Cell and Vascular Response to Infection and Injury 5

Total Page:16

File Type:pdf, Size:1020Kb

Cell and Vascular Response to Infection and Injury 5 Chapter 5 Cell and Vascular Response 5 to Infection and Injury Activation of the defense systems gives rise to inflam- small numbers (1–6%). Their life span is somewhat mation which, if microbes are involved, is called in- longer than that of the neutrophils. Under normal fection. The reactions may be acute or chronic and condition they migrate into the tissues and are found involve different types of inflammatory cells together scattered everywhere, but especially in the mucosa with lymphatics and blood vessels. of the gastrointestinal tract. In hypersensitivity reac- tions a high number of eosinophils may be present in tissues as well as in the circulating blood. Mostly 5.1 the nucleus has no more than two segments and the Inflammatory Cells cytoplasm carries large, bright, eosinophilic granules, The types, number and proportion of inflammatory which differentiate them from old neutrophils with cells taking part in an inflammatory reaction depend eosinophilic cytoplasm. Eosinophilic granules contain on the type of inflammation/infection. cationic (positively charged) proteins, three of which are major basic protein (MBP), eosinophilic cationic protein (ECP), and eosinophilic derived neurotoxin 5.1.1 (EDN) (Peters et al. 1986). These positively charged Neutrophils proteins make eosinophils able to bind to negatively Neutrophils or granulocytes (i.e., white blood cells charged molecules on other cells and make them toxic with discreet granules in the cytoplasm) are continu- for worms and other large parasites. ously produced in the bone marrow and make up the main part of the white blood cells that normally circu- late in the blood (40–75%). At need more neutrophils 5.1.3 are recruited, which is followed by an increased num- Lymphocytes ber in the circulation. Neutrophils are end cells and As already mentioned, B cells originate in the bone thus cannot divide. Their life span is short (3–4 days). marrow and T cells in the thymus. Together they make The nucleus of the cell is divided into two to five seg- up 20–45% of the white cells circulating in the periph- ments depending on the age of the cell (Fig. 12.1b). eral blood. Mature lymphocytes are small and have a The cytoplasm carries two types of fine, inconspicuous, round, compact and dark nucleus, and sparse cyto- and enzyme-containing granules. Neutrophils engulf plasm (Fig. 15.1). In routinely stained sections, B and (phagocytose) microbes and kill them by means of the T cells look alike. However, it is possible to differenti- enzymes stored in the cytoplasm. When released into ate between them and also between their subgroups by the tissue these enzymes also have the ability to de- means of immunohistochemical staining techniques grade dead cells and tissue fragments. Neutrophils do using monoclonal antibodies directed against their not reside in the tissues under normal condition, but surface antigens. are called upon at need, and thus are the dominating Stimulated lymphocytes are larger than mature lym- cells in acute inflammation. In old multisegmented phocytes. In routinely prepared sections stimulated B neutrophils the cytoplasm becomes eosinophilic and cells are easily identified in the fully developed germi- the cells may be mistaken for eosinophils. nal center of a lymphocytoma. They have large, light, and somewhat irregular nuclei, which contain one or two nucleoli (Fig. 18.2c). However, stimulated T cells, 5.1.2 usually components of a mixed lymphocytic infiltrate, Eosinophils stand out because they have a slightly irregular form Like neutrophils, eosinophils are end cells, produced and are larger and seem more compact than the sur- in the bone marrow. They circulate in the blood in rounding normal lymphocytes (Fig. 20.5c). The latter 22 5 Cell and Vascular Response to Infection and Injury Fig. 5.1 Mast cells. a ACA. Between three dilated venules there ter (arrow); H&E, ×1000. c ACA. A small mast cell with hazy are two large mast cells (large arrows) and two small heav- cytoplasm (arrow). The vessel is an arteriole; H&E, ×1000. ily charged with granules (small arrows); toluidine blue, ×400. d Mastocytoma. Arrows binuclear cells; H&E, ×400 b ACA. A large mast cell stuffed with large granules in the cen- is an artifact probably due to too much stain and/or blood, but are present in connective tissue through- thick sections. The reason for this proposition is that out the body. Morphologically