Browsing by Subject "Lipopolysaccharide"

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    Dataset used for the article: "Temporal dynamics of inflammation in gilthead seabream (Sparus aurata) induced by λ-carrageenan, LPS, and Poly I:C: from behaviour to gene expression"
    (2024-07-11) Campos Sánchez, Jose Carlos; Cabrera-Álvarez, Maria José; Oliveira, Ana Rita; Duarte Oliveira, Gonçalo; Soares, Florbela; Saraiva , João L.; Esteban Abad, María de los Ángeles; Guardiola Abellán, Francisco Antonio; Biología Celular e Histología
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    Effect of repeated administration of lipopolysaccharide on inflammatory and stress markers in saliva of growing pigs
    (Elsevier, 2014-04-16) Campos, Paulo H.R.F.; Gutiérrez Montes, Ana María; Le Floc’h, Nathalie; Cerón Madrigal, José Joaquín; Merlot, Elodie; Escribano Tortosa, Damián; Producción Animal
    Although saliva could be considered to be an ideal biological sample for evaluation of biomarkers relat- ing to stress and inflammatory responses in pigs, little is known about how these might be influenced by the presence of endotoxaemia. In the present study, the response to repeated administrations of li- popolysaccharide (LPS) was investigated, using a panel of salivary stress markers such as chromogranin A (CgA) and cortisol, as well as inflammatory/immune markers such as haptoglobin (Hp), C-reactive protein (CRP) and immunoglobulin A (IgA). Sixteen growing pigs were adapted to experimental conditions for 3 weeks, after which, 10 of the pigs were selected to receive three doses of LPS at 48 h intervals. Saliva samples were taken from all pigs prior to any LPS administration (baseline) and at time points corresponding to 3 h after each injection of LPS (T1, T2 and T3). Results showed that repeated administration of LPS induced significant elevation of salivary markers of hypothalamic-pituitary-adrenal (cortisol) and immune (Hp, CRP and IgA) activity compared to base- line levels (P < 0.05). However, rectal temperature, CRP and cortisol data suggested that the amplitude of the inflammatory response decreased with successive LPS administrations. Thus, measurement of sal- ivary biomarkers could be a practical tool for evaluating the inflammatory response to endotoxaemia in pigs. In the case of chronic inflammatory states, salivary Hp and IgA might be more sensitive markers than CRP or cortisol.
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    Electroacupuncture preconditioning attenuates acute lung injury in mice through transient receptor potential vanilloid 4-mediated anti-inflammation via inhibiting the p38 MAPK signaling pathway
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2026) Jiangtian Yan; Nina Yin; Wan Liu; Zhigang Wang; Lin Zeng; Biología Celular e Histología
    The objective of this study was to investigate the protective effect of electroacupuncture (EA) preconditioning on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice. The changes in inflammatory factors and total protein content in bronchoalveolar lavage fluid (BALF) were quantified using enzyme-linked immunosorbent assay (ELISA) and bicinchoninic acid assay (BCA). Hematoxylin and eosin (H&E) staining was employed to assess the extent of lung injury, while Ly-6G immunohistochemistry was used to examine the infiltration of inflammatory cells. Western blot analysis was employed to detect the expression of TRPV4 and proteins associated with the mitogen-activated protein kinase (MAPK) signaling pathway. In comparison with the sham-operated group, the model group demonstrated an elevated production of inflammatory factors in the BALF, augmented total protein content, elevated lung injury score, increased number of Ly-6G-positive cells, upregulation of TRPV4 expression in the lung, and enhanced p38 phosphorylation. The aforementioned pathological changes were significantly improved by EA preconditioning. Furthermore, the protective effect of EA preconditioning on ALI mice was verified by the use of GSK1016790A, an agonist of TRPV4, which demonstrated that this effect is exerted through the TRPV4-mediated p38 MAPK signaling pathway.
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    Ex vivo detection of lipopolysaccharide immunopositivity in Rushton bodies
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2023) Virkkunen, Sirke; Willberg, Jaana; Haglund, Caj; Sund, Malin; Sorsa, Timo; Hagström, Jaana
    Aim. Our aim was to investigate how bacterial lipopolysaccharide (LPS) is immunoexpressed in periapical lesions. By surprise we detected Rushton bodies (RBs) whose origin has been debatable to be positive for LPS. Methodology. Samples of radicular cysts (N=70) were stained in order to identify variations in LPS immunoexpression indicating bacterial background. For immunostaining, we used an anti-LPS antibody from Escherichia coli, and for visualization Horse Radish Peroxidase labeled polymer as the secondary antibody. Results. RBs showed positivity for LPS in radicular cysts. After collection of radicular cyst samples (70 in total), we noted that all RBs (N=25) histologically detected in tissue samples were positive for LPS. Furthermore, calcification in the cyst capsule showed immunopositivity. Conclusion. We demonstrate for the first time that LPS is present in RBs, indicating that host response to bacteria might be the initial cause of the formation of these hyaline bodies in the cyst epithelium and cyst capsule calcifications.
