A critical role of pentraxin 3 in severe sepsis and septic shock

Carbone, Federico; Montecucco, Fabrizio; Rigamonti, Fabio

doi:10.1111/eci.12855

Cited by 1 publication

(1 citation statement)

References 15 publications

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“…(PRRs). The interaction between PAMPs and PRRs promotes the activation of pro-inflammatory pathways releasing cytokines, chemokines, and acute-phase proteins such as tumor necrosis factor alpha (TNF-α), interleukin (IL)-1β, IL-6, and pentraxin-3 (PTX-3) PMID [2][3][4]. Additionally, endogenous constituents from damaged tissue or those actively released from cells during inflammatory processes can bind and activate PRRs.…”

Section: Introductionmentioning

confidence: 99%

Long-Term Cognitive Outcomes After Sepsis: a Translational Systematic Review

et al. 2018

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Sepsis is systemic inflammatory response syndrome with a life-threatening organ dysfunction that is caused by an unbalanced host immune response in an attempt to eliminate invasive microorganisms. We posed questions, "Does sepsis survivor patients have increased risk of neuropsychiatric manifestations?" and "What is the mechanism by which sepsis induces long-term neurological sequelae, particularly substantial cognitive function decline in survivor patients and in pre-clinical sepsis models?" The studies were identified by searching PubMed/MEDLINE (National Library of Medicine), PsycINFO, EMBASE (Ovid), LILACS (Latin American and Caribbean Health Sciences Literature), IBECS (Bibliographical Index in Spanish in Health Sciences), and Web of Science databases for peer-reviewed journals that were published until January 2018. A total of 3555 papers were included in the primary screening. After that, 130 articles were selected for the study. A number of pre-clinical studies have shown an auto amplification of pro-inflammatory cytokines such as tumor necrosis factor alpha (TNF-α), interleukin (IL)-1β, and IL-6 in the first few hours after sepsis induction, also increased blood-brain barrier permeability, elevated levels of matrix metalloproteinases, increased levels of damage-associated molecular patterns were demonstrated. In addition, the rodents presented long-term cognitive impairment in different behavioral tasks that were prevented by blocking the mechanism of action of these inflammatory mediators. Clinical studies have showed that sepsis survivors presented increased bodily symptoms such as fatigue, pain, visual disturbances, gastrointestinal problems, and neuropsychiatric problems compared to before sepsis. Sepsis leaves the survivors with an aftermath of physiological, neuropsychiatric, and functional impairment. Systematic review registration: CRD42017071755.

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Section: Introductionmentioning

confidence: 99%