Ultrastructure of in situ perfusion-fixed avian liver, with special reference to structure of the sinusoids

Broiler chicken and laying hen livers were fixed using a simple technique of in situ puncture perfusion of cacodylate-buffered fixative, which allowed characterisation of the fine structure of hepatic parenchyma, hepatocytes, bile ductules, and, in particular, the sinusoidal cells including endothelial, Kupffer, and Ito cells. Sinusoidal endothelial cells with their bulging perinuclear cytoplasm, evident in both transmission and scanning electron micrographs, were easily distinguishable from Kupffer cells, which possessed numerous pseudopodia. Bile ductular epithelium and hepatocytes of the laying hens contained large amounts of lipid. The ultrastructural characteristics of intercalated cells (putative extra-sinusoidal macrophages of chicken liver) are described and their possible role as precursors of Kupffer cells is discussed.     

Amphibia Kupffer cells

Amphibia Kupffer cells (i.e., liver resident macrophages) show many common characteristics when compared with Mammalia Kupffer cells: filopodia, microvillous-like structures, lamellipodia, fuzzy coat, coated vesicles, bristled vacuoles, nonspecific esterase activity, and pinocytotic and phagocytic activity are present both in Amphibia and Mammalia Kupffer cells. On the other hand, some differences are present between Kupffer cells of both zoological classes: phagocytosed red cells and their derivatives, iron-protein complexes, and lipofuscin bodies are normally present in Amphibia Kupffer cells, but absent in the same cells of healthy mammals. Worm-like structures are not seen in Amphibia and endogenous peroxidase activity is very weak in these animals compared with Mammalia. The most important difference lies in the ability of Amphibia Kupffer cells to produce melanins: in fact the tyrosinase gene is expressed, "melanosome centers" are present, and dopa oxidase activity is demonstrable.     

Fine structure and function of kupffer cells

Kupffer cells are macrophages that are attached to the luminal surface or inserted in the endothelial lining of hepatic sinusoids. In this site, Kupffer cells play a key role in host defense by removing foreign, toxic and infective substances from the portal blood and by releasing beneficial mediators. Under some conditions, toxic and vasoactive substances also are released from Kupffer cells which are thought to play a role in a variety of liver diseases. Many of these activities may be modulated by the levels of gut derived endotoxin normally present in the portal blood. The ultrastructural aspects of Kupffer cell structure function in situ are best studied using perfused-fixed livers. In fixed livers, transmission and scanning electron microscopy reveal Kupffer cells during health to be irregular in shape with their exposed surfaces presenting numerous microvilli, filopodia, and lamellopodia. Long filopodia penetrate endothelial fenestrae to secure Kupffer cells to the sinusoid lining. Specific membrane invaginations known as worm-like bodies or vermiform processes are seen in the cytoplasm of Kupffer cells as are numerous endocytotic vesicles and lysosomes which vary in density, shape and size. Sometimes, annulate lamellae connected to the rough endoplasmic reticulum also are found. The principal endocytic mechanisms of Kupffer cells are phagocytosis of particulates and cells, and bristle-coated micropinocytosis for fluid-phase endocytosis of smaller substances. Many of these events are mediated by specific receptors. In some species, Kupffer cells can be distinguished from other sinusoidal lining cells and monocytes by specific cytoplasmic staining or monoclonal antibodies. Kupffer cells have been shown to be of monocytic origin as well as having the capacity for self-replication.     

