Mediators of inflammation

Determination of soluble ICAM-1 and TNFalphaR in the cerebrospinal fluid and serum levels in a population of Brazilian patients with relapsing-remitting multiple sclerosis

“…Moreover, MS patients with clinically active disease showed altered MRI and very high levels of soluble ICAM-1 in both serum and CSF. The evidence of increased serum levels of sICAM-1 during acute relapses are in accordance with recently reported data 11,14,[24][25][26] showing elevated expression of adhesion molecules (ICAM-1) on the luminal surface of endothelial cells in active MS lesions. In this sense, high concentrations of sICAM-1 and VCAM-1 in the peripheral blood during active disease would reflect BBB damage and may further serve as an adhesion ligand during extravasation of activated leukocytes into the brain tissue 24,27 .…”

“…Indeed, the severity of the relapse, measured by the EDSS score, highly correlate to the TNF production 29,30 . TNF-α up regulate expression of adhesion molecules on endothelial cells and leukocytes thus facilitating adherence and extravasation of leukocytes into the CNS to initiate local tissue damage 14,30 . The results reported herein indicate that regardless clinical course of disease (relapse or remission) MS patients showed a steady inflammatory process within the CNS microenvironment.…”

“…Indeed constitutive adhesion molecules expressed or induced during active immune response, can be released from cerebral endothelial cell membranes following cytokine stimulation 14,15 . Moreover soluble TNF receptors (sTNF-R) capable of antagonize TNF action in vivo also up regulate TNF-α levels thus inducing TNF-associated activities 10,11,17,18 , such as cytotoxicity.…”

Lymphotoxin Plays a Crucial Role in the Development and Function of Nasal-Associated Lymphoid Tissue through Regulation of Chemokines and Peripheral Node Addressin

“…7 However, even though the NALT is detectable, it is sparsely populated, and in the tumor necrosis factor (TNF)/LT-␣ Ϫ/Ϫ mouse a loss of T-and B-cell compartmentalization is apparent, reminiscent of the defects seen in the spleens of LT-␣ Ϫ/Ϫ mice. 7,15 Members of the LT/TNF family play crucial, but not completely redundant roles in the development of LNs, Peyer's patches, and spleen, 8 in part through regulation of chemokines 9 and adhesion molecules. 10 Therefore, we wished to identify the mechanism by which the individual family members contribute to the development and function of the NALT to determine whether a similar pattern would emerge even in an organ in which the cytokines were not essential for its initiation.…”

Acute lung injury: how the lung inflammatory response works

“…Products of the acute inflammatory response in lung causing tissue injury are released from recruited PMN and activated lung macrophages [4]. These include toxin oxygen (O 2 , hydrogen peroxide, etc.)…”