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Long Term Intravital Multiphoton Microscopy Imaging of Immune Cells in Healthy and Diseased Liver Using CXCR6.Gfp Reporter Mice
Published on: March 24, 2015
Relationship between Kuppfer cells, inflammation, and fibrosis in chronic hepatitis B and C
N Stănculeţ1, Adriana Grigoraş1, Roxana Avădanei1
1University of Medicine and Pharmacy Grigore T. Popa-lasi, Faculty of Medicine.
Abstract:
Kupffer cells are liver parenchymal components of the immune system able of intervention in pathogenic mechanisms involved in viral hepatitis and tumoral lesions. Our study aimed to evaluate the Kupfferian hyperplasia in chronic hepatitis B and C, and to correlate with the severity of liver lesions, focusing on the modality in which Kupffer cells modulate the necroinflammatory events and fibrosis specific for chronic hepatitis morphologic substrate. We investigated 33 cases with chronic hepatitis B and 38 cases with chronic hepatitis C, diagnosed according to Ishak score (in chronic hepatitis B and C) and METAVIR score (in chronic hepatitis C). Kuppfer cells were immunohistochemical labeled, by using an anti-CD68 antibody and heat-induced epitope retrieval (HIER) technique. The sinusoidal reaction expressed by CD68 (+) cells hyperplasia progressively increases along with the intensity of necroinflammatory activity and with the amplitude of fibrosis lesions. Statistically significant differences between Kupffer cells number and the degree of necroinflammatory activitiy and fibrosis, respectively (Ishak score) have been identified in both types of chronic hepatitis. However, no significant differences have been registered when comparing the Kupffer cells number corresponding to each degree of necroinflammatory activity and of fibrosis, in chronic hepatitis B versus C, respectively. Our results demonstrate the relationship between Kupffer cells and the severity degree of the disease, without differences between chronic hepatitis B and C. Consequently, we may appreciate that the chronic hepatitis C specific lesions progression, different from that of chronic hepatitis B, is influenced by a different behavior of Kupffer cells, and not by their effective
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