there are two variants in smears (Fig. 26.3c) and in sections, slightly faded of mast cells, a larger and a smaller. The large cells are after demonstration using a carbon arc lamp projec- also called connective tissue mast cells, and the small tor, these cells also reveal large nuclei containing one cells mucosal mast cells. In spite of this, both variants or two nucleoli and many mitotic figures (Fig. 26.3f). may be present together in the skin as well as in the In routinely stained sections, stimulated T cells are mucous membranes. The large mast cell is triangular, impossible to differentiate from T cell lymphoma cells has a round nucleus and a rich cytoplasm stuffed with (Sect. 26.3.4). large granules. The small mast cell is round or slightly oval. It has a round nucleus and because of densely packed small granules the cytoplasm is hazy. Among 5.1.4 other substances the granules contain histamine. In Plasma Cells normal skin, mast cells are located around vessels in Plasma cells, the effector cells of B cells, are larger than the papillary dermis and close to nerves and append- lymphocytes. They are oval and have a round and ec- ages. centrically located nucleus. In the cytoplasm close to A greatly increased number of mast cells are found the nucleus there is a typical crescent-like light area. in urticaria pigmentosa, mastocytoma, and related In longstanding lesions binuclear plasma cells may be conditions. However, the number of mast cells is also present (Figs. 18.1 and 18.4b). Plasma cells are com- increased in lesions of common dermatoses such as mon in chronic inflammation and are often numer- chronic dermatitis, psoriasis, and lichen planus (Tharp ous in infections caused by spirochetes and Leishma- 2001). According to the experience of the author there nia protozoa. They develop and mature in the lymph is also an increase in mast cells in infectious diseases nodes and migrate to the skin. such as acrodermatitis chronica atrophicans (ACA), a kind of borreliosis, and secondary syphilis, and in amalgam tattoo. In acute inflammation/infection to- 5.1.5 gether with basophils they release histamine (Sect. Mast Cells 5.2.1). Mast cells originate from the bone marrow and are Once recognized in H&E-stained sections, mast able to divide. They do not normally circulate in the cells are not difficult to identify, but they are better 5.2 Acute Inflammation 23 Fig. 5.2 Phagocytosis. Smear from a subepidermal vesicle. with a newly engulfed neutrophil. In the middle there is a group There are two old neutrophils with a multisegmented nucleus of macrophages which contain the remains of neutrophils in (arrowheads) and several macrophages. Arrow, top left macro- various stages of processing in the cytoplasm. In the macro- phage in close contact with a neutrophil containing a disinte- phage in the top right corner the remains of a nucleus are lying grating, swollen neutrophil; arrow, bottom right macrophage in a vacuole (arrow). Mayer staining, ×1000 displayed by means of special stains such as toluidine of phagocytosis are often, as in this book, called his- blue or Giemsa stains, which accentuate the granules tiocytes. Macrophages (histiocytes) are a common (Figs. 5.1 and 29.7b). In sections stained with tolu- component of inflammatory cell infiltrates in chronic idine and Giemsa, granules become blue and with infections and in the healing stage of acute infections May-Grünwald Giemsa metachromatically red. (Fig. 5.2). 5.1.6 5.2 Basophils Acute Inflammation Basophils are bone marrow-derived granulocytes The histologic hallmarks of acute inflammation are which circulate in the blood in small numbers (0–1%). exudation of plasma and migration of inflammatory They have a segmented nucleus and like mast cells cells, predominantly neutrophils, from postcapillary carry basophilic granules containing histamine in the venules into the perivascular tissue. cytoplasm. They are not precursors of mast cells. 