Fine structure of hepatic sinusoids and sinusoidal cells in disease

Liver sinusoids are special capillaries that are limited by fenestrated endothelial cells, without a genuine basement membrane, surrounded by perisinusoidal cells storing vitamin A, and harbouring Kupffer cells and pit cells, resident macrophages, and large granular lymphocytes, respectively. Each nonparenchymal cell and parenchymal cell of the liver interacts with all others and with the extracellular matrix. Therefore, the functional ability of each cell is constantly being modified by the metabolic activity of the others. Human liver biopsies (132), needle or surgical, perfusion-fixed with glutaraldehyde and processed for transmission electron microscopy (TEM), and occasionally for scanning electron microscopy (SEM), were examined. The study included liver diseases (such as alcoholic liver diseases, benign and malignant liver tumors, cholestasis of various origins, fulminant hepatitis, acute rejection after orthotopic liver transplantation, Budd-Chiari syndrome), as well as general or extrahepatic diseases (such as diabetes, hemochromatosis, hypervitaminosis A, various hematological disorders), and normal controls. Ultrastructural abnormalities are described and illustrated under two different headings: (1) elementary lesions of sinusoidal cells (endothelial, Kupffer, perisinusoidal and pit cells), nonsinusoidal cells (in the space of Disse and/or in the lumen), the extracellular matrix; and (2) the major pathological entities including perisinusoidal fibrosis, capillarization of sinusoids, sinusoidal dilatation, and peliosis. In the discussion, an overview of the major abnormalities reported in the literature is presented, and some specific questions regarding (1) perisinusoidal fibrosis in liver with normal histology, (2) the overload of perisinusoidal cells with lipids in non-hypervitaminosis A intoxication and (3) the etiological relationship of sinusoidal dilatation, peliosis, perisinusoidal fibrosis, or sinusoidal tumors with drugs and toxic compounds are discussed. In the event that lesions are not specific to any diagnosis, the knowledge of the ultrastructure of sinusoids is extremely useful from the perspective of the liver as an ecosystem.     

Myelin phagocytosis by macrophages and nonmacrophages during Wallerian degeneration

The literature concerning Schwann cells (SCs) and macrophages in myelin phagocytosis during Wallerian degeneration is reviewed. SCs carry out the first step in the removal of myelin by segmenting myelin and then incorporating the degraded myelin. The recruited macrophages then join in the myelin-phagocytosis event, appearing to make full use of their original phagocyte abilities until the end of myelin clearance. The molecular mechanisms of the two cells underlying myelin phagocytosis are thought to be different; myelin phagocytosis by SCs being lectin-mediated, i.e., opsonin-independent, whereas that of macrophages is mainly opsonin-dependent. It is important to note that SCs and macrophages cooperatively accomplish myelin phagocytosis.     

Morphological aspects of particle uptake by lung phagocytes

Macrophages residing on the inner epithelial surfaces of airways and alveoli are the only lung phagocytes exposed directly to the environment. Their phagocytic and microbicidal activities are essential for maintaining this organ in a clean and sterile state. The morphology of these phagocytes can be investigated in situ only after implementing special techniques, which involve intravascular triple-perfusion of aqueous fixatives or instillation of nonpolar ones. Such studies have revealed the engulfment of particles by these cells to be rapid, the process being essentially complete within a day. Particles are entrapped within phagosomes and the host cells eventually transported out of the lungs by mucociliary action, macrophages with higher loads being more rapidly eliminated than those with lower ones. Very small particles or those persisting on the epithelial surfaces may be taken up by the eponymous cells. Translocation of particles into the underlying connective tissue and their subsequent phagocytosis by interstitial macrophages prolongs their retention time in the lungs. The still poorly studied pleural macrophages might be involved in cell-mediated immune responses within the pleural space. Intravascular pulmonary macrophages figure largely in the phagocytosis of circulating particles. The role played by dendritic cells in particle uptake by the lungs is not well understood. Airway and alveolar macrophages are the primary phagocytes of the lung. In nonoverload situations and for particles >1 microm, a small proportion of those recruited suffices to remove material from the epithelial surface before other phagocytes, with an apparently greater immunological potential, gain access to it.     

Tracing DiO-labelled tumour cells in liver sections by confocal laser scanning microscopy

Investigating rare cellular events is facilitated by studying thick sections with confocal laser scanning microscopy (CLSM). Localization of cells in tissue sections can be done by immunolabelling or by fluorescent labelling of cells prior to intravenous administration. Immunolabelling is technically complicated because of the preservation of antigens during fixation and the problems associated with the penetration of the antibodies. In this study, an alternative and simple approach for the labelling of cells in vitro with the fluorescent probe DiO and its subsequent application in vivo will be outlined. The method was applied to trace DiO‐labelled colon carcinoma cells (CC531s) in 100 µm thick liver sections. In vitro and in vivo experiments revealed that DiO‐labelling of CC531s cells had no cytotoxic or antiproliferative effect and the cells preserved their susceptibility towards hepatic NK cells or Kupffer cells. In addition, DiO remained stable for at least 72 h in the living cell. DiO‐labelled CC531s cells could be traced all over the tissue depth and anti‐metastatic events such as phagocytosis of tumour cells by Kupffer cells could be easily observed. In situ staining with propidium iodide (nucleic acids) or rhodamine‐phalloidin (filamentous actin) resulted in additional tissue information. The data presented improved the understanding of the possible effects of the vital fluorescent probe DiO on cell function and provided a limit of confidence for CLSM imaging of DiO‐labelled cells in tissue sections.     

