Diagnosis of intestinal malakoplakia by fine needle aspiration cytology

Two cases of intestinal malakoplakia were diagnosed by fine needle aspiration (FNA) cytology. Clinically, these cases were mistaken for a lymphoma and a tuberculosis. Percutaneous abdominal FNA material showed numerous macrophages with the characteristic Michaelis-Gutmann bodies. These bodies were easily identified both inside and outside the macrophages in the smears.     

Bisphosphonate-related osteonecrosis of jaw (BRONJ): an anti-angiogenic side-effect?

Malakoplakia is a disease especially of the urinary tract with typical plaques most frequently observed in the urinary bladder's mucosa. In the context of immunosuppression malakoplakia can also occur in other organs. Some of these extravesical malakoplakias are associated with an infection by Rhodococcus equi, a rare human pathogen well known from veterinary medicine. Here we present the first case of a pleural malakoplakia without lung involvement caused by a proved Rhodococcus equi infection.     

Malakoplakia of bone. A case report

BACKGROUND: Malakoplakia is an uncommon but distinctive granulomatous disease, characterized by an accumulation of histiocytes or Von Hansemann cells containing intracytoplasmic, laminated Michaelis-Gutmann bodies. CASE: A 3-year-old male presented with a tender swelling in the left gluteal region that had been present for one month. Smears made from a fine needle aspirate showed large histiocytic cells containing intracytoplasmic, basophilic, laminated, targetoid Michaelis-Gutmann bodies resembling Von Hansemann cells in malakoplakia. Histopathology confirmed the diagnosis of malakoplakia of bone. CONCLUSION: This case, histologically proven to be malakoplakia, demonstrated regression of the lesion following therapy. The characteristic cytologic features and presence of Von Hansemann cells may in themselves be diagnostic and obviate the need for biopsy.     

Effect of adherence to plastic on peripheral blood monocyte and alveolar macrophage chemiluminescence

The chemiluminescence of peripheral blood monocytes and alveolar macrophages was determined in the presence of luminol and lucigenin, either before or after the cell adherence to the luminometer curvettes. In the case of monocytes, cell adherence induces an increase of luminol-dependent chemiluminescence and has almost no effect on the lucigenin-dependent chemiluminescence. However, it shows a strong inhibition of the lucigenin-dependent chemiluminescence and almost no effect on luminol-dependent chemiluminescence, in the case of alveolar macrophages. These results show that adhesion to plastic alters the metabolic burst of both monocytes and alveolar macrophages. Although the mechanisms are poorly understood, they seem to be related to the modifications that take place during the differentiation of peripheral monocytes to alveolar macrophages.     

Leishmania donovani: Superoxide dismutase level in infected macrophages

Superoxide dismutase (SOD), a metal containing enzyme is present in parasiteLeishmania donovani as well as in host macrophages both resident and activated in a detectable amount, although the level is much higher in the latter case. It is observed that at any particular protein concentration, the SOD activity is highest in the case of parasite infected macrophages and lowest in the case of normal resident macrophages; the SOD activity of thioglycolate activated macrophages lies in between the two. It is also noticed that formalin-killedLeishmania donovani neither attach to macrophages nor do they increase the SOD activity of the host. Thus, the processes, e.g. attachment of the parasite to the host membrane, subsequent membrane perturbation and thus activation of membrane bound enzyme NADPH oxidase leading to respiratory burst, may be responsible for an enormous increase in the SOD level in macrophages during infection. Moreover, the chemical nature of the SOD found in infected macrophages has been investigated by using an inhibitor, e.g. NaCN, which specifically inhibits Cu–Zn SOD but not Fe–SOD. A considerable inhibition of SOD activity by NaCN in infected macrophages confirms the chemical nature of the increased SOD to be of Cu–Zn type, usually found in host. Presumably, Cu–Zn SOD or host SOD plays a protective role at the time of parasite infection although the role of parasitic SOD or some other mechanisms for the survival of the parasite within the toxic phagolysosome environment, of the macrophage cannot be ruled out.     

In vitro cytochemical and cytophysiological study of in vivo activated mouse peritoneal macrophages

The morphological, cytochemical (acid phosphatase activity) and cytophysiological (phagocytosis) features of mouse peritoneal macrophages activated in vivo by two bacterial agents. Corynebacterium parvum parvum and Polidin, were investigated in vitro. Both immunostimulants induced an increase in cytochemical and phagocytic activities of the activated peritoneal macrophages but in different degrees, the changes being more extensive in the case of Corynebacterium parvum-activated macrophages.     

Enhancement of Host Resistance against Listeria Infection by Lactobacillus casei: Activation of Liver Macrophages and Peritoneal Macrophages by Lactobacillus casei

The functions of liver macrophages and peritoneal macrophages obtained after injection of Lactobacillus casei were examined. Listericidal activity in vivo was enhanced in liver macrophages 13 days after L. casei injection but was somewhat suppressed in the macrophages 2 days after the injection. The listericidal activity in vitro was enhanced in peritoneal macrophages obtained 13 days after L. casei injection but was suppressed in cells obtained 2 days later. The PMA-triggered respiratory burst in the liver macrophages elicited by L. casei was higher than that of resident macrophages. Alkaline phosphodiesterase activity in the liver macrophages was decreased by L. casei injection, as was also the case with peritoneal macrophages. These observations indicate that L. casei augmented cellular functions of both liver and peritoneal macrophages.     

