Liver macrophages include mostly Kupffer cells
, which are usual constituents of the liver, but during inflammation, monocytes are recruited from the periphery that can differentiate into macrophages in this tissue (45).
In addition, during the ischemia period, the lack of oxygen to hepatocytes causes mitochondrial deenergization, and finally the swelling of the sinusoidal endothelial cells and the Kupffer cells
. The production of reactive oxygen species, activation of Kupffer cells
, upregulation of proinflammatory cytokines, resulting in neutrophil-mediated injury are the major factors contributing to inflammation-associated damages (22).
Mouse RAW264.7 macrophages were obtained from ATCC, ImKCs (immortalized Kupffer cells
) were obtained from EMD Millipore Corporation (Temecula, CA, USA), and E.
Dedousis et al., "Depletion of liver Kupffer cells
prevents the development of diet-induced hepatic steatosis and insulin resistance," Diabetes, vol.
The importance of this axis has been clarified through TLR4 mutant mice resistant to the development of NAFLD ; furthermore, a direct link between TLR4 and Kupffer cells
was described in the pathogenesis of steatohepatitis, as the experimental destruction of Kupffer cells
was shown to prevent the increased expression of TLR4 .
Specific super-paramagnetic iron oxide-based (eg, ferucarbotran [Resovist; Schering, Berlin, Germany]) and manganese-based (ie, mangafodipirtrisodium [Tesla-scan; Nycomed Amersham, Oslo, Norway]) contrast media are targeted at the Kupffer cells
and hepatocytes, respectively.
Liver: Histopathological changes of liver were restricted to rabbits (group A3) consisting of hyperplasia of Kupffer cells
; severe congestion and hemorrhage and degeneration of hepatocytes.
Depletion of kupffer cell
function by gadolinium chloride attenuates thioacetamide-induced hepatotox-icity: expression of metallothionein and HSP70.
Saito et al., "Crucial role of impaired Kupffer cell
phagocytosis on the decreased Sonazoid-enhanced echogenicity in a liver of a nonalchoholic steatohepatitis rat model," Hepatology Research, vol.
Morphological Observations: There was disruption of liver cell plates at some sites and mild Kupffer cell
hyperplasia in two days heat exposed experimental animals.
In rats exposed to heat for two times, morphological changes of increased variation in size and staining of hepatocytes nuclei (anisocytosis) at some sites with disrupting liver cell plates in lobules, mild Kupffer cell
hyperplasia were present.
This finding confirmed that the binding of endotoxin to its receptors on Kupffer cells
and the resulting Kupffer cell
activation and production of TNF-[alpha] are key events in the development of alcoholic liver injury.