A new role for chondrocytes as non-professional phagocytes. An in vitro study

Chondrocytes are capable of engulfing latex particles, cell detritus, and necrotic and apoptotic remains in vitro. It is conceivable that chondrocytes might be involved in the clearance by phagocytosis of different materials within the cartilage. In fact, so far there is no evidence for the presence of "professional phagocytes" (macrophages and neutrophils) in this tissue. Chondrocyte suspensions obtained from rat knees and hips were cultured to assess phagocytosis of latex particles (1 microm), articular cartilage detritus, and necrotic and apoptotic chondrocyte remains (induced by VP-16 1 mM). We observed that chondrocytes phagocytosed latex particles as evaluated by confocal microscopy and flow cytometry. In addition, we observed that chondrocytes phagocytosed articular cartilage detritus and necrotic and apoptotic VP-16 induced-chondrocytes, as observed by bright field microscopy and transmission electron microscopy.     

Functional expression and localization of P-glycoprotein at the blood brain barrier

Until recently, the blood-brain barrier was viewed as a static lipid membrane barrier. Physical attributes of the cerebral endothelial cells such as the presence of tight junctions, paucity of vesicles or caveolae, and high electrical resistance were believed to be the primary components that provide the membrane selectivity of the blood-brain barrier to a variety of circulating compounds from the periphery. However, results from molecular biology, immunocytochemistry, biochemistry, and transport studies show that the cerebral endothelial cells possess an asymmetrical array of metabolic enzymes (i.e., alkaline phosphatase, cytochrome P450 enzymes, glutathione transferases) and energy-dependent efflux transport proteins (i.e., P-glycoprotein and Multidrug-resistance proteins) that are instrumental to the barrier function. P-glycoprotein, a membrane-associated, energy-dependent, efflux transporter, is expressed in brain parenchyma (i.e., astrocytes and microglia) as well as in blood-brain and blood-cerebrospinal fluid barriers. Its function along the blood-brain barrier is believed to prevent the accumulation of potentially harmful compounds in the brain by actively removing them from the brain into the peripheral circulation. This is a brief review on the expression and activity of P-glycoprotein at the blood-brain barrier, which reports on the localization of the protein in rat brain capillaries in situ as well as in a well-characterized in vitro model of the blood-brain barrier, an immortalized rat brain endothelial cell line, the RBE4. Immunocytochemical analysis employing various P-glycoprotein monoclonal antibodies, demonstrated the presence of the protein along the plasma membrane, in plasmalemmal vesicles and nuclear envelope of rat cerebral endothelial cells, both in situ and in vitro. Western blot analysis revealed a single band with a molecular weight of 170-180 kDa, a size previously reported for P-glycoprotein, in RBE4 cells. In addition, results from functional studies show that the accumulation of the P-glycoprotein substrate digoxin by RBE4 monolayer cells is significantly enhanced in the presence of standard P-glycoprotein inhibitors (verapamil, cyclosporin A, PSC 833), protease inhibitors (saquinavir, ritonavir, indinavir), and the metabolic inhibitor, sodium azide. These results demonstrate the functional expression of P-glycoprotein in the immortalized rat brain endothelial cell line, RBE4. Novel in situ and in vitro intracellular locations of P-glycoprotein in cerebral endothelial cells have been identified suggesting that this transporter may play a significant role in the subcellular distribution of substrates in the brain.     

Alanine minimises hepatocyte injury after ischemia-reperfusion in an <i>ex vivo</i> rat liver model

Ischemia-reperfusion injury is a determinant in liver injury occurring during surgery, ischemic states and multiple organ failure. The pre-existing nutritional status of the liver, i.e., fasting, might contribute to the extent of tissue injury. This study investigated whether alanine, an amino acid precursor of glucose, could protect ex vivo perfused livers of fasting rats from reperfusion injury. The portal vein was cannulated, the liver removed and perfused in a closed ex vivo system. Isolated livers were perfused either with glucose 1 g/L and 10 g/L, or with equal concentrations of alanine (n = 10 in each group). The experiment consisted of perfusion for 15 min, ischemia for 60 min, and reoxygenation during 60 min. Enzymes, glucose, lactate and bilirubin were analysed in perfusate samples. The proportion of glycogen as well as activation of caspase 3 was determined in biopsies. Alanine at a concentration of 10 g/L attenuated enzymes release in the perfusate during reoxygenation when compared to glucose-treated groups. Lactate level in the perfusate was lowest in alanine groups. Ischemia-reperfusion and mainly alanine activated apoptosis, specifically in Kupffer and endothelial cells. Alanine presents a protective effect on normothermic ischemia-reperfusion injury of the fasting rat liver when compared to glucose     