5.2.1 5.1.7 Active Phase Monocytes/Macrophages In response to injury or bacterial infection, histamine Monocytes have an abundant cytoplasm and a large and serotonin, short-lived vasoactive chemical media- bean-shaped nucleus. They originate from the bone tors stored in the tissue (histamine in mast cells and marrow and circulate in the blood (2–10%). However, basophils and serotonin in platelets) are released and after a short time in the circulation they migrate into start the inflammatory process. Histamine and sero- connective tissue where they become larger, acquire tonin cause dilatation of arterioles, which increases the capacity to phagocytose and when doing so be- the blood flow and capillary pressure. Closed capillar- come activated. Like neutrophils, macrophages rec- ies open up and become filled with blood. Due to the ognize bacteria by surface receptors that are specific increased capillary flow and pressure, postcapillary for bacterial products. On activation they become venules become distended and gaps appear between even larger, and their ability to phagocytose and kill the endothelial cells, through which plasma leaks out bacteria increases. Tissue macrophages without signs into the surrounding tissue. The gaps are the result of 24 5 Cell and Vascular Response to Infection and Injury contraction of two adjacent endothelial cells brought but then they suddenly stop and stick to the intima about by the influence of the vasoactive mediators. before they sneak through the wall using the gaps be- Contracted cells bulge into the vascular lumen and tween the epithelial cells.
Recommended publications
  • Pigmentation Associated Histopathological Variations in Sympathetic Ophthalmia
    Br J Ophthalmol: first published as 10.1136/bjo.64.3.220 on 1 March 1980. Downloaded from British Jolarnal of Ophthalmology, 1980, 64, 220-222 Pigmentation associated histopathological variations in sympathetic ophthalmia GEORGE E. MARAK, JR., AND HIROSHI IKUI From the Department of Ophthalmology, Georgetown University, Washington, DC, USA, and the Department of Ophthalmology, Kyishia University, Fukiioka, Japani SUMMARY The severity of inflammation in sympathetic ophthalmia is related to the degree of pigmentation, and the granulomatous response seems to be related to pigmentation. Eosinophilia is also associated with pigmentation, but this association appears to be fortuitous and is a result of the association of eosinophilia with severity of the inflammation. Elsching presented his most confusing pearl to the reasonably be considered intermediate in pigmen- ophthalmological community when he proposed tation between North American black and white that sympathetic ophthalmia represented an autoim- populations. mune response to uveal pigment.12 Recent obser- The magnitude of choroidal thickening by the vations have raised considerable doubts about the inflammatory infiltrate, the intensity of tissue role of uveal pigment as the offending antigenin eosinophilia, and the proportion of the epithelioid sympathetic ophthalmia.34 The function of the uveal cell response in the choroid compared to the melanocytes in sympathetic ophthalmia is not well lymphocytic infiltration were rated by a single understood, but pigmentary disturbances occur
    [Show full text]
  • Fine Structure and Histochemistry of Epithelioid Cells in Sarcoidosis
    Thorax: first published as 10.1136/thx.29.1.115 on 1 January 1974. Downloaded from Thorax (1974), 29, 115. Fine structure and histochemistry of epithelioid cells in sarcoidosis E. M. VALERIE JAMES and W. JONES WILLIAMS Pathology Department, Welsh National School of Medicine, The Heath, Cardiff James, E. M. Valerie and Jones Williams, W. (1974). Thorax, 29, 115-120. Fine structure and histochemistry of epithelioid cells in sarcoidosis. In this fine structure study of epithelioid cells in the granulomata of sarcoidosis we confirm our previous findings that they appear to be synthesizing rather than phagocytosing cells. The numerous characteristic intracyto- plasmic vesicles, 0 5 ,u in size, are shown to contain mucoglycoprotein and only rarely acid phosphatase activity. Epithelioid cells show varying quantities of extravesicular acid phos- phatase activity which is sometimes on the outer surface of the protein-containing vesicles. The possible role of secretory products of epithelioid cells in the formation and persistence ofgranulomata is discussed. It is suggested that epithelioid cells may be forming lymphokines. We have previously demonstrated that the fine that of Ericsson and Trump (1965) using the lead structure of granulomata in sarcoidosis and tuber- nitrate Gomori technique. Substrate-free and sodium culosis (Jones Williams, Erasmus, James, and fluoride control blocks were also prepared. After being Davies, 1970), in the Kveim test lesion (Jones washed in acetate buffer solutions the tissues were post-fixed in Millonig's osmium tetroxide, dehydrated, Williams, 1972), and in chronic beryllium disease and embedded in Araldite. Sections were cut on an (Jones Williams, Fry, and James, 1972a) are LKB ultramicrotome and 0.5 ,u sections were stained http://thorax.bmj.com/ similar.
