Kupffer Cell Hyperplasia Research Articles

Comparative effects of gamma and microwave irradiation on anticarcinogenic effect of red chili in colon and liver of male albino rats

The comparative effect of raw red chili and red chili treated by gamma irradiation or microwave pasteuriza- tion with or without 5-fluorouracil on experimentally induced colon cancer in rats was investigated. Dimethylhydrazine was used to induce colon cancer which is histologically similar to and comparable with human neoplasm. Histopathological examination of dimethylhydrazine-treated rats demonstrated epithelial and goblet cell hyperplasia as well as preneoplastic changes of the rat colon expressed by loss of polarity of the nuclei and abnormal mitosis. The preneoplastic changes were developed to adenocarcinoma in 80% of cases. The liver showed different pathological pictures that included dysplas- tic changes, preneoplastic foci, and oval cell proliferation. We observed that red chili with or without 5-fluorouracil inhibited colon adenocarcinoma. The gamma red chili either alone or with5-fluorouracilwasthe bestgroups.The gamma irradiated red chili alone decreased epithelial and goblet cell hyperplasia and preneoplastic changes in colon and dysplastic changes, oval cell proliferation, and Kupffer cell hyperplasia in the liver. The gamma irradiated red chili with 5-fluorouracil inhibited the preneoplastic changes in colon. It was concluded that the sanitization of red chili by gamma irradiation either alone or with 5-fluorouracil was more beneficial from the human health point of view than that by microwave.

Protective Effects of Hyperoside against Carbon Tetrachloride-Induced Liver Damage in Mice

In this study, the hepatoprotective effects of hyperoside (1), a flavonoid glycoside isolated from Artemisia capillaris, have been examined against carbon tetrachloride (CCl4)-induced liver injury. Mice were treated intraperitoneally with vehicle or 1 (50, 100, and 200 mg·kg(-1)) 30 min before and 2 h after CCl4 (20 μL·kg(-1)) injection. Levels of serum aminotransferases were increased 24 h after CCl4 injection, and these increases were attenuated by 1. Histological analysis showed that 1 prevented portal inflammation, centrizonal necrosis, and Kupffer cell hyperplasia. Lipid peroxidation was increased and hepatic glutathione content was decreased significantly after CCl4 treatment, and these changes were reduced by administration of 1. Protein and mRNA expression of tumor necrosis factor-α (TNF-α), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and heme oxygenase-1 (HO-1) and nuclear protein expression of nuclear factor erythroid 2-related factor 2 (Nrf2) significantly increased after CCl4 injection. Compound 1 suppressed TNF-α, iNOS, and COX-2 protein and mRNA expression and augmented HO-1 protein and mRNA expression and Nrf2 nuclear protein expression. These results suggest that 1 has protective effects against CCl4-induced acute liver injury, and this protection is likely due to enhancement of the antioxidative defense system and suppression of the inflammatory response.

Gold nanoparticles administration induced prominent inflammatory, central vein intima disruption, fatty change and Kupffer cells hyperplasia