Action of the chemical agent fipronil (active ingredient of acaricide Frontline®) on the liver of mice: an ultrastructural analysis

Fipronil, active ingredient of the acaricide Frontiline®, is a phenyl‐pyrazolic derivative, and its efficacy in the elimination of several plagues, even in low concentrations, has already been demonstrated; however, its effect on nontarget organisms has not been thoroughly explained. In this sense, the objective of this study was to evaluate the effects of different dosages of fipronil on the liver of mice in artificial conditions. Results showed that the animals exposed to fipronil present significant ultrastrucutural changes in hepatic cells with evident cellular and cytoplasm disorganization in hepatocytes characterized by an increase in the number of organelles, mainly mitochondria and rough endoplasmic reticulum, organelles that, in the case of the exposed animals, were probably responsible for the enzymes' synthesis that have the function of inactivating the toxic metabolites. A fat accumulation in the hepatocytes' cytoplasm (steatosis) was observed, in addition to extended vacuolated areas, mainly in regions next to the cell nucleus. Alterations observed in the nuclei of the hepatocytes pointed out cell death processes. Moreover, Kupffer cells increased in number (hyperplasia) suggesting an increase in the phagocytic activity of the liver in the exposed animals. Microsc. Res. Tech., 2011. © 2011 Wiley Periodicals, Inc.     

Ultrastructural characterization of isolated rat Kupffer cells by transmission X-ray microscopy

The ultrastructure of primary cultured rat Kupffer cells was studied using transmission X-ray microscopy as well as transmission electron microscopy. X-ray microscopical images of intact, hydrated Kupffer cells demonstrated structures such as cell nucleus separated by a nuclear membrane and filaments concentrated in the perinuclear area. Within the cytoplasm, a number of vacuoles were visible; some of these were crescent-shaped vacuoles that were half X-ray lucent, half X-ray dense; others were uniformly dense. The number of crescent-shaped vacuoles was predominant. After phagocytosis of haematite particles, enlarged vacuoles containing the ingested material were visible within the cytoplasm of Kupffer cells while crescent-shaped vacuoles were no longer detectable. Densitometric analysis of the two types of vacuole revealed that the X-ray absorption of the uniform vacuole was approximately half that of the dense part of the crescent-shaped vacuoles. This observation led to speculation on the existence of only one type of vacuole in the cytoplasm of Kupffer cells. The different morphological aspects — crescent-shaped versus uniform vacuoles — might be due to different three-dimensional orientation with respect to the image plane. Using transmission electron microscopy, the morphology of vacuoles differed more widely in diameter, density and shape. Two main types of vacuole were identified: electron-lucent and electron-dense. Based on the observation of only one type of vacuole by transmission X-ray microscopy, the different morphological aspects of vacuoles obtained by transmission electron microscopy could be explained by imaging several different sections of a crescent-shaped vacuole. From the present data it can be concluded that transmission X-ray microscopy is a versatile technique that reveals the ultrastructure of intact, unsectioned biological specimens in their aqueous environment, thereby allowing a more comprehensive interpretation of data obtained by transmission electron microscopy.     

Cytotoxic effects of permethrin on mouse liver and spleen cells

This study analyzed the histopathological and histochemical effects of different dosages of permethrin on liver and spleen cells of mice, in order to evaluate the toxic potential of this substance and the possible impairments that this chemical causes in different tissues of nontarget organisms (laboratorial conditions). The results showed that permethrin caused severe alterations in the liver cells, reducing the size of the nuclei and causing hydropic degeneration of the hepatocytes, in addition to stimulating the proliferation of Kupffer cells, altered the amount of proteins, polysaccharides, lipids, and vacuoles in the cytoplasm of the hepatocytes and congested the hepatic capillaries. As for the spleen of the treated mice, no alterations were observed in the morphology in relation to the control group, what would suggest that the spleen would continue performing its functions, without suffering morphological alterations even in the presence of the toxic agent.     