    [Show full text]
  • Review Article
    J Clin Pathol: first published as 10.1136/jcp.36.7.723 on 1 July 1983. Downloaded from J Clin Pathol 1983;36:723-733 Review article Granulomatous inflammation- a review GERAINT T WILLIAMS, W JONES WILLIAMS From the Department ofPathology, Welsh National School ofMedicine, Cardiff SUMMARY The granulomatous inflammatory response is a special type of chronic inflammation characterised by often focal collections of macrophages, epithelioid cells and multinucleated giant cells. In this review the characteristics of these cells of the mononuclear phagocyte series are considered, with particular reference to the properties of epithelioid cells and the formation of multinucleated giant cells. The initiation and development of granulomatous inflammation is discussed, stressing the importance of persistence of the inciting agent and the complex role of the immune system, not only in the perpetuation of the granulomatous response but also in the development of necrosis and fibrosis. The granulomatous inflammatory response is Macrophages and the mononuclear phagocyte ubiquitous in pathology, being a manifestation of system many infective, toxic, allergic, autoimmune and neoplastic diseases and also conditions of unknown The name "mononuclear phagocyte system" was aetiology. Schistosomiasis, tuberculosis and leprosy, proposed in 1969 to describe the group of highly all infective granulomatous diseases, together affect phagocytic mononuclear cells and their precursors more than 200 million people worldwide, and which are widely distributed in the body, related by http://jcp.bmj.com/ granulomatous reactions to other irritants are a morphology and function, and which originate from regular occurrence in everyday clinical the bone marrow.' Macrophages, monocytes, pro- histopathology. A knowledge of the basic monocytes and their precursor monoblasts are pathophysiology of this distinctive tissue reaction is included, as are Kupffer cells and microglia.
    [Show full text]
  • 2016 Essentials of Dermatopathology Slide Library Handout Book
    2016 Essentials of Dermatopathology Slide Library Handout Book April 8-10, 2016 JW Marriott Houston Downtown Houston, TX USA CASE #01 -- SLIDE #01 Diagnosis: Nodular fasciitis Case Summary: 12 year old male with a rapidly growing temple mass. Present for 4 weeks. Nodular fasciitis is a self-limited pseudosarcomatous proliferation that may cause clinical alarm due to its rapid growth. It is most common in young adults but occurs across a wide age range. This lesion is typically 3-5 cm and composed of bland fibroblasts and myofibroblasts without significant cytologic atypia arranged in a loose storiform pattern with areas of extravasated red blood cells. Mitoses may be numerous, but atypical mitotic figures are absent. Nodular fasciitis is a benign process, and recurrence is very rare (1%). Recent work has shown that the MYH9-USP6 gene fusion is present in approximately 90% of cases, and molecular techniques to show USP6 gene rearrangement may be a helpful ancillary tool in difficult cases or on small biopsy samples. Weiss SW, Goldblum JR. Enzinger and Weiss’s Soft Tissue Tumors, 5th edition. Mosby Elsevier. 2008. Erickson-Johnson MR, Chou MM, Evers BR, Roth CW, Seys AR, Jin L, Ye Y, Lau AW, Wang X, Oliveira AM. Nodular fasciitis: a novel model of transient neoplasia induced by MYH9-USP6 gene fusion. Lab Invest. 2011 Oct;91(10):1427-33. Amary MF, Ye H, Berisha F, Tirabosco R, Presneau N, Flanagan AM. Detection of USP6 gene rearrangement in nodular fasciitis: an important diagnostic tool. Virchows Arch. 2013 Jul;463(1):97-8. CONTRIBUTED BY KAREN FRITCHIE, MD 1 CASE #02 -- SLIDE #02 Diagnosis: Cellular fibrous histiocytoma Case Summary: 12 year old female with wrist mass.