BackgroundAdvances in nanotechnology have identified promising candidates for many biological, biomedical and biomedicine applications. They are being increasingly exploited for medical uses and other industrial applications. The aim of the present study was to investigate the effects of administration of gold nanoparticles (GNPs) on inflammatory cells infiltration, central vein intima disruption, fatty change, and Kupffer cells hyperplasia in the hepatic tissue in an attempt to cover and understand the toxicity and the potential threat of their therapeutic and diagnostic use.MethodsA total of 70 healthy male Wistar-Kyoto rats were exposed to GNPs received 50 or 100 μl of GNPs infusion of 10, 20 and 50 nm GNPs for 3 or 7 days. Animals were randomly divided into groups, 12 GNPs-treated rats groups and one control group (NG). Groups 1, 2 and 3 received infusion of 50 μl GNPs of size 10 nm (3 or 7 days), size 20 nm (3 or 7 days) and 50 nm (3 or 7 days), respectively; while groups 4, 5 and 6 received infusion of 100 μl GNPs of size 10 nm, size 20 nm and 50 nm, respectively.ResultsIn comparison with respective control rats, exposure to GNPs doses has produced alterations in the hepatocytes, portal triads and sinusoids. The alterations in the hepatocytes were mainly vacuolar to hydropic degeneration, cytopasmic hyaline vacuolation, polymorphism, binucleation, karyopyknosis, karyolysis, karyorrhexis and necrosis. In addition, inflammatory cell infiltration, Kupffer cells hyperplasia, central veins intima disruption, hepatic strands dilatation and occasional fatty change together with a loss of normal architechiture of hepatic strands were also seen.ConclusionsThe alterations induced by the administration of GNPs were size-dependent with smaller ones induced more affects and related with time exposure of GNPs. These alterations might be an indication of injured hepatocytes due to GNPs toxicity that became unable to deal with the accumulated residues resulting from metabolic and structural disturbances caused by these NPs. These histological alterations may suggest that GNPs interact with proteins and enzymes of the hepatic tissue interfering with the antioxidant defense mechanism and leading to reactive oxygen species (ROS) generation which in turn may induce stress in the hepatocytes to undergo necrosis.

A BALB/c mouse model shows that liver involvement in dengue disease is immune-mediated

In the present study, BALB/c mice were used to develop a model for the hepatic injury associated to dengue infection. Histological analysis after subcutaneous inoculation with a low viral dose of dengue-2 virus showed Kupffer cell hyperplasia and an increased inflammatory cellular infiltrate next to the bile ducts on days 5, 7 and 14 post-inoculation, mainly characterized by the presence of mononuclear cells. The liver mRNA transcription level of IL-1β was highest on the 5th day post-infection ( p.i.) and decreased by the 21st day, TNF-α showed a peak of mRNA transcription after 14 days p.i. coinciding with the regression of cellular infiltrates and elevated expression of TGF-β mRNA. Serum AST and ALT levels were slightly elevated at 7 and 14 days post-infection. Dengue-2 RNA levels were undetectable in the liver on any of the days following inoculation. Our observations suggest that, as it is true for humans, the animals undergo a transient and slight liver inflammation, probably due to local cytokine production and cellular infiltration in the liver.

Suspected Yellow Fever Vaccine-Associated Viscerotropic Adverse Events (1973 and 1978), United States

Two cases of yellow fever vaccine-associated viscerotropic adverse events (YEL-AVD) were identified by review of correspondence received at the Centers for Disease Control and Prevention (CDC; Ft. Collins, CO). The cases occurred in Indiana and Maryland in 1973 and 1978, respectively. One patient, a 75-year-old man with multi-organ failure died, and the other, a 31-year-old woman, was hospitalized for 14 days. Onset was 3-6 days after vaccination. The illness was characterized by fever, headache, myalgia, gastrointestinal symptoms, hepatic and renal dysfunction, and (in the fatal case), shock and coagulopathy, compatible with YEL-AVD. Liver pathology showed diffuse, spotty necrosis, acidophilic degeneration, Kupffer cell hyperplasia, and microvesicular fat. No virological confirmation was obtained, so that both cases remain classified as "suspect." The 1973 case is the earliest record of YEL-AVD; until now, the earliest known case of YEL-AVD had been in 1975 in Brazil, and most subsequent cases have been reported after 1995.

Fumigaclavine C improves concanavalin A-induced liver injury in mice mainly via inhibiting TNF-alpha production and lymphocyte adhesion to extracellular matrices.

