Alarmins Initiate Host Defense

Oppenheim, Joost J.; Tewary, Poonam; Rosa, Gonzalo de la; Yang, De

doi:10.1007/978-0-387-72005-0_19

Cited by 166 publications

(136 citation statements)

References 40 publications

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“…70 Stressed, damaged, and injured cells release endogenous danger signals, which trigger local inflammatory responses needed for tissue repair and regeneration. 21,[71][72][73] Damage-associated molecular patterns (DAMPs) play an important role in the propagation of the proinflammatory cascade of innate immunity, promoting the release of cytokines and other inflammatory mediators. 70,74 DAMPs initiate the innate immune response through the activation of APCs, which up-regulate costimulatory and major histocompatibility complex molecules.…”

Section: Discussionmentioning

confidence: 99%

Reversal of Established Traumatic Brain Injury-Induced, Anxiety-Like Behavior in Rats after Delayed, Post-Injury Neuroimmune Suppression

Rodgers

Deming

Bercum

et al. 2014

Journal of Neurotrauma

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Traumatic brain injury (TBI) increases the risk of neuropsychiatric disorders, particularly anxiety disorders. Yet, there are presently no therapeutic interventions to prevent the development of post-traumatic anxiety or effective treatments once it has developed. This is because, in large part, of a lack of understanding of the underlying pathophysiology. Recent research suggests that chronic neuroinflammatory responses to injury may play a role in the development of post-traumatic anxiety in rodent models. Acute peri-injury administration of immunosuppressive compounds, such as Ibudilast (MN166), have been shown to prevent reactive gliosis associated with immune responses to injury and also prevent lateral fluid percussion injury (LFPI)-induced anxiety-like behavior in rats. There is evidence in both human and rodent studies that post-traumatic anxiety, once developed, is a chronic, persistent, and drug-refractory condition. In the present study, we sought to determine whether neuroinflammation is associated with the long-term maintenance of post-traumatic anxiety. We examined the efficacy of an anti-inflammatory treatment in decreasing anxiety-like behavior and reactive gliosis when introduced at 1 month after injury. Delayed treatment substantially reduced established LFPI-induced freezing behavior and reactive gliosis in brain regions associated with anxiety and continued neuroprotective effects were evidenced 6 months post-treatment. These results support the conclusion that neuroinflammation may be involved in the development and maintenance of anxiety-like behaviors after TBI.

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Section: Discussionmentioning

confidence: 99%

Reversal of Established Traumatic Brain Injury-Induced, Anxiety-Like Behavior in Rats after Delayed, Post-Injury Neuroimmune Suppression

Rodgers

Deming

Bercum

et al. 2014

Journal of Neurotrauma

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“…In the last years, growing attention has been dedicated to endogenous alarm signals, which although heterogeneous, share some relevant features. They are released from necrotic cells, have chemotactic properties, and activate innate and possibly acquired immune responses [25,26]. The best-characterized among such signals is HMGB1, which has been shown to be active on mesoangioblasts [17]; it is involved in the activation of endothelia [27], and it has antiapoptotic and differentiation actions that could favor survival and function of stem cells in the tissues [28].…”

Section: Discussionmentioning

confidence: 99%

Inflammatory and alternatively activated human macrophages attract vessel-associated stem cells, relying on separate HMGB1- and MMP-9-dependent pathways

Lolmède

Campana

Vezzoli

et al. 2009

Journal of Leukocyte Biology

194

167

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“…This mechanism also appears effective in limiting the replication of other intracellular pathogens, including Legionella and Burkholderia [24]. In addition to removing the bacterial replicative niche, pyroptosis also passively releases multiple alarmins [26,27] such as ATP, IL-33 [28] and HMGB1 [29] to alert and recruit immune cells to the site Brought to you by | University of Queensland -UQ Library Authenticated Download Date | 4/9/15 1:05 AM of infection [30]. The oligomeric form of the adaptor protein ASC can also act as an unusual alarmin released during pyroptosis that can propagate inflammasome signalling in surrounding macrophages [31,32].…”

Section: Pyroptosis As a Pathogen Clearance Mechanismmentioning

confidence: 99%

Burn the house, save the day: pyroptosis in pathogen restriction

Boucher¹,

Chen²,

Schroder³

2016

Inflammasome

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Many programmed cell death pathways are essential for organogenesis, development, immunity and the maintenance of homeostasis in multicellular organisms. Pyroptosis, a highly proinflammatory form of cell death, is a critical innate immune response to prevent intracellular infection. Pyroptosis is induced upon the activation of proinflammatory caspases within macromolecular signalling platforms called inflammasomes. This article reviews our understanding of pyroptosis induction, the function of inflammatory caspases in pyroptosis execution, and the importance of pyroptosis for pathogen clearance. It also highlights the situations in which extensive pyroptosis may in fact be detrimental to the host, leading to immune cell depletion or cytokine storm. Current efforts to understand the beneficial and pathological roles of pyroptosis bring the promise of new approaches to fight infectious diseases.

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Alarmins Initiate Host Defense

Cited by 166 publications

References 40 publications

Reversal of Established Traumatic Brain Injury-Induced, Anxiety-Like Behavior in Rats after Delayed, Post-Injury Neuroimmune Suppression

Reversal of Established Traumatic Brain Injury-Induced, Anxiety-Like Behavior in Rats after Delayed, Post-Injury Neuroimmune Suppression

Inflammatory and alternatively activated human macrophages attract vessel-associated stem cells, relying on separate HMGB1- and MMP-9-dependent pathways

Burn the house, save the day: pyroptosis in pathogen restriction

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