    [Show full text]
  • Perivascular Epithelioid Cell Tumor of Gastrointestinal Tract Case Report and Review of the Literature
    Perivascular Epithelioid Cell Tumor of Gastrointestinal Tract Case Report and Review of the Literature Biyan Lu, MD, PhD, Chenliang Wang, MD, Junxiao Zhang, MD, Roland P. Kuiper, PhD, Minmin Song, MD, Xiaoli Zhang, MD, Shunxin Song, MD, Ad Geurts van Kessel, PhD, Aikichi Iwamoto, MD, PhD, Jianping Wang, MD, PhD, and Huanliang Liu, MD, PhD Perivascular epithelioid cell tumors of gastrointestinal tract (GI PECo- markers. Molecular pathological assays confirmed a PSF-TFE3 gene mas) are exceedingly rare, with only a limited number of published fusion in one of our cases. Furthermore, in this case microphthalmia- reports worldwide. Given the scarcity of GI PEComas and their associated transcription factor and its downstream genes were found to relatively short follow-up periods, our current knowledge of their exhibit elevated transcript levels. biologic behavior, molecular genetic alterations, diagnostic criteria, Knowledge about the molecular genetic alterations in GI PEComas and prognostic factors continues to be very limited. is still limited and warrants further study. We present 2 cases of GI PEComas, one of which showed an (Medicine 94(3):e393) aggressive histologic behavior that underwent multiple combined che- motherapies. We also review the available English-language medical Abbreviations: AML = angiomyolipoma, CCMMT = clear cell literature on GI PEComas-not otherwise specified (PEComas-NOS) and myomelanocytic tumor of the falciform ligament/ligamentum teres, discuss their clinicopathological and molecular genetic features. CCST = clear cell ‘‘sugar’’ tumor of the lung, CDK2 = cyclin- Pathologic analyses including histomorphologic, immunohisto- dependent kinase 2, C-MET = met proto-oncogene, CRP = C- chemical, and ultrastructural studies were performed to evaluate the reactive protein, CT = computed tomography, DCT = dopachrome clinicopathological features of GI PEComas, their diagnosis, and differ- tautomerase, GAPDH = glyceraldehyde-phosphate dehydrogenase, ential diagnosis.
    [Show full text]
  • Avian Blood. the Transformed Cells Occurred in Incubated Blood
    THE FORMATION OF MACROPHAGES, EPITHEIID CELLS AND GIANT CELLS FROM LEUCOCYTES IN INCUBATED BLOOD * MAGARET REED LEWIS (From th Carxge Laboratory of Embryology, Johns Hopkixs edical Scho) While tissue cultures would seem to afford an appropriate technic for the study of the part taken by the white blood-cells in various conditions, this method has seldom been employed. In 1914 Awro- row and Tlmofejewskij studied the white blood-cells of leukemic blood in plasma cultures, Loeb (i92o) followed the amebocytes of the king crab in dotted blood, and Carrel (192I) observed the growth of the buffy coat of the centrifuged blood of the adult chicken in plasma cultures. The method by which the observations incor- porated in this paper were made is simpler than that of any of the above investigators, consisting merely of the incubation of hanging drops of blood taken, by means of a paraffined pipette, either from the heart or from the peripheral circulation. The transformation and growth of the leucocytes into macro- phages, epithelioid cells, and giant cells were observed in the blood of the chick embryo, young chicken, adult hen, mouse, guinea-pig and dog, and i human blood. In every kind of blood emined there developed first a large wandering cell, several times larger than any of the normal leucocytes, which was phagocytic for red blood- cells, melanin granules, carbon partides, dead granulocytes, and tuberde bacili Somewhat later there appeared a cell more like a prmitive mesenchyme cell, and still later the epithelioid cell was formed. This cell was sometimes binudeate and in some instances a :ypical multinudeated giant cell (Lahans giant cell) was formed.