Bacteria-hemocyte interactions and phagocytosis in marine bivalves

Marine bivalves (such as mussels, oysters, and clams) are widespread mollusks in coastal waters at different latitudes; due to their filter-feeding habits, they accumulate large numbers of bacteria from the harvesting waters and may act as passive carriers of human pathogens. To cope with this challenge, bivalves possess both humoral and cellular defense mechanisms with remarkably effective capabilities. The circulating cells, or hemocytes, are primarily responsible for defense against parasites and pathogens; microbial killing results from the combined action of the phagocytic process with humoral defense factors such as agglutinins (e.g., lectins), lysosomal enzymes (e.g., acid phosphatase, lysozyme), toxic oxygen intermediates, and various antimicrobial peptides. In this work, current knowledge of the mechanisms underlying the interactions between bacteria and the hemolymph components of marine bivalves is summarized. Bacterial susceptibility to hemolymph killing in different bivalve species may be a consequence of the different ability of bacterial products to attract phagocytes, the presence or absence of specific opsonizing molecules, the hemocyte capability to bind and engulf different bacteria, and the different bacterial sensitivity to intracellular killing. The role of soluble (e.g., agglutinins and opsonins) and surface-bound factors in bacterial phagocytosis by hemocytes of the most common marine bivalve species is described and the possibility that environmental temperatures and other seasonal factors may influence this process is considered. Moreover, the potential strategies used by bacteria to evade phagocytic killing by hemocytes are discussed. From the available data it is clear that several questions need further investigation; the elucidation of the factors influencing phagocytosis in bivalves and the fundamental strategies used by bacteria to escape hemolymph killing are important not only to understand bivalve immune defenses but also to explain the persistence of pathogenic bacteria in bivalve tissues and to predict the consequent impact on human health.     

Phagocytosis--the mighty weapon of the silent warriors

Professional phagocytes, comprising polymorphonuclear neutrophils and monocyte/macrophage cells, play an important role in the host defense. Any defect in their function exposes the organism to microbial intruders terminating in fatal diseases. The functional responses of the phagocytes to bacterial and fungal infections include chemotaxis, actin assembly, migration, adhesion, aggregation, phagocytosis, degranulation, and reactive oxygen species production. Superoxide generation by phagocytic NADPH oxidase is an imperative step toward bacterial killing. Phagocytes participate in inflammatory reactions and exert tumoricidal activity. They are supported by serum factors such as immunoglobulins, cytokines, complement, the acute phase reactant C-reactive protein, production of antibacterial proteins, and others. In addition to their principal task to eliminate bacteria, they are engaged in removing damaged, senescent, and apoptotic cells. Engulfed cell debris, large particles such as latex beads, fat, and oil droplets, are examples of phagocytic activity illustrated in the present review with transmission and scanning electron microscope micrographs. Numerous factors, such as diseases and stressful conditions, affect the engulfing activity of the professional phagocytes. Our experience regarding the impaired phagocytic capacity of cells in patients with diabetes and chronic renal failure is discussed. The results obtained in our laboratory from experiments detecting the effect of strenuous physical exercise, hypothermia, fasting, and abdominal photon irradiation on the phagocytic capacity of human polymorphonuclear neutrophils and rat peritoneal macrophages are hereby summarized and the reports on those subjects in the recent literature are reviewed. A variety of assays are applied for quantifying phagocytosis. Flow cytometry based on incubation of phagocytic cells with fluorescent conjugated particles and measuring the amount of fluorescence as an indicator of the engulfing capacity of the cells is a useful method. A direct visualization of the ingested particles using light or electron microscopy is a valuable tool for estimation of phagocytic function. In our hands, the use of semithin sections of embedded phagocytes following their incubation with latex particles provided satisfactory results for measuring the total number of phagocytic cells, as well as the internalizing capacity of each individual cell. Microbiological assays, the nitroblue tetrazolium test, quantitation of antibody- and antigen-mediated phagocytosis, as well as methods reviewed in detail in other reports are additional applications for determination of this intricate process.     

