Development of diagnostic and prophylactic methodologies is dependent on knowledge of the host's defence system and reaction to different vaccine adjuvants. Here we present a sequential morphological study of peritonitis and inflammatory cell processing of incomplete Freund's adjuvant (IFA) in intraperitoneally injected Atlantic cod. The peritoneal tissue responses were characterised using necropsy, histology and electron microscopy. An extensive inflammatory response as characterised by leukocyte morphology and contents of enzymes, presence of apoptotic cells and IFN-γ-expressing cells was observed. Three days post injection, IFA droplets were surrounded by different types of inflammatory cells and two different patterns could be discerned. The first was characterised by flattened and concentrically arranged interdigitating cells connected by desmosomes and with macrophage-like cells (MLCs) predominant in the periphery. The second type possessed four stratified layers with an inner layer containing many apoptotic MLCs; a second layer containing flattened and shrunken cells and outer layers comprising moderately flattened cells and an outermost layer of mononuclear cells expressing IFN-γ. Oil was detected both inside and outside MLCs. The two types of processes, of which the second was clearly stratified, were similar to those observed in other teleosts, indicating a variety of reaction modes or alternatively sequential process development. The numerous dead MLCs contributed to inflammation.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.fsi.2011.11.003 | DOI Listing |
Trans R Soc Trop Med Hyg
January 2025
Conse jo Nacional de Investigaciones Científicas y Técnicas (CONICET), Instituto de Química Básica y Aplicada del Nordeste Argentino (IQUIBA-NEA), CP3400 Corrientes, Argentina.
Background: The WHO states that antivenom is the only safe and effective treatment to neutralize snake venom. Snakebite antivenom typically involves horse hyperimmunization with crude venom and Freund's adjuvant.
Methods: In the current work, we analyzed the ascorbyl palmitate liquid crystal structure with snake protein or PLA2, the carrier charge capacity, and we evaluated the immune response induced by the enzyme P9a(Cdt-PLA2) formulated in a nanostructure using CpG-ODN, determining the titer of IgG antibodies.
Brain Behav
January 2025
Department of Anesthesiology & Clinical Research Center for Anesthesia and Perioperative Medicine & Key Laboratory of Anesthesia and Analgesia Application Technology, Huzhou Central Hospital, The Fifth School of Clinical Medicine of Zhejiang Chinese Medical University, Huzhou, China.
Cardiovasc Pathol
December 2024
Wits Integrated Molecular Physiology Research Initiative, Wits Health Consortium (PTY) Ltd, School of Physiology, Faculty of Health Sciences, University of the Witwatersrand, 2193 Johannesburg, South Africa.
Background: Interleukin-6 (IL-6) is an attractive therapeutic target due to its diverse roles in the pathogenesis of conditions characterized by systemic inflammation. IL-6 has also been implicated in the pathophysiology of heart failure. This study aimed to investigate the impact of IL-6 receptor blockade with tocilizumab on the molecular pathways underlying systemic inflammation-induced left ventricular (LV) dysfunction in a collagen-induced arthritis (CIA) rat model.
View Article and Find Full Text PDFLancet Neurol
January 2025
Spinal Cord Injury Center, Balgrist University Hospital, University of Zurich, Zurich, Switzerland.
Background: Spinal cord injury results in permanent neurological impairment and disability due to the absence of spontaneous regeneration. NG101, a recombinant human antibody, neutralises the neurite growth-inhibiting protein Nogo-A, promoting neural repair and motor recovery in animal models of spinal cord injury. We aimed to evaluate the efficacy of intrathecal NG101 on recovery in patients with acute cervical traumatic spinal cord injury.
View Article and Find Full Text PDFNaunyn Schmiedebergs Arch Pharmacol
December 2024
Department of Human Biology to the Physiology, School of Medicine, International Medical University, 57000, Kuala Lumpur, Malaysia.
Rheumatoid arthritis (RA) can cause blood pressure (BP) elevation in estrogen-deficient, post-menopausal women; however, the underlying mechanisms are not well understood. In this study, the aortic involvement and its underlying mechanisms that contribute to the BP elevation in estrogen-deficient, RA condition were identified. Ovariectomy was performed to create a state of estrogen deficiency and RA was then induced in ovariectomized rats by using incomplete Freund's adjuvant and immune-mediated collagen type-II.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!