    [Show full text]
  • Differentiation of Macrophages from Normal Human Bone Marrow in Liquid Culture
    Differentiation of macrophages from normal human bone marrow in liquid culture. Electron microscopy and cytochemistry. D R Bainton, D W Golde J Clin Invest. 1978;61(6):1555-1569. https://doi.org/10.1172/JCI109076. Research Article To study the various stages of human mononuclear phagocyte maturation, we cultivated bone marrow in an in vitro diffusion chamber with the cells growing in suspension and upon a dialysis membrane. At 2, 7, and 14 days, the cultured cells were examined by electron microscopy and cytochemical techniques for peroxidase and for more limited analysis of acid phosphatase and arylsulfatase. Peroxidase was being synthesized in promonocytes of 2- and 7-day cultures, as evidenced by reaction product in the rough-surfaced endoplasmic reticulum, Golgi complex, and storage granules. Peroxidase synthesis had ceased in monocytes and the enzyme appeared only in some granules. By 7 days, large macrophages predominated, containing numerous peroxidase-positive storage granules, and heterophagy of dying cells was evident. By 14 days, the most prevalent cell type was the large peroxidase-negative macrophage. Thus, peroxidase is present in high concentrations in immature cells but absent at later stages, presumably a result of degranulation of peroxidase-positive storage granules. Clusters of peroxidase-negative macrophages with indistinct borders (epithelioid cells), as well as obvious multinucleated giant cells, were noted. Frequently, the interdigitating plasma membranes of neighboring macrophages showed a modification resembling a septate junction--to our knowledge, representing the first documentation of this specialized cell contact between normal macrophages. We suggest that such junctions may serve as zones of adhesion between epithelioid cells.
    [Show full text]
  • Modulation of Neutrophil Influx in Glomerulonephritis in the Rat with Anti-Macrophage Inflammatory Protein-2 (MIP-2) Antibody
    Modulation of neutrophil influx in glomerulonephritis in the rat with anti-macrophage inflammatory protein-2 (MIP-2) antibody. L Feng, … , T Yoshimura, C B Wilson J Clin Invest. 1995;95(3):1009-1017. https://doi.org/10.1172/JCI117745. Research Article The role of the chemokine, macrophage inflammatory protein-2 (MIP-2), during anti-glomerular basement membrane (GBM) antibody (Ab) glomerulonephritis (GN) was studied. Rat MIP-2 cDNA had been cloned previously. Recombinant rat MIP-2 (rMIP-2) from Escherichia coli exhibited neutrophil chemotactic activity and produced neutrophil influx when injected into the rat bladder wall. By using a riboprobe derived from the cDNA and an anti-rMIP-2 polyclonal Ab, MIP-2 was found to be induced in glomeruli with anti-GBM Ab GN as mRNA by 30 min and protein by 4 h, with both disappearing by 24 h. The expression of MIP-2 correlated with glomerular neutrophil influx. A single dose of the anti-MIP- 2 Ab 30 min before anti-GBM Ab was effective in reducing neutrophil influx (40% at 4 h, P < 0.01) and periodic acid-Schiff deposits containing fibrin (54% at 24 h, P < 0.01). The anti-rMIP-2 Ab had no effect on anti-GBM Ab binding (paired-label isotope study). Functional improvement in the glomerular damage was evidenced by a reduction of abnormal proteinuria (P < 0.05). These results suggest that MIP-2 is a major neutrophil chemoattractant contributing to influx of neutrophils in Ab-induced glomerular inflammation in the rat. Find the latest version: https://jci.me/117745/pdf Modulation of Neutrophil Influx in Glomerulonephritis in the Rat with Anti-Macrophage Inflammatory Protein-2 (MIP-2) Antibody Lili Feng, Yiyang Xia, Teizo Yoshimura,* and Curtis B.