Three‐dimensional morphometric comparison of normal and apoptotic endothelial cells based on laser scanning confocal microscopy observation

Three‐dimensional (3D) morphometric analysis of cellular and subcellular structures provides an effective method for spatial cell biology. Here, 3D cellular and nuclear morphologies are reconstructed to quantify and compare morphometric differences between normal and apoptotic endothelial cells. Human umbilical vein endothelial cells (HUVECs) are treated with 60 μM H₂O₂ to get apoptotic cell model and then a series of sectional images are acquired from laser scanning confocal microscopy. The 3D cell model containing plasma membrane and cell nucleus is reconstructed and fused utilizing three sequential softwares or packages (Mimics, Geomagic, and VTK). The results reveal that H₂O₂ can induce apoptosis effectively by regulating the activity of apoptosis‐related biomolecules, including pro‐apoptotic factors p53 and Bax, and anti‐apoptotic factor Bcl‐2. Compared with the normal HUVECs, the apoptotic cells exhibit significant 3D morphometric parameters (height, volume and nucleus‐to‐cytoplasm ratio) variation. The present research provides a new perspective on comparative quantitative analysis associated with cell apoptosis and points to the value of LSCM as an objective tool for 3D cell reconstruction. Microsc. Res. Tech. 76:1154–1162, 2013. © 2013 Wiley Periodicals, Inc.     

Cell and matrix morpho-functional analysis in chondrocyte micromasses

Micromass cultures represent a convenient means of studying chondrocyte physiology in the context of a tridimensional culture model. In this study, we present the first ultrastructural analysis of the distribution and organization of the extracellular components in micromasses in comparison with their cartilaginous counterparts. Primary chondrocytes obtained from osteoarthritis patients were pelleted in micromasses. Transmission electron microscopy and immunofluorescence were used to evaluate the distribution of major extracellular matrix proteins, i.e., aggrecan, chondroitin-4-sulfate, chondroitin-6-sulfate, and collagen I and II. Both approaches revealed a number of morphological features shared by micromass and cartilage chondrocytes. In particular, in micromasses, chondrocytes are in close contact with an organized extracellular matrix that adequately mimics that of cartilage. Cells were observed to establish specialized junctions for cell-extracellular matrix crosstalk. Noteworthy, cells seem endowed in a chondroitin sulfate-rich microenvironment, and thus possibly ensuring the immobilization of chemokines, a family of molecules emerging in osteoarthritis pathogenesis, in a haptotactic-like gradient to the chondrocytes, which facilitates the binding to their receptors. To determine the suitability of this model to investigate osteoarthritis pathogenesis, a potential apoptotic stimulus (endothelial IL-8) was used, and ultrastructural analysis assessed apoptosis induction. Micromass cultures were proved to be an experimental technique providing a large number of properly differentiated chondrocytes, and thus allowing reliable biochemical and morphological studies. They represent, therefore, a novel approach to osteoarthritis investigation that promises more thorough understanding of chondrocyte physiology in osteoarthritis.     

Actin machinery of phagocytic cells: universal target for bacterial attack

Uptake of microorganisms by eukaryotic cells depends on proper functioning of the actin machinery. It creates a driving force for the cell membrane deformations necessary for ingestion and killing of microbes by phagocytes. Therefore, specific alterations in the activity of the actin apparatus could be favorable for pathogenic bacteria, representing an efficient mechanism in their virulence. Such alterations are supposed to be achieved in two principle ways. One is accomplished via binding of bacterial ligands to certain surface receptors, which initiate subsequent actin cytoskeleton rearrangements. Another is to introduce cytoskeleton-targeted products directly into eukaryotic cells and in this way modulate the activity of the actin apparatus. Indeed, Legionella and some other intracellular parasites possess ligands able to stimulate certain receptors on the surface of phagocytes and possess devices suitable for translocation of effector molecules into eukaryotic cytoplasm. The results of such events could be increased uptake of these microbes and their subsequent transportation to permit multiplication in their intracellular niche. On the contrary, representatives of Clostridium and a number of other extracellular pathogens create products which penetrate eukaryotic cells and disorganize the actin cytoskeleton network, thus making uptake of these pathogens by phagocytes impossible.     

Evaluating Virtual Cells and Multistage Flow Shops: An Analytical Approach

The implementation of cellular manufacturing can be carried out through the creation of manufacturing cells (i.e., groups of dissimilar machines dedicated to a set of part types that are placed in close proximity to one another) or virtual cells (i.e., the dedication of specific machines within the current departments to a prespecified set of part types). Typically, the former involves the reorganization of the shop floor and provides the operational benefit of reduced materials handling. On the other hand, the latter configuration is simpler to implement and easier to reconfigure in light of product demand changes, but it may not offer the same operational benefits. In this paper, we propose and validate analytical approximations for comparing the performance of virtual cells and multistage flow shops. Using these approximations and hypothetical data, we identify some key factors that influence the implementation of virtual cells in a multistage flow shop environment. We conclude with an application of our approximations to industrial data.