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The patient with acute gastrointestinal problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
Rebecca Maindonald, Adrian Jugdoyal
The Kupffer cells are phagocytic and are very efficient in digesting bacteria, viruses and other foreign matter. These cells are particularly important because they destroy bacteria that are constantly entering the portal blood flow directly from the GI tract. The main functions of Kupffer cells are: phagocytosis of bacteria, debris and other foreign matter in hepatic blood.a defence mechanism when bacterial translocation occurs.
Structural Organization of the Liver
Published in Robert G. Meeks, Steadman D. Harrison, Richard J. Bull, Hepatotoxicology, 2020
The main function of Kupffer cells is clearance of particulate and non-particulate materials from the blood. Particulate materials phagocytized by Kupffer cells include cellular debris (e.g., necrotic cells, organelles, and membranes) circulating tumor cells, microorganisms including viruses and exogenous particulate materials (e.g., colloidal gold, latex particles). Kupffer cells also endocytize a wide variety of macromolecules, e.g., immunoglobulins (IgA, IgG), immune complexes, enzymes, bacterial toxins, etc. Endotoxin appears to be taken up selectively by Kupffer cells, whereas many other nonparticulate macromolecules are taken up by endothelial cells as well (Jones and Summerfield, 1988; Plaaning-van Dalen et al., 1981). These functions primarily involve endocytosis and lysosomal digestion of endocytosed materials. Reflecting such a functional requirement, lysosomes comprise 14% of the cellular volume of Kupffer cells, in contrast to 7% in endothelial cells and hardly any space in fat storing cells. Kupffer cells account morphometrically for 17% of the lysosomal volume of the liver (Blouin, 1977).
Tissue Distribution And Cellular Expression Of Ia Antigens
Published in Soldano Ferrone, Chella S. David, Ia Antigens, 2019
Kupffer cells in the liver have long been thought to be related to tissue macrophages. Their origin was shown to be of bone marrow in the late 1970s and not surprisingly they expressed Ia.97,98 Again, purification of these cells shows they can in fact stimulate mixed lymphocyte cultures, act as accessory cells, and function in antigen presentation.98 The Ia expression by Kupffer cells seems identical to that of Ia+ macrophages.
Microanatomy of the metabolic associated fatty liver disease (MAFLD) by single-cell transcriptomics
Published in Journal of Drug Targeting, 2023
Lijun Wang, Kebing Zhou, Qing Wu, Lingping Zhu, Yang Hu, Xuefeng Yang, Duo Li
Metabolic-associated fatty liver disease remains a prominent risk factor for many chronic diseases, including obesity, diabetes, cardiovascular disease, and cancer [16]. Moreover, MAFLD can progress to steatohepatitis or cirrhosis. However, there is no definite target and therapeutic mechanism for MAFLD. Single-cell sequencing has guiding significance for screening potential therapeutic targets and molecular mechanisms of MAFLD. In the present study, we conducted transcriptome profiling of 30,038 single cells, including hepatocytes and non-hepatocytes, from normal and steatosis adult mouse livers. Comparative analysis of hepatocytes and non-hepatocytes revealed significant heterogeneity, and non-hepatocytes acted as major cell communication hubs. Systematic analysis of cellular compositions and cell-cell interaction networks showed that hepatocyte metabolism was significantly correlated with changes in liver function. We also uncovered the active involvement of non-hepatocyte cells in regulating the behaviour of hepatocytes, exemplified by Kupffer cells, which could preserve liver function after steatosis.
Hepatoprotective effects of norgalanthamine on carbon tetrachloride induced-hepatotoxicity in mice
Published in Drug and Chemical Toxicology, 2023
Nayeon Yang, Myungsoon Ko, Meejung Ahn, Taekyun Shin
Kupffer cells/macrophages are activated during liver injury (Ahn et al. 2016). In the mouse livers in the normal control group, Iba-1-positive Kupffer cells were detected along the sinusoids (Figure 5(D)), but no infiltration of inflammatory cells was observed. By contrast, in the livers of CCl4-injured mice, activated Kupffer cells and an inflammatory cell infiltrate were detected (Figure 5(E)). Pretreatment with 1 mg/kg and 10 mg/kg norgalanthamine (Figure 5(F,G)) and silymarin (Figure 5(H)) reduced the numbers of Iba1-positive cells. Furthermore, while the percentages of Iba-1-positive areas were significantly higher in the vehicle-treated group than in the normal control group (p < 0.001), they were significantly lower in the norgalanthamine (NG1, p < 0.01; NG10, p < 0.001, respectively) and silymarin (p < 0.01) groups than in the vehicle-treated group (Figure 5(I)).
Spotlight on liver macrophages for halting injury and progression in nonalcoholic fatty liver disease
Published in Expert Opinion on Therapeutic Targets, 2022
Tea Lund Laursen, Anders Mellemkjær, Holger Jon Møller, Henning Grønbæk, Konstantin Kazankov
In the present review, we bring an update on the role of macrophages for NAFLD disease development and progression, describing the role of resident macrophages viz. Kupffer cells and the recruitment of monocytes and macrophages to the liver. Activation of macrophages during NAFLD development and progression can be initiated by several stimuli including DAMPS and PAMPS with specific cross talk of the liver with the gut microbiome and adipose tissue. It is expected that a better characterization of the gut microbiome of importance for macrophage activation and NAFLD development may lead to interventions targeting the gut microbiota resulting in less macrophage activation inflammation and fibrosis. Along the same lines, DAMPS or molecules and pathways involved in the development of DAMPS may be future targets. In addition, disturbances of both hepatic and adipose tissues insulin sensitivity have been linked to macrophage activation, suggesting that interventions including pharmaceuticals that improve insulin resistance and the metabolic syndrome may ameliorate NAFLD. This effect may occur directly but also indirectly through macrophage activation.