Fumigaclavine C, an alkaloidal metabolite, was produced by Aspergillus fumigatus (strain No. CY018). This study examined the effect of this compound on concanavalin A (Con A)-induced liver injury in mice, a T cell-dependent model of liver damage. Con A administration resulted in severe liver injury, T lymphocyte activation and a strong increment in spleen cell adhesion, as well as in tumour necrosis factor-alpha (TNF-alpha) production. Against this liver injury, the intraperitoneal administration of fumigaclavine C dose-dependently inhibited the elevation in transaminase activity, TNF-alpha production in serum and the histological changes, including inflammatory infiltration, hepatocyte necrosis and degeneration and Kupffer cell hyperplasia. In addition, this compound in-vitro also inhibited the proliferation of spleen cells induced by Con A, and reduced their IL-2 and TNF-alpha production. Moreover, the intraperitoneal administration of fumigaclavine C inhibited the potential of spleen cells isolated from the liver-injured mice to adhere to fibronectin, laminin and type IV collagen. These results suggest that the improvement of this T cell-mediated liver injury by fumigaclavine C may be related to the inhibition of lymphocyte activation, proliferation and adhesion to extracellular matrices as well as the reduction in TNF-alpha production.

Aqueous extract of Yin-Chen-Hao decoction, a traditional Chinese prescription, exerts protective effects on concanavalin A-induced hepatitis in mice through inhibition of NF-kB

In traditional oriental medicine, Yin-Chen-Hao decoction is used for the remedy of liver diseases such as hepatitis, fatty liver, hepatocirrhosis and jaundice. However, despite extensive pharmacological study, the molecular mechanism of the anti-inflammatory effect of Yin-Chen-Hao decoction is poorly understood. In this study, we have investigated the pharmacological action on the mechanism of concanavalin A-induced T cell-dependent hepatitis in mice. Concanavalin A administration resulted in a severe liver injury. This was shown through increased levels of serum transaminase and lactic dehydrogenase, and increased liver DNA fragmentation and caspase-3 activity. Pretreatment with the aqueous extract from Yin-Chen-Hao decoction dose-dependently inhibited the elevation in transaminase and lactic dehydrogenase activity, and reduced liver DNA fragmentation and caspase-3 levels. There was an improvement in histological changes including inflammatory infiltration, hepatocyte necrosis and degeneration, and Kupffer cell hyperplasia. In addition, Yin-Chen-Hao decoction significantly inhibited tumour necrosis factor-alpha (TNF-alpha) production in-vitro and in-vivo. Moreover, the activation of nuclear factor kappa B (NF-kappaB), which regulates TNF-alpha production, was blocked by Yin-Chen-Hao decoction in-vitro and in-vivo. In conclusion, Yin-Chen-Hao decoction was capable of regulating T-cell-mediated liver injury in-vivo. This event may have depended on the decrease of TNF-alpha production through the inhibition of NF-kappaB activation.

Astilbin prevents concanavalin A-induced liver injury by reducing TNF-alpha production and T lymphocytes adhesion.

The aim of this study was to evaluate the effect of astilbin on concanavalin A (Con A)-induced hepatitis, a T cell-dependent model of liver injury. Con A administration resulted in a severe liver injury in mice, with a strong increment in spleen cell adhesion and liver infiltration of T cells, as well as in tumour necrosis factor (TNF)-alpha production. Against this liver injury, astilbin significantly inhibited the elevation in transaminase activity, reduced the TNF-alpha production, and improved the histological changes, including inflammatory infiltration, hepatocyte necrosis and degeneration and Kupffer cell hyperplasia. In addition, astilbin inhibited the adhesion of spleen cells and purified T lymphocytes isolated from the liver-injured mice to fibronectin, laminin and type IV collagen.Moreover, the adhesion of human Jurkat T cells to endothelial cell line ECV-304 was also inhibited by astilbin. These results suggest that the improvement of the T cell-mediated liver injury by astilbinmay be related to the reduction in TNF-alpha production and in T cell adhesion to extracellular matrices and endothelial cells.

