Interleukin-1 Is Responsible for Acute Lung Immunopathology but Increases Survival of Respiratory Influenza Virus Infection

Schmitz, Nicole; Kurrer, Michael; Bachmann, Martin F.; Köpf, Manfred

doi:10.1128/jvi.79.10.6441-6448.2005

Cited by 335 publications

(336 citation statements)

References 46 publications

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“…For analysis of primary CD8 + T-cell responses, mice were infected with 0.1 LD50 (1 × 10 7 CFU) of either ΔactA/inlB or ΔactA/inlB L. monocytogenes-L.p.FlaA (both expressing full length OVA and B8R [20][21][22][23][24][25][26][27] epitope) and spleens were harvested on day 7. Spleens were dissociated and red blood cells removed using red blood cell lysing buffer (Sigma).…”

Section: Methodsmentioning

confidence: 99%

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Listeria monocytogenes engineered to activate the Nlrc4 inflammasome are severely attenuated and are poor inducers of protective immunity

Sauer¹,

Pereyre

Archer³

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

122

190

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Inflammasomes are intracellular multiprotein signaling complexes that activate Caspase-1, leading to the cleavage and secretion of IL-1β and IL-18, and ultimately host cell death. Inflammasome activation is a common cellular response to infection; however, the consequences of inflammasome activation during acute infection and in the development of long-term protective immunity is not well understood. To investigate the role of the inflammasome in vivo, we engineered a strain of Listeria monocytogenes that ectopically expresses Legionella pneumophila flagellin, a potent activator of the Nlrc4 inflammasome. Compared with wild-type L. monocytogenes , strains that ectopically secreted flagellin induced robust host cell death and IL-1β secretion. These strains were highly attenuated both in bone marrow-derived macrophages and in vivo compared with wild-type L. monocytogenes . Attenuation in vivo was dependent on Nlrc4, but independent of IL-1β/IL-18 or neutrophil activity. L. monocytogenes strains that activated the inflammasome generated significantly less protective immunity, a phenotype that correlated with decreased induction of antigen-specific T cells. Our data suggest that avoidance of inflammasome activation is a critical virulence strategy for intracellular pathogens, and that activation of the inflammasome leads to decreased long-term protective immunity and diminished T-cell responses.

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Section: Methodsmentioning

confidence: 99%

“…4A). It was previously shown that inflammasome-mediated control of infection by influenza virus is partially mediated by IL-1β (25). Additionally, IL-18 has been shown to mediate resistance to variety of pathogens, including Mycobacterium tuberculosis and Shigella flexneri (26,27).…”

Section: Monocytogenes Ectopically Expressing Flagellin Hyperactivatementioning

confidence: 99%

Listeria monocytogenes engineered to activate the Nlrc4 inflammasome are severely attenuated and are poor inducers of protective immunity

Sauer¹,

Pereyre

Archer³

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

122

190

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show abstract

“…Par exemple, au cours de l'infection par le virus de la grippe, la mortalité est supé-rieure chez les souris déficientes en IL-1R ou en IL-18 par rapport aux souris sauvages [42,43]. Par ailleurs, l'infection par le virus herpès de type 1 (HSV1) de souris déficientes en IL-1 résulte en une charge virale sanguine augmentée, un taux d'encéphalites à HSV1 plus élevé, et ce dans un contexte moins inflammatoire.…”

Section: Infections Viralesunclassified

Les inflammasomes

Jamilloux

Henry

2013

Med Sci (Paris)

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“…Activated caspase-1 cleaves inactive cytokines precursors to a secreted and biologically active form such as IL-1β, IL-18, IL-33 and IL-17. These proinflammatory cytokines further recruit monocytes and neutrophils into the lung to control influenza infection and pathogenesis [71]. Moreover, activation of CD4+ T cells is also mediated by this complex.…”

Section: Dendritic Cell Functional Changes With Agingmentioning

confidence: 99%

The Innate Immune System and Aging: What is the Contribution to Immunosenescence ?

Fülöp

Fortin²,

Lesur³

et al. 2012

TOLSJ

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Abstract:The immune system plays an important role in the defence against various threats to health, such as pathogens, cancer cells or modified-self proteins. With aging there is a decrease in the immune response, called immunosenescence, concomitantly with the increase in some age-related diseases such as infections, autoimmune disorders, chronic inflammatory diseases and cancer. The immune response is traditionally divided between innate and adaptive immune responses. Accumulating evidence suggests that immunosenescence is not only restricted to the adaptive but also affects the innate immune system. Assessment of innate immune system functions revealed that it is also susceptible to age-related dysregulation. Furthermore, it is becoming clear that the sustained function of innate cells is indispensable for the adequate functioning of the adaptive immune response. This review will describe the changes in the innate immune response with aging and the recent discoveries, which may shed new light on its contribution to immunosenescence.

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Interleukin-1 Is Responsible for Acute Lung Immunopathology but Increases Survival of Respiratory Influenza Virus Infection

Abstract: Interleukin-1␣ (IL-1␣

Cited by 335 publications

References 46 publications

Listeria monocytogenes engineered to activate the Nlrc4 inflammasome are severely attenuated and are poor inducers of protective immunity

Listeria monocytogenes engineered to activate the Nlrc4 inflammasome are severely attenuated and are poor inducers of protective immunity

Les inflammasomes

The Innate Immune System and Aging: What is the Contribution to Immunosenescence ?

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