Proinflammatory cytokines tumor necrosis factor-α and interferon-γ alter tight junction structure and function in the rat parotid gland Par-C10 cell line

Abstract

Baker OJ, Camden JM, Redman RS, Jones JE, Seye CI, Erb L, Weisman GA. Proinflammatory cytokines tumor necrosis factor-␣ and interferon-␥ alter tight junction structure and function in the rat parotid gland Par-C10 cell line.

Aquaporin gene therapy corrects Sjögren’s syndrome phenotype in mice

“…Restoration of flow could increase the release of these peptides and contribute to decreasing innate immune activation. In addition, transepithelial barrier integrity is reported to be decreased in patients with pSS (48,49), likely leading to exposure to new antigens and inflammation. Restoration of flow could lead to decreased antigen exposure, lowering glandular inflammation and inducing a return to immune homeostasis.…”

Lipoxin A4 inhibits immune cell binding to salivary epithelium and vascular endothelium

“…Binding of lymphocytes to salivary epithelium in SS is associated with an increased production of proinflammatory cytokines such as IL-1␤, interleukin-6 (IL-6), TNF-␣, and interferon-␥ (10,34,42,71). These proinflammatory cytokines cause alteration of epithelial integrity leading to salivary gland dysfunction (5). Previous studies indicate that activation of P2Y 2 nucleotide receptor, and TNF receptor in salivary epithelium upregulates VCAM-1 expression and stimulates lymphocyte adherence (6).…”

Neuroprotective roles of the P2Y2 receptor

“…Since both P2Y 2 Rmediated transactivation of growth factor receptors and integrins contribute to cell migration [21,24,91], it is intriguing to postulate that FLNa binding to the SH3-binding domains of the P2Y 2 R links nucleotide-induced EGFR transactivation to the RGD-dependent integrin signaling pathway that regulates cytoskeletal rearrangements required to increase cell motility. In other studies, P2Y 2 R-mediated monocyte diapedesis (i.e., transendothelial migration) has been shown to occur by disruption of intercellular adherens junctions, suggesting that cytoskeletal rearrangements promoted by the P2Y 2 R also can affect cell polarization [89,93,95,[101][102][103]. Therefore, these data suggest a mechanism whereby the tropism of monocytic cells (e.g., microglia) into damaged areas of the CNS can be induced by activation of P2Y 2 Rs.…”