Pathological Effects of Crud Trichothecenes on Swiss Mice

Trichothecenes are natural secondary metabolites causing economic losses and health hazard to human and farm animals which are produced by several species of Fusarium and some other genera on different agricultural commodities. Study on trichothecenes mycotoxicosis revealed morphological, biochemical, and histopathological changes. After intraperitoneal injection of the toxin in male mice with different concentration for 35 days shows marked increase in body weight, dyspanea, shivering, bristling up of hair, hair falling, anomalies of eyes, and irritation around neck, also abdominal hemorrhage and clot accumulation in abdomen. In addition to inclusion (retention) cyst forms on liver. The biochemical studies on liver function by measuring GPT and GOT enzymes level have been done. An increase level of these enzymes in treated animal in comparison with control animal which indicating abnormal function of liver observed. The histopathological study on sections from the liver of treated animal with trichothecenes revealed many alterations in liver which includes congestion, kupffer cells hyperplasia, dilated sinusoids and mononuclear cells infiltration around the portal area.

Comparative 90-day dietary study of paraffin wax in Fischer-344 and Sprague–Dawley rats

Highly refined mineral hydrocarbons (MHCs) such as low melting point paraffin wax (LMPW) and low viscosity white oils can cause inflammatory changes in the liver and mesenteric lymph nodes (MLNs) of the Fischer-344 (F-344) rat. In contrast, only minimal MLN changes are seen in the Sprague–Dawley (S–D) rat with no changes in the liver. In this study, the response of female F-344 and S–D rats was compared after 90 days dietary treatment with 0%, 0.2% or 2% LMPW. Effects in the F-344 rats were significantly greater than in the S–D rats: increased liver and splenic weights and inflammatory changes (hepatic microgranulomas) in these tissues were observed only in the F-344 rats. Microgranulomas in the MLNs were observed in both strains but the effects were substantially greater in the F-344 rats. Cellular markers of inflammation were examined in a subset of rats from each group using immunohistochemical staining. An increase in staining for CD3 (T-cells), CD8a (suppresser/cytotoxic T-cells) and CD4 (helper T-cells) correlated with an increase in lymphoid cells in the livers of treated F-344 rats. The majority of macrophages in the hepatic microgranulomas of treated F-344 rats were negative for the ED2 marker, indicating a likely origin from non-resident macrophages. Electron microscopy showed Kupffer cell hypertrophy and hyperplasia in treated F-344 rats. However, lysozyme staining (indicating activation of epithelioid macrophages) decreased with increasing granuloma size. Non-ED2 expressing cells may have been recruited but not sufficiently activated to be lysozyme positive. Inflammatory changes in the cardiac mitral valve noted in previous studies of LMPW were also seen in the F-344 rats in this study but not in the S–D rats. Chemical analysis showed that MHC accumulated in livers from treated F-344 but not S–D rats and the concentration was more than 2-fold greater in MLNs from the F-344 than from the S–D rats. The F-344 appears to be more immunologically sensitive to a number of agents than other rat strains and the results of this study suggest that this may contribute, along with pharmacokinetic differences, to the inflammatory response of F-344 rats to dietary MHCs.

Histological and histochemical alterations induced by lead in the liver of the quail Coturnix coturnix

Adult males of the quail Coturnix coturnix were exposed to lead acetate trihydrate in drinking water (0.1, 0.25, 0.5, and 1% for one–six months) to investigate histological and histochemical alterations induced by lead intoxication in the liver. Chronic exposure to subtoxic concentrations of lead produced changes in hepatocytes, portal veins, Kupffer cells, and blood sinusoids. Alterations in hepatocytes mainly involved cytoplasmic vacuolation, necrosis, cytolysis, and glycogen accumulation. Kupffer cell hyperplasia, hemosiderosis, blood sinusoidal dilatation, portal vein congestion, and edema were also observed. No fibrosis or cirrhosis in the liver of any member of the dose groups over the entire period of the study was noted. The findings revealed that chronic exposure to lead produced mild histological and histochemical changes in the liver of the quail Coturnix coturnix.

