Granulomatous liver disease

Abstract

Granulomas are mainly composed of macrophages and T cells. The immune phenotype that triggers them and their histological appearance differ according to their etiology and to the host immune status. 1,4,5 For example, exposure to weakly antigenic agents results in the formation of persistent low-turnover granulomas (e.g., sutures), also called foreign-body granulomas (Figure 1). On the other hand, exposure to highly antigenic stimuli (e.g., Mycobacterium tuberculosis) results in additional activation of adaptive immune responses and in the formation of more complex granulomas (immune granulomas) (Figure 2). 1,6 Both, the innate and adaptive immune systems, are involved in their formation and maintenance. 7 In the case of Mycobacterium tuberculosis, its recognition through various macrophage receptors (e.g., complement receptor 4), among others, allows the T-helper cells activation into Th1, Th2, Th17 or regulatory T cells, as well as recruitment of other inflammatory cells (macrophages, neutrophils, B-cells). This results in the formation of the granuloma structure: a center composed

Microscopic changes in the digestive organs of domestic canaries poisoned with canthaxanthin

“…The same factors also condition the development of fatty infiltration of hepatocytes. The mechanism of its development is related to the infiltration of the cytoplasm with lipids introduced from blood, and also, perhaps, with decomposition of lipoprotein complexes of organelles' membranes under the impact of canthaxanthin (Ortiz-Brizuela et al, 2018). In this case, cellular infiltration of the liver stroma is a sign of chronic interstitial inflammatory reaction initiated by the influence of canthaxanthin (Samour, 2015).…”