Results 91 to 100 of about 20,066 (195)

Inactivation of the complement anaphylatoxin C5a by secreted products of parasitic nematodes

open access: yesInternational Journal for Parasitology, 2010
Given the importance of the complement anaphylatoxins in cellular recruitment during infection, the ability of secreted products from larval stages of Brugia malayi and Trichinella spiralis to influence C5a-mediated chemotaxis of human peripheral blood granulocytes in vitro was examined. Secreted products from B.
Rees-Roberts, D   +3 more
openaire   +3 more sources

The Oral‐Gut Axis: Bidirectional Interactions Between Microbiome and Diseases

open access: yesJournal of Periodontal Research, EarlyView.
This study aims to summarize the mechanisms underlying ectopic colonization of the gut by oral pathobionts and the microbial and host factors that regulate this process. ABSTRACT Increased colonization of typically oral microorganisms is frequently observed in the gut mucosa or lumen of individuals with gastrointestinal disorders, including patients ...
Shinya Ebihara, Nobuhiko Kamada
wiley   +1 more source

Complement–Eosinophil Crosstalk Links Complement Activation to Fibrin Deposition in Eosinophilic Chronic Rhinosinusitis

open access: yes
Allergy, EarlyView.
Ryo Hasegawa   +18 more
wiley   +1 more source

Young Adult Microglial Deletion of C1q Reduces Engulfment of Synapses and Partially Mitigates Cognitive Impairment in an Aggressive Alzheimer's Disease Mouse Model

open access: yesGlia, Volume 74, Issue 9, September 2026.
Young adult deletion of microglial C1q reduced engulfment of Vglut1+ synapses and mitigated spatial cognitive deficits at 10 months of age in the amyloidopathy Arctic mouse model of AD. Neither fibrillar amyloid plaques nor soluble or insoluble Aβ levels in the hippocampus were affected by young adult microglial loss of C1q despite reduced phagocytosis
Tiffany J. Petrisko   +4 more
wiley   +1 more source

Aseptic meningitis due to intravenous immunoglobulin therapy (IVIG) in therapy‐refractory pyoderma gangraenosum

open access: yes
JDDG: Journal der Deutschen Dermatologischen Gesellschaft, EarlyView.
Katharina A. Kälber   +3 more
wiley   +1 more source

The Immuno‐Cardiovascular Storm of Pre‐Eclampsia: Cytokine‐Mediated Endothelial Injury, Thrombosis, and Maternal Cardiovascular Instability

open access: yesComprehensive Physiology, Volume 16, Issue 4, August 2026.
Placental ischemia in pre‐eclampsia initiates cytokine‐driven endothelial dysfunction, angiogenic imbalance, oxidative stress, and thromboinflammation. Elevated TNF‐α, IL‐6, IL‐17, sFlt‐1, and complement activation promote vasoconstriction, thrombosis, and cardiovascular instability.
Emmanuel Ifeanyi Obeagu
wiley   +1 more source

Neopterin, PMN Elastase, and Complement Components as Monitoring Parameters in Women with the Syndrome of Hemolysis, Elevated Liver Enzymes and Low Platelet Count

open access: yesPteridines, 1993
Preeclampsia is a pregnancy induced hypertensive disease with an incidence of about 5% in primigravida and it significantly contributes to maternal and neonatal morbidity and mortality. The primary cause remains unknown but might be immunologic.
Haeger Magnus   +2 more
doaj   +1 more source

From scarring to healing: Emerging regenerative therapies for pulmonary fibrosis using MSCs and exosomes

open access: yesClinical and Translational Discovery, Volume 6, Issue 4, August 2026.
MSCs exert anti‐inflammatory, anti‐fibrotic and regenerative effects in pulmonary fibrosis. MSC‐derived exosomes reproduce many therapeutic benefits of parental MSCs. Preconditioning and genetic modification improve MSC therapeutic performance. Current preclinical and clinical evidence supports the translational potential of MSC‐based therapies ...
Hajar Nasiri   +8 more
wiley   +1 more source

Thromboinflammatory biomarkers in obstetric pathophysiology: Predictive insights into placental insufficiency and feto‐maternal adverse outcomes

open access: yesClinical and Translational Discovery, Volume 6, Issue 4, August 2026.
Placental insufficiency is a thromboinflammatory disorder driven by angiogenic imbalance, complement activation, endothelial dysfunction and coagulation dysregulation, leading to microvascular thrombosis, impaired uteroplacental perfusion and adverse maternal and fetal outcomes, including pre‐eclampsia, fetal growth restriction and stillbirth. Abstract
Emmanuel Ifeanyi Obeagu
wiley   +1 more source

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