P11: Megalocytic nodules in P53 heterozygous and wild-type mice exposed to Fumonisin B1

This project was undertaken in order to validate the p53+/- mouse model as an alternative to the 2 year carcinogenicity test. Groups of 10 male mice, either heterozygote (Taconic, P53N5-T) or wild type (Taconic, P53N5-W), were fed AIN-76A diet containing the non-genotoxic carcinogen fumonisin B1 (FB1) at levels of 0, 5, 50 or 150 ppm for 6 months. At necropsy the livers of all mice showed a characteristic nodular appearance. Microscopic studies revealed more or less defined nodules of variable diameters consisting of megalocytic hepatocytes. These distinct cells occupied portions of single lobules and in various places extended into adjacent lobules. The megalocytes had large nuclei that were hyperchromatic. Their cytoplasm was intensely eosinophilic. Nodules were separated by dense, cellular regions composed of small, vacuolated hepatocytes with micronuclei. They were accompanied by numerous apoptotic bodies and oval cells. There was minimal fibrosis and stromal condensation. Minor Kupffer cell hyperplasia and modest, multifocal oncotic necrosis completed the picture. In the liver of high dose groups there were increased apoptotic and oncotic necrosis and increased numbers of altered foci and tumors (adenomas, cholangiomas) relative to the 0 ppm group. The megalocytic liver nodules were an unusual and unexpected result. These megalocytic cells are thought to be mitotically inhibited. The effects of FB1 were dose- but not strain-dependent and therefore unrelated to the status of the p53 gene.

Hepatic changes in fatal malaria: an emerging problem

Over the last few years there has been a rise in the incidence of fatal malaria in urban areas of India, and this worrying trend is a major cause of concern for the national health authorities. The spectrum of histopathological changes that occur in the livers of Indian subjects with fatal malaria has recently been investigated, in a retrospective autopsy-based study. This investigation involved the 151 fatal cases of malaria seen at a tertiary-care hospital in Mumbai between January 2001 and December 2007. The diagnosis of malaria was made on the basis of the examination of a smear of peripheral blood (81 cases) or a histopathological examination (70 cases). For each subject of the present study, at least two blocks were prepared, using routine histological methods, from a liver sample collected at autopsy. The sections produced from these blocks were stained with various compounds, including Prussian Blue (which was used to distinguish malarial pigment from non-malarial). The pattern of liver necrosis seen in the malaria cases was compared with that seen in 11 cases of acute viral hepatitis, and with the liver histology seen in 50 control subjects, who had died of causes other than malaria or liver disease. The most common clinical presentation of the subjects who died of malaria was fever (85%), followed by jaundice (68%). The presence of jaundice often led to an initial misdiagnosis of acute viral hepatitis. In the livers of the fatal malaria cases, Kupffer-cell hyperplasia and the retention of haemozoin pigment were the two most common histological features. Necrosis was seen in 63 (41%) of these cases, with predominant centrilobular haemorrhagic necrosis in 16 (10%). The inflammation in the sections of liver from the malaria cases with hepatic necrosis was sparse compared with that in the corresponding sections from patients with acute viral hepatitis, although mixed portal inflammation was frequently noted in the malaria cases. None of the liver sections from the 50 control subjects showed evidence of pigment, necrosis or any other pathology. In conclusion, jaundice was one of the commonest clinical presentations of the fatal cases of malaria and could mimic viral hepatitis on clinical examination. The characteristic histopathological features of the livers of those with fatal malaria were Kupffer-cell hyperplasia, malarial pigment within the Kupffer cells, and liver-cell necrosis, with portal inflammation, steatosis and cholestasis also observed.

