The role of IL-1β in Pseudomonas aeruginosa in lung infection

Wonnenberg, Bodo; Bischoff, Markus; Beißwenger, Christoph; Dinh, Thai; Bals, Robert; Singh, Baljit; Tschernig, Thomas

doi:10.1007/s00441-016-2387-9

Cited by 29 publications

(21 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Local production of cytokines in the lungs influences host defense mechanisms against P. aeruginosa infection (17)(18)(19). However, the excessive production of proinflammatory cytokines can lead to tissue damage and other detrimental effects for the host.…”

Section: Downloaded Frommentioning

confidence: 99%

Mice Lacking γδ T Cells Exhibit Impaired Clearance of Pseudomonas aeruginosa Lung Infection and Excessive Production of Inflammatory Cytokines

et al. 2020

View full text Add to dashboard Cite

Pseudomonas aeruginosa is an opportunistic pathogen that causes chronic and life-threatening infections in immunocompromised patients. A better understanding of the role that innate immunity plays in the control of P. aeruginosa infection is crucial for therapeutic development. Specifically, the role of unconventional immune cells like γδ T cells in the clearance of P. aeruginosa lung infection is not yet well characterized. In this study, the role of γδ T cells was examined in an acute mouse model of P. aeruginosa lung infection. In the absence of γδ T cells, mice displayed impaired bacterial clearance and decreased survival, outcomes which were associated with delayed neutrophil recruitment and impaired recruitment of other immune cells (macrophages, T cells, natural killer cells, and natural killer T [NKT] cells) into the airways. Despite reduced NKT cell recruitment in the airways of mice lacking γδ T cells, NKT cell-deficient mice exhibited wild-type level control of P. aeruginosa infection. Proinflammatory cytokines were also altered in γδ T cell-deficient mice, with increased production of interleukin-1β, interleukin-6, and tumor necrosis factor. γδ T cells did not appear to contribute significantly to the production of interleukin-17A or the chemokines CXCL1 and CXCL2. Importantly, host survival could be improved by inhibiting tumor necrosis factor signaling with the soluble receptor construct etanercept in γδ cell-deficient mice. These findings demonstrate that γδ T cells play a protective role in coordinating the host response to P. aeruginosa lung infection, both in contributing to early immune cell recruitment and by limiting inflammation.

show abstract

Section: Downloaded Frommentioning

confidence: 99%

Mice Lacking γδ T Cells Exhibit Impaired Clearance of Pseudomonas aeruginosa Lung Infection and Excessive Production of Inflammatory Cytokines

et al. 2020

View full text Add to dashboard Cite

show abstract

“…Innate immune defence molecules 73 , 74 , CD95-mediated apoptosis of epithelial cells 75 , 76 , and killing by polymorphonuclear neutrophilic granulocytes (PMNs) 77 play critical roles in fighting P. aeruginosa . PMNs are primarily recruited by chemokines to the diseased microenvironment.…”

Section: The Response Of the Mammalian Immune System To P mentioning

confidence: 99%

Recent advances in understanding Pseudomonas aeruginosa as a pathogen

2017

View full text Add to dashboard Cite

The versatile and ubiquitous Pseudomonas aeruginosa is an opportunistic pathogen causing acute and chronic infections in predisposed human subjects. Here we review recent progress in understanding P. aeruginosa population biology and virulence, its cyclic di-GMP-mediated switches of lifestyle, and its interaction with the mammalian host as well as the role of the type III and type VI secretion systems in P. aeruginosa infection.

show abstract

“…These multi-molecular signaling platforms assemble in macrophages and dendritic cells when bacterial products are bound by PRRs, and result in the cleavage and activation of procaspase-1, which leads to processing and secretion of the pro-inflammatory cytokines IL-1β and IL-18 and/or pyroptotic cell death (reviewed in [37–39]). Of the numerous inflammasomes described thus far, the NLRC4 and NLRP3 inflammasomes appear to contribute most significantly to P. aeruginosa pathogenesis.…”

Section: Immune Recognition and Response To P Aeruginosa Infectionmentioning

confidence: 99%

Inflammation: A Double-Edged Sword in the Response to <b><i>Pseudomonas aeruginosa</i></b> Infection

Lin

Kazmierczak²

2017

J Innate Immun

View full text Add to dashboard Cite

The Gram-negative opportunistic pathogen Pseudomonas aeruginosa exploits failures of barrier defense and innate immunity to cause acute infections at a range of anatomic sites. We review the defense mechanisms that normally protect against P. aeruginosa pulmonary infection, as well as the bacterial products and activities that trigger their activation. Innate immune recognition of P. aeruginosa is critical for pathogen clearance; nonetheless, inflammation is also associated with pathogen persistence and poor host outcomes. We describe P. aeruginosa adaptations that improve this pathogen's fitness in the inflamed airway, and briefly discuss strategies to manipulate inflammation to benefit the host. Such adjunct therapies may become increasingly important in the treatment of acute and chronic infections caused by this multi-drug-resistant pathogen.

show abstract

The role of IL-1β in Pseudomonas aeruginosa in lung infection

Cited by 29 publications

References 31 publications

Mice Lacking γδ T Cells Exhibit Impaired Clearance of Pseudomonas aeruginosa Lung Infection and Excessive Production of Inflammatory Cytokines

Mice Lacking γδ T Cells Exhibit Impaired Clearance of Pseudomonas aeruginosa Lung Infection and Excessive Production of Inflammatory Cytokines

Recent advances in understanding Pseudomonas aeruginosa as a pathogen

Inflammation: A Double-Edged Sword in the Response to <b><i>Pseudomonas aeruginosa</i></b> Infection

Contact Info

Product

Resources

About