    [Show full text]
  • Innate and Adaptive Immune Responses in Pulmonary Sarcoidosis
    From Department of Medicine Solna, Respiratory Medicine Unit Karolinska Institutet, Stockholm, Sweden Innate and Adaptive Immune Responses in Pulmonary Sarcoidosis Maria Wikén Stockholm 2010 The figure on the front page shows a lung with a granuloma and two T cells hit by laser beams, and was made by help from Victor Wikén. All previously published papers were reproduced with permission from the publisher. Published by Karolinska Institutet. Printed by Larserics Digital Print AB. © Maria Wikén, 2010 ISBN 978-91-7409-894-5 Till min familj ABSTRACT Sarcoidosis is an inflammatory disease characterized by formation of granulomas in various organs and tissues. Although it is a systemic disorder, the lungs are commonly affected, and an infiltration of T cells, in particular CD4pos T helper 1 (Th1) cells, is seen in the lower airways. HLA-DRB1*0301pos (HLA-DR3pos) patients commonly present with acute disease onset, typically with Löfgren´s syndrome, accumulation of lung CD4pos T cells expressing the T cell receptor (TCR) gene segment AV2S3 (AV2S3pos T cells) and good prognosis. In contrast, HLA-DR3neg patients show insidious disease onset and are at risk of developing lung fibrosis. The aetiology of sarcoidosis is still unknown; however, several studies indicate an infectious cause, suggesting a role for innate immune receptors, including toll-like receptors (TLRs) and nod-like receptors (NODs). Recently, the mycobacterial protein mKatG was identified in sarcoidosis tissues but not in healthy subjects, and T cell responses have been reported to mKatG. However, their specificity and cytokine profile, as well as the phenotype of lung-accumulated T cells in general, has not been that well described.
    [Show full text]
  • Chairman: Dr H. L. Israel, M.D. the Fine Structure of Sarcoid and Tuberculous Granulomas
    Postgraduate Medical Journal (August 1970) 46, 496-500. SESSION III Chairman: Dr H. L. Israel, M.D. The fine structure of sarcoid and tuberculous granulomas W. JONES WILLIAMS D. A. ERASMUS E. M. VALERIE JAMES T. DAVIES Welsh National School of Medicine and University College, Cardiff Summary are obviously metabolically active cells, with pro- The granulomas of sarcoidosis and non-caseating perties suggesting both phagocytosis and biosyn- tuberculosis show similar cell-types: two forms of thesis. epithelioid cells, A and B, giant cells, lymphocytes The published accounts of the fine structure of and 'activated' mononuclear cells. The morphology sarcoid granulomas have also not demonstrated any of epithelioid cells suggests that they are primarily causative agent but most investigators agree that biosynthetic rather than phagocytic. epithelioid cells are active cells though there is no The relationship of these various cells to each other unanimity as to their exact function (Bassett et al., is discussed and the following sequence of granuloma 1967; Gusek & Behrend, 1969; Hirsch, Fedorko & development is suggested: circulating lymphocyte -- Dwyer, 1967; Kalifat, Bouteille & Delarue, 1967; activated mononuclears -> A -* B epithelioid cell Kelemen, Soltesz & Mandi, 1969; Wanstrup & whose secretory product stimulates transformation Christensen, 1966). of other circulating lymphocytes. We shall present and discuss our initial fine structural findings and compare the features of the sarcoid granulomas with that of non-caseating Introduction tuberculosis. The fascination of the search for the causation of sarcoidosis continues and embraces ever widening Materials and methods techniques. The sarcoid granuloma, on light micro- The material examined was obtained from one scopy, consists of closely apposed epithelioid cells, sarcoid spleen and two bacteriologically proven intermingled giant cells, often of the Langhan, tuber- tuberculous lymph nodes.