Effects of contrast media on the hepato-pancreato-biliary system

To determine the effects of high osmolarity contrast media (HOCM) and iso-osmolar contrast media (CM) application, with or without pressure, on hepato-pancreato-biliary (HPB) system. Sixty rats were divided into six equal groups as follows: Group 1: (0.9% NaCl, control), Group 2: (diatrizoate meglumine Na, ionic HOCM, Urographin), Group 3: (iodixanol, iso-osmolar non-ionic CM, Visipaque); each of which was applied without pressure, whereas the animals of the remaining three groups (1p, 2p, 3p) were subjected to the same CM with pressure. We performed a duodenal puncture and introduced a catheter into the ampulla. After the catheterization, 0.2 mL CM or 0.9% NaCl was injected with or without pressure. Blood samples were taken for biochemical evaluations. The histopathological examinations of liver, common bile duct, and pancreas were performed. There were no significant differences between the six groups for blood amylase, alanine aminotransferases, aspartate aminotransferases, bilirubin levels (P > 0.05). Alkaline phosphatase and gamma glutamyl transaminase levels were higher (P < 0.05) in the Urographin groups (2, 2p) than the Visipaque groups (3, 3p), or control groups (1, 1p). Hepatocyte necrosis, portal area inflammation, and Kupffer's cell hyperplasia were higher (P < 0.05) in the study groups than the control group. However, there were no significant differences (P > 0.05) between HOCM (2, 2p) and iso-osmolar CM (3, 3p) groups. Bile duct proliferation and regeneration in the Urographin groups (2, 2p) were significantly higher (P < 0.05) than the Visipaque groups (3, 3p) or the control groups (1, 1p). Although CM caused minor damage to the pancreas, there were no statistically significant differences (P > 0.05) between the groups. Application of the CM with pressure did not cause additional damage to the HPB system. Iso-osmolar, non-ionic CM could be more reliable than the ionic HOCM, whereas the application of pressure during the CM application had no effect on the HPB system.

Protective Effect of Baicalin Against Carbon Tetrachloride–Induced Acute Hepatic Injury in Mice

This study examined the effects of baicalin, a bioactive flavonoid isolated from Scutellariae Radix, on carbon tetrachloride (CCl4)-induced liver injury. Mice were treated intraperitoneally with 0.5 ml/kg CCl4and different groups of animals received 25, 50, 100, and 200 mg/kg baicalin. At 24 h after the CCl4treatment, the level of serum aminotransferases and lipid peroxidation was significantly elevated, whereas the hepatic glutathione content was decreased. These changes were attenuated by baicalin. The histological studies showed that baicalin inhibited the portal inflammation, centrizonal necrosis, and Kupffer cell hyperplasia, which are the three most common characteristics of CCl4-induced liver damage. The serum level and mRNA expression of tumor necrosis factor-α were markedly increased by the CCl4treatment but suppressed by baicalin. The mRNA and protein expression levels of inducible nitric oxide synthase and heme oxygenase-1 increased significantly at 24 h after the CCl4treatment. Baicalin attenuated the increase in the protein and gene expression of inducible nitric oxide synthase but augmented the increase in those of heme oxygenase-1. These findings suggest that baicalin protects hepatocytes from the oxidative damage caused by CCl4, and this protection is likely due to the induction of HO-1 expression and the inhibition of the proinflammatory mediators.

Vanishing bile duct syndrome in a patient with advanced AIDS. HIV Med 2007; 8: 70–72

Vanishing bile duct syndrome in a patient with advanced AIDS. <i>HIV Med</i> 2007; 8: 70–72

Exoerythrocytic development of Plasmodium gallinaceum in the White Leghorn chicken

Plasmodium gallinaceum typically causes sub-clinical disease with low mortality in its primary host, the Indian jungle fowl Gallus sonnerati. Domestic chickens of European origin, however, are highly susceptible to this avian malaria parasite. Here we describe the development of P. gallinaceum in young White Leghorn chicks with emphasis on the primary exoerythrocytic phase of the infection. Using various regimens for infection, we found that P. gallinaceum induced a transient primary exoerythrocytic infection followed by a fulminant lethal erythrocytic phase. Prerequisite for the appearance of secondary exoerythrocytic stages was the development of a certain level of parasitaemia. Once established, secondary exoerythrocytic stages could be propagated from bird to bird for several generations without causing fatalities. Infected brains contained large secondary exoerythrocytic stages in capillary endothelia, while in the liver primary and secondary erythrocytic stages developed primarily in Kupffer cells and remained smaller. At later stages, livers exhibited focal hepatocyte necrosis, Kupffer cell hyperplasia, stellate cell proliferation, inflammatory cell infiltration and granuloma formation. Because P. gallinaceum selectively infected Kupffer cells in the liver and caused a histopathology strikingly similar to mammalian species, this avian Plasmodium species represents an evolutionarily closely related model for studies on the hepatic phase of mammalian malaria.