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    Lipopolysaccharide induces the early enhancement of mice colonic mucosal paracellular permeability mainly mediated by mast cells
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2019) Sun, Tingyi; Wang, Yaxi; Hu, Shilong; Sun, Haimei; Yang, Shu; Wu, Bo; Ji, Fengqing; Zhou, Deshan
    The alteration of intestinal mucosal barrier is considered to be the central pathophysiological process in response to gastrointestinal infections, and mucosal microstructural damage is a major factor for enhancing epithelial permeability in persistent bacterial infections. However, the mechanism involved in hyperpermeability in the early stage of acute bacterial infections is not fully understood. In the present study, fluorescein isothiocyanate-dextran across and transepithelial resistance measured in Ussing chambers were used to assess the intestinal paracellular permeability. Mast cell activation was evaluated by western blotting for the presence of tryptase released from mast cells. Serum levels of interleukin-6 were evaluated using enzymelinked immunosorbent assay. Our results indicated that mast cells played a pivotal role in colonic mucosal hyperpermeability in wild type mice treated with lipopolysaccharide (LPS) for 2 h. And the effect of LPS was mainly dependent on mast cell degranulation, while no change in permeability was observed in the mast celldeficient mice (Wads-/- ) after LPS administration. No obvious changes of the mucosal structure including histomorphological architecture and expression of intercellular junction proteins were obtained in either wild type or Wads-/- mice after LPS stimulation by hematoxylin and eosin staining, immunofluorescence staining and western blot analysis. Furthermore, the selfrenewal of intestinal epithelia, detected by using proliferation marker 5’-bromo-2’-deoxyuridine, was not involved in increased permeability. Collectively, activation of mast cells induced by LPS mediated intestinal hyperpermeability in the initial stage, and played a crucial role in barrier dysfunction rather than mucosal microstructural damage in acute enterogenous bacterial infection.
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    Systemic inflammation aggravates retinal ganglion cell vulnerability to optic nerve trauma in adult rats
    (MDPI, 2026-02-03) Rovere, Giuseppe ; Caja Matas, Yolanda; Vidal Villegas, Beatriz; Bernal Garro, José M. ; Sobrado Calvo, Paloma; Salinas Navarro, Manuel Ángel; Nucci, Carlo; Villegas Pérez, Maria Paz; Vidal Sanz, Manuel; Agudo Barriuso, Marta; Nadal-Nicolás, Francisco Manuel; Oftalmología, Optometría, Otorrinolaringología y Anatomía Patológica; Facultades de la UMU::Facultad de Medicina
    Systemic inflammation is increasingly recognized as a modifier of neurodegenerative outcomes in the central nervous system; however, its impact on retinal ganglion cell (RGC) survival and retinal microglial responses following optic nerve (ON) injury in vivo remains incompletely understood. In this study, we investigated how systemic lipopolysaccharide (LPS)-induced inflammation influences retinal microglial activation and RGC vulnerability under physiological conditions and after traumatic ON damage. In adult female rats, systemic LPS administration by intraperitoneal injection induced rapid and robust microglial activation, characterized by process retraction and soma hypertrophy within hours and promoting microglial proliferation at later stages but without causing RGC loss in intact retinas. Following ON crush, systemic inflammation did not affect early RGC degeneration but significantly exacerbated neuronal loss during the late acute phase. This increased vulnerability was accompanied by a marked rise in microglial density and a pronounced redistribution of microglia toward the central retina and the ON head, a region of heightened anatomical and metabolic susceptibility. Together, these findings demonstrate that, in rats, systemic inflammation alone is insufficient to induce RGC degeneration but acts as a potent priming factor that amplifies neurodegeneration in the context of axonal injury. The temporal and spatial specificity of microglial responses underscores their context-dependent role in retinal pathology and identifies systemic inflammatory status as a critical determinant of retinal outcome after trauma. Targeted, time-dependent modulation of microglial activation may therefore represent a promising therapeutic strategy for optic neuropathies.