    [Show full text]
  • Epithelioid Cell Granulomas Experimentally Induced by Prototheca in the Skin of Mice: a Light Microscopic Study
    21 Hiroshima J. Med. Sci. Vol.44, No.2, 21-27, June, 1995 HIJM 44-5 Epithelioid Cell Granulomas Experimentally Induced by Prototheca in the Skin of Mice: A Light Microscopic Study Yasuhiro HORIUCHI and Mikio MASUZAWA Department of Dermatology, Kitasato University School of Medicine, Sagamihara, Japan ABSTRACT Prototheca wickerhamii, an achlorophyllous algae, was previously found to induce massive epithelioid cell granulomas in the skin of mice. By means of light microscopy, examination was made of the histological reactions involved in epithelioid cell granulomas induced by intrader­ mal and/or subcutaneous inoculation of Prototheca wickerhamii in BALB/c and ICR mice. Six BALB/c mice showed granuloma nodules while only three of six ICR mice did so. Based on the results of the present and previous studies, BALB/c mice may be considered a strain particularly vulnerable to contracting epithelioid cell granuloma and ICR mice, a resistant strain. In very early lesions at one week following initial prototheca inoculation, cellular infiltration with varying numbers of polymorphonuclear leukocytes, lymphocytes and some macrophages was observed throughout the dermis and subcutaneous fat tissue. In early lesions at one to two months after inoculation, focal granulomas composed of histiocytic cells and/or macro­ phages were observed. Mast cells were occasionally present among the histiocytic cell infil­ trates. In the granulomatous lesions at two to three months, scattered eosinophils and some lymphocytes were seen. Central necrosis, with numerous neutrophils and many endospores surrounded by the granuloma, was often observed. In late stage lesions at six months, massive lymphocyte and plasma cell infiltration surrounding and/or intervening between vacuolated epithelioid cell clusters was evident.
    [Show full text]
  • 354030245X Dermatopathology.Pdf
    Eva Brehmer-Andersson Dermatopathology Eva Brehmer-Andersson Dermatopathology With 138 Figures in 445 Separate Illustrations and 5 Tables 123 Eva Brehmer-Andersson Värtavägen 17 115 53 Stockholm Sweden ISBN-10 3-540- 30245-X Springer-Verlag Berlin Heidelberg NewYork ISBN-13 978-3-540- 30245-2 Springer-Verlag Berlin Heidelberg NewYork Library of Congress Control Number: 2006920598 This work is subject to copyright. All rights are reserved, whether the whole or part of the material is concerned, speci.cally the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on micro.lms or in any other way, and storage in data banks. Duplication of this publication or parts thereof is permitted only under the provisions of the German Copyright Law of September 9, 1965, in its current version, and permission for use must always be obtained from Springer-Verlag. Violations are liable for prosecution under the German Copyright Law. Springer is a part of Springer Science+Business Media springer.com © Springer-Verlag Berlin Heidelberg 2006 Printed in Germany The use of general descriptive names, registered names, trademarks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. Product liability: the publishers cannot guarantee the accuracy of any information about dos- age and application contained in this book. In every individual case the user must check such information by consulting the relevant literature. Editor: Gabriele Schröder, Heidelberg Desk Editor: Ellen Blasig, Heidelberg Production and Typesetting: LE-TEX Jelonek, Schmidt & Vöckler GbR, Leipzig Cover Design: Frido Steinen-Broo, EStudio Calamar, Spain Printed on acid-free paper 24/3100/YL 5 4 3 2 1 0 Preface The purpose of this book is to introduce future pathologists and dermatolo- gists to the exciting field of dermatopathology.
    [Show full text]