Results 101 to 110 of about 18,973 (244)

Platelet-derived HMGB1 induces NETosis, exacerbating brain damage in the photothrombotic stroke model

open access: yesMolecular Medicine
Following cerebral ischemia, neutrophil extracellular traps (NETs) contribute significantly to brain damage by exacerbating delayed immune cell infiltration and vascular injury. They are detected both in brain tissue and within blood vessels.
Sang-A. Oh   +4 more
doaj   +1 more source

Sepsis Induces a Dysregulated Neutrophil Phenotype That Is Associated with Increased Mortality

open access: yesMediators of Inflammation, 2018
Background. Neutrophil dysfunction in sepsis has been implicated in the pathogenesis of multiorgan failure; however, the role of neutrophil extracellular traps (NETs) remains uncertain.
Jaimin M. Patel   +6 more
doaj   +1 more source

Vaspin identified as a DNA‐binding serpin with functional consequences for protease inhibition

open access: yesThe FEBS Journal, EarlyView.
Vaspin is a serpin that is expressed in skin, adipose tissue, and liver. It binds to single‐ and double‐stranded DNA with high affinity. This binding is unaffected by mutation of the known heparin‐binding site, accelerates the inhibition of the inflammatory protease KLK7, and may contribute to vaspin's nuclear localization.
Kevin Möhlis   +9 more
wiley   +1 more source

JNK Activation Turns on LPS- and Gram-Negative Bacteria-Induced NADPH Oxidase-Dependent Suicidal NETosis

open access: yesScientific Reports, 2017
Neutrophils cast neutrophil extracellular traps (NETs) to ensnare microbial pathogens. Nevertheless, the molecular rheostats that regulate NETosis in response to bacteria are not clearly established.
Meraj A. Khan   +6 more
doaj   +1 more source

Platelets as mediators of Thromboinflammation in chronic Myeloproliferative Neoplasms [PDF]

open access: yes, 2019
Chronic myeloproliferative neoplasms (MPN) are stem cell disorders driven by mutations in JAK2, CALR, or MPL genes and characterized by myeloid proliferation and increased blood cell counts.
Heller, Paula Graciela   +1 more
core   +1 more source

Genetic Susceptibility to Periodontitis

open access: yesJournal of Periodontal Research, EarlyView.
Aim: The aim of this narrative review was to identify genes carrying risk alleles associated with an increased risk of periodontitis and to place them in a biological context. Methods: The literature was reviewed based on predefined criteria. Results: The identified genes largely fall into functions linking immune response with tissue repair. The genes
Gesa M. Richter, Arne S. Schaefer
wiley   +1 more source

Neutrophil swarms require LTB4 and integrins at sites of cell death in vivo [PDF]

open access: yes, 2013
Neutrophil recruitment from blood to extravascular sites of sterile or infectious tissue damage is a hallmark of early innate immune responses, and the molecular events leading to cell exit from the bloodstream have been well defined1,2. Once outside the
Afonso, P.   +6 more
core   +2 more sources

Farklı yönleriyle NETosis

open access: yes, 2021
Gelişmiş ve gelişmekte olan ülkelerde otoimmün ve otoinflamatuar hastalıkların görülme sıklığında ciddi bir artış vardır. Bu hastalıkların etiyolojisi karmaşık ve multifaktöriyel nedenlere bağlı gelişmektedir. Sistemik otoimmün hastalıkların temelinde otoantijenler olduğu düşünülmektedir.
Sürsal, Neslihan, Yıldız, Kader
openaire   +1 more source

Inflammatory and Immunological Basis of Periodontal Diseases

open access: yesJournal of Periodontal Research, EarlyView.
The periodontal lesion emerges as an evolving immunological battlefield, where host–microbiome interactions, dysregulated immune responses, fragile resolution mechanisms, and inflammophilic dysbiosis converge to shift the balance from homeostasis to unrestrained tissue destruction.
Giacomo Baima   +3 more
wiley   +1 more source

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