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Infection-driven periodontal disease
Published in Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald, Principles of Mucosal Immunology, 2020
Thomas E. Van Dyke, Mike Curtis
Endothelial cells activated by the cytokines are active participants in the pathogenesis of periodontal inflammation. Secretion of endothelial cell chemokines (CXCL8, CCL2) and expression of adhesion molecules (P- and E-selectin and intercellular adhesion molecule (ICAM)-1 and ICAM-2) on the surface of endothelial cells promote leukocyte extravasation. P- and E-selectins bind glycoproteins on leukocytes and promote rolling of cells along the vessel wall. Firm binding of leukocytes to endothelium is mediated by integrins (leukocyte function-associated antigen-1 [LFA-1]), and leukocytes attach firmly to ICAM-1 expressed on endothelial cells; TNFα, PGE2, and histamine increase vascular permeability and permit leukocyte diapedesis. Chemokines, such as IL-8, that are produced at the site of infection, along with bacterial chemoattractants (the tripeptide fMLP [N-formyl-methionine-leucine-phenylalanine]), form a concentration gradient for leukocytes to migrate to the focus of infection. Circulating pro-inflammatory cytokines from the site of inflammation activate hepatocytes in the liver to release acute-phase proteins, including LPS-binding protein and sCD14 that are important for the recognition of LPS. Complement proteins and C-reactive protein (CRP) are also released to opsonize bacteria for phagocytosis. Figure 29.2 illustrates the initiation sequence of inflammation at the gingiva.
Angiogenesis and Roles of Adhesion Molecules in Psoriatic Disease
Published in Siba P. Raychaudhuri, Smriti K. Raychaudhuri, Debasis Bagchi, Psoriasis and Psoriatic Arthritis, 2017
Asmita Hazra, Saptarshi Mandal
The leukocytes unbound to quiescent endothelium generally pass through at a relatively high local speed unless loosely captured to endothelial cells by interactions between the adhesion molecules and their ligands. Leukocyte extravasation has been known for more than a quarter of a century. It happens through different stages. The multistep paradigm for the recruitment of circulating leukocytes to a tissue-like skin is the following:
Maturation, Barrier Function, Aging, and Breakdown of the Blood–Brain Barrier
Published in Shamim I. Ahmad, Aging: Exploring a Complex Phenomenon, 2017
Elizabeth de Lange, Ágnes Bajza, Péter Imre, Attila Csorba, László Dénes, Franciska Erdő
While peripheral blood leukocyte infiltration plays an essential role in lesion development, there is also evidence suggesting that BBB dysfunction precedes immune cell infiltration. Recent evidence suggests that immune-mediated activation (or damage) of the various BBB cellular components significantly contributes to lesion development and progression (McQuaid et al. 2009, Alvarez et al. 2011a, b). Chemokines seem to play an important role in the cascade of leukocyte extravasation. Chemokines displayed along the endothelial lumen bind chemokine receptors on circulating leukocytes, initiating intracellular signaling that culminates in integrin activation, leukocyte arrest, and extravasation (Holman et al. 2011).
Temporal pathway analysis of cerebrospinal fluid proteome in herpes simplex encephalitis
Published in Infectious Diseases, 2023
Anja Nääs, Peng Li, Clas Ahlm, Elisabeth Aurelius, Josef D. Järhult, Silvia Schliamser, Marie Studahl, Wenzhong Xiao, Jonas Bergquist, Gabriel Westman
A majority of the significantly activated pathways are involved in regulating the immune system and the response to infection. In some cases the role in the immune system is quite evident, like the Acute phase response pathway and the Leukocyte extravasation pathway [25,26]. Further, the MSP-RON, 14-3-3 and the Rho GTPase signalling are all involved in activating a variety of leukocytes including macrophages, T cells and neutrophils [27–29]. Further, ERK5, MSP-RON, ARE mediate mRNA degradation and Rho GTPase signalling are all involved in cytokine production [27,29–31]. From a CNS perspective, it is interesting to note that RhoA and the Multiple sclerorsis signalling pathway are linked to neurodegenerative disorders [32]. Appearing more general, some affected pathways are central for essential cell functions, such as the PI3K/Akt pathway, the ILK pathway and the Gluconeogenesis and Glycolysis pathways [33,34]. A common denominator of several of the pathways (e.g. MSP-RON, 14-3-3, RhoA, ERK5) is the harmful effects of dysregulated signalling where an overactivation can lead to extra inflammation and tissue damage [27,28,30,32].
EPA’s pleiotropic mechanisms of action: a narrative review
Published in Postgraduate Medicine, 2021
John R. Nelson, Matthew J. Budoff, Omar R. Wani, Viet Le, Dhiren K. Patel, Ashley Nelson, Richard L. Nemiroff
The potential benefit of shifting the EPA:arachidonic acid ratio has long been recognized with regard to platelet aggregation [94]. Whereas cyclooxygenase in platelets converts arachidonic acid to the pro-aggregatory thromboxane-A2, it converts EPA to the anti-aggregatory thromboxane-A3. Similarly, in the vessel wall arachidonic acid is converted to the pro-aggregatory prostacyclin PGI2 while EPA is converted to the anti-aggregatory prostacyclin PGI3 [94]. Production of resolvins, notably resolvin E1, may also play a role in reducing platelet activation and thrombosis [54]. RvE1 has been shown to regulate leukocyte extravasation via the cell surface adhesion molecule L-selectin, which has a role in leukocyte rolling and tethering, as well as reducing ADP and thromboxane-A2 receptor-stimulated platelet aggregation. These effects also extend to platelets, with RvE1 blocking platelet aggregation and reducing ADP-stimulated P-selectin expression and surface mobilization. This suggests that RvE1 may also block initial platelet–leukocyte interactions [54,95].
Recent efforts in drug discovery on vascular inflammation and consequent atherosclerosis
Published in Expert Opinion on Drug Discovery, 2021
Alma Martelli, Valentina Citi, Vincenzo Calderone
Simultaneously, endothelial cells, which physiologically avoid leukocyte attachment to the vessel wall, overexpress P-selectin, and E-selectin, triggering the adhesion of leukocytes to the vascular wall. Then, also the overexpression of leukocyte adhesion molecules, such as vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) occur, promoting a tighter adhesion due to the interaction between the very late antigen-4 (VLA-4) on the leukocyte surface and ICAM-1 and VCAM-1, leading to leukocyte extravasation (monocytes and neutrophils), from the bloodstream toward the subendothelial matrix [5]. Once internalized into the vascular tissue, monocytes undergo differentiation into macrophages due to the action of growth factors (macrophage-colony stimulating factor (M-CSF)) and incorporate oxidized LDL, evolving into lipid-laden macrophages, known as foam cells, which aggregate to form a yellow-colored fatty streak in the vessel wall [6].