Observations on pathological and histochemical changes in piglet livers infected with Taenia saginata asiatica

To study the pathological and histochemical characteristics of lesions in piglet livers infected with Taenia saginata asiatica (T. saginata asiatica) throughout the different stages, piglets were fed with eggs of T. saginata asiatica and raised in isolation in an animal center to establish the T. saginata asiatica infection model with normal piglets as control. The pathological changes in the piglet livers were observed after the infection using liver sections stained with hematoxylin and eosin. Histochemical methods were used to check the changes in lipid, glycogen and protein content in the liver. The data collected by image analysis were analyzed statistically with Statistical Package for the Social Science. The results show that T. saginata asiatica-exposed piglets were indeed infected. Inflammatory reactions began on the fourth day and progressed rapidly. Kupffer cell hyperplasia, hepatic hydropic degeneration and ballooning degeneration were found in the 10th-20th days after infection. Hepatic central veins and hepatic sinusoids were dilated and congested. Spotty necrosis occurred in some local liver tissues. In the 40th-60th days, granulomatous reactions and mild hepatocirrhosis were the main lesions. In the 70th-80th days, hepatocirrhosis and bile duct proliferation were observed in the liver. In the different stages, lipid drops were increased while glycogen and protein levels were decreased to some degree. There was a significant difference in metabolism between the infected group and the control group (P < 0.01). It is concluded that pigs are the favorable intermediate host of T. saginata asiatica and its infection can result in serious pathological and histochemical lesions in host organs.

The Liver in Brucellosis

Brucellosis involves the liver in varying ways, ranging from benign subclinical increases in serum aminotransferase levels to ominous chronic suppurative disease. Data on histopathology of the liver in brucellosis are scarce and contradictory. We sought to determine the liver histologic patterns present in a series of brucellosis patients and review the existing knowledge about liver involvement in this worldwide, prevalent zoonotic infection. Fourteen patients from 2 referral centers were retrospectively studied. They had brucellosis caused by Brucella melitensis and had undergone liver biopsy at the time of diagnosis. All patients exhibited granuloma formation in the liver parenchyma and in the majority in portal spaces. Varying degrees of cellular infiltration of parenchymal tissue and portal spaces, giant cells in granulomas, parenchymal necroses, and Kupffer's cell hyperplasia were also noted. No significant epidemiological or clinical correlations with liver involvement were exhibited. Thus, liver involvement was not increased in men vs women, young vs old patients, or complicated vs uncomplicated disease. The liver is involved in Brucella melitensis infection contrary to past beliefs. Different histologic patterns can be observed in liver involvement in brucellosis, the most common being granuloma formation. The pathogenetic role of brucellosis in development of liver fibrosis and cirrhosis remains limited and understudied.

Hepatoprotective effect of a protein-enriched fraction from the maggots (Musca domestica) against CCl4-induced hepatic damage in rats

The hepatoprotective potential of a protein-enriched fraction (PEF) isolated from the maggots of housefly (Musca domestica) was evaluated in rats against carbon tetrachloride (CCl4)-induced acute hepatic damage. Activities of serum aspartate aminotransferase and alanine aminotransferase increased by 4- and 13-fold induced by CCl4, were significantly inhibited by pretreatment with 50, 100 and 200 mg PEF/kg. The formation of malondialdehyde was also significantly decreased in PEF-treated group compared with CCl4-treated group. The treatments with PEF also elevated total protein levels significantly. These results were further supplemented by histopathological examination of liver sections. Hyperplasia of kupffer cells was observed after treatment with PEF (100 and 200 mg/kg). We conclude that PEF is effective in this model of liver damage.