Role of Kupffer Cells in Lung Injury in Rats Administered Endotoxin11

Triggering Receptor in Myeloid Cells (TREM-1) Specific Expression in Peripheral Blood Mononuclear Cells of Sepsis Patients with Acute Cholangitis

“…One mechanism may be related to excessive activation of the Kupffer cell [28][29][30]. Endotoxins are known to induce liver parenchyma cell damage [31,32], while Kupffer cells promote delivery of inflammatory factors such as TNF-α, IL-1 and IL-6 [33][34][35][36]. In addition, there may be some relationship with activation of the Kupffer cell during infection of the biliary tract.…”

Influx of macrophages into livers of rats treated with hepatotoxicants (thioacetamide, allyl alcohol, d-galactosamine) induces expression of HSP25

“…Perhaps both NAC and indomethacin diminish oxidative stress, and in consequence HSP25 expression is not stimulated so distinctly. Enlargement of ED1 + cells observed after NAC and indomethacin treatment may reflect the functional changes of these cells, and the shift from production of pro-inflammatory to anti-inflammatory cytokines in large ED1 + cells, as was observed by Kono et al (2005). It is also worth to mention that the combined treatment of rats with TAA and indomethacin or NAC cause not only the enlargement of recruited macrophages, but also their distinct vacuolization.…”

“…Such an effect is attributed to inflammatory mediators released by activated Kupffer cells, as well as to their involvement in further recruitment of monocytes (Mosher et al 2001), although the mechanisms involved in hepatotoxicant-induced activation of monocytes/macrophages are still a matter of a debate. Since the expression of HSP25 in liver treated with GdCl 3 and TAA was not altered in comparison to the liver treated with TAA alone, one can consider ED2 + cells as not The recent observations of Kono et al (2005) indicate that the population of monocytes/macrophages is heterogeneous and the differences concern their morphology and function. The distinguished subclasses differ markedly in their ability to synthesize TNF-a, IL-6 and IL-10 and phagocytosis: the expression of TNF-a was distinctly greater in small ED1 + cells and in contrast IL-6 and IL-10 were expressed mainly in intermediate and large ED1 + macrophages.…”

The Kupffer Cell Inhibition Exacerbates but Splenectomy Prevents Mortality in a Rat Septic Peritonitis Model

“…Serum HMGB1 concentrations, moreover, had dramatically increased by 4 h after CLP in a modified model that preserves blood flow [34]. These results may indicate that the expression of HMGB1 in the early phase after CLP most likely is caused predominantly by [19,37]. In contrast, phagocytosis was barely detectable in small Kupffer cells.…”

“…6). On the other hand, the mRNA expression of anti-inflammatory cytokine IL-10 was greater in intermediate and large Kupffer cells than small Kupffer cells activated with LPS [37]. Thus, large and intermediate Kupffer cells act as anti-inflammatory cells, whereas small Kupffer cells act as inflammatory cells [22,35,36].…”