inflammation. IL-10 null mice show prolonged and excessive proinflammatory cytokine production and neutrophil infiltration in the airways after P. aeruginosa infection.
Formal Description
Interaction-ID: 17792

gene/protein

IL10

decreases_activity of

process

P. aeruginosa infection

Comment Administration of IL-4 enhances bacterial clearance from the lungs of wild-type mice and decreases mortality after infection. The protective effects of IL-4 may be related to its ability to modulate leukocyte function. IL-4 enhances expression of complement receptors CR1, CR3, and CR4 and increases complement-dependent phagocytosis.
Formal Description
Interaction-ID: 17794

gene/protein

IL4

decreases_activity of

process

P. aeruginosa infection

Comment Syndecan-1 null mice are resistant to P. aeruginosa lung infection, suggesting the importance of this mechanism in pathogenesis of P. aeruginosa pneumonia.
Formal Description
Interaction-ID: 17830

gene/protein

SDC1

increases_activity of

process

P. aeruginosa infection

Comment The role of T cells is being investigated and suggests that a Th1-type response is beneficial to the host.
Formal Description
Interaction-ID: 24258

decreases_activity of

process

P. aeruginosa infection