Binding of activated macrophages to tumor cells through a macrophage lectin and its role in macrophage tumoricidal activity

A 45-60 kDa Gal/GalNAc-specific macrophage lectin was found to participate in the interaction between tumor cells and tumoricidal macrophages activated by an antitumor streptococcal preparation, OK-432, and in the tumoricidal activity of the activated macrophages. The binding between OK-432-elicited activated macrophages and murine mastocytoma P-815 cells was inhibited on preincubation of the macrophages with a neoglycoprotein (Gal-BSA) or a complex-type glycopeptide (unit B) which was a specific inhibitor of the macrophage lectin. This binding of the macrophages to P-815 cells was also inhibited on the addition of anti-macrophage lectin antiserum. Contrary to the case of OK-432-elicited macrophages, the binding of thioglycolate-elicited (responsive) macrophages to P-815 cells was inhibited only a little by Gal-BSA and unit B, and not inhibited by the antiserum. Furthermore, the tumoricidal activity of the activated macrophages was inhibited by the addition of the anti-macrophage lectin antiserum. These results suggest that the binding of activated macrophages to tumor cells through the Gal/GalNAc-specific macrophage lectin is an important part of the tumor cell killing mechanism.     

Evaluation of nitrite production by human monocyte-derived macrophages.

Reactive nitrogen intermediates are important in the anti-tumor and anti-microbial activities of rodent macrophages, but it is not known whether this is the case for human macrophages. In the present study, nitrite concentrations in vitro were used as an indicator of reactive nitrogen intermediate production by mouse, rat, and human macrophages. Human macrophages derived by culturing peripheral blood monocytes did not consistently produce detectable nitrite levels in response to any stimulus examined. Human macrophages were viable and metabolically active as indicated by the MTT assay, and their respiratory burst response to phorbol myristate acetate was increased following incubation with Interferon-gamma, as expected for typical macrophages. In contrast, rat or mouse peritoneal macrophages produced nitrite concentrations of approximately 20-100 microM in response to lipopolysaccharide, Interferon-gamma, or both. These results demonstrate substantial differences in the production of nitrites by rodent and human macrophages. Because of the heterogeneity among macrophage populations, these findings may not be applicable to all human macrophage populations, but they suggest a need for caution in extrapolating from rodent studies regarding the role of reactive nitrogen intermediates in anti-tumor or anti-microbial functions of human macrophages.     

Macrophage tropism determinants of human immunodeficiency virus type 1 in vivo.

Strains of human immunodeficiency virus type 1 differ in their abilities to infect and replicate in primary human macrophages. Chimeric clones were constructed from a provirus unable to infect macrophages (NLHX) and envelope sequences (V3 loop) of viruses derived without cultivation from brain (YU2 and w1-1c1) or spleen (w2-1b4) tissues. The substituted V3 loop sequences in each case were sufficient to confer upon NLHX the ability to infect macrophages. Furthermore, an envelope domain immediately N terminal to the V3 loop also was found to modulate the level of replication in macrophages. These results demonstrate that an envelope determinant derived directly from patients with AIDS confers HIV-1 tropism for macrophages.     

Effect of phenothiazines on protein kinase C- and calcium-dependent activation of peritoneal macrophages

The effects of some phenothiazines (promethazine, PMZ; chlorpromazine, CPZ; levomepromazine, LVPZ; thioridazine, TRDZ; trifluoperazine, TFPZ) on the activation and viability of rat peritoneal macrophages were investigated. The macrophage activation was estimated by measuring of luminol-dependent chemiluminescence, induced by phorbol-12-myristate-13-acetate (PMA) (a protein kinase C activator) or calcium ionophore A23187. The viability of macrophages was determined using ATP bioluminescence as a criterion of cell viability. It was observed that all drugs, in concentrations higher than 1 mol/L, markedly decreased the chemiluminescent index of PMA-activated or A23187-activated macrophages. The inhibitory effect was dose-dependent. It was better expressed in the case of CPZ, followed by TFPZ and TRDZ, and less expressed in the case of PMZ and LVPZ. The suppression of chemiluminescence of PMA-/A23187-activated macrophages by phenothiazines was not a result of their cytotoxic effect. Moreover, it was found that all drugs dose-dependently enhanced the viability of macrophages, estimated by ATP production. The inhibitory effects of phenothiazines on the chemiluminescence of PMA-/A23187-activated macrophages were greater than their ability to decrease KO₂-induced chemiluminescence as a result of interaction with superoxide radicals. It may be supposed that the inhibitory effect of phenothiazines on PMA-/A23187-induced chemiluminescence of macrophages is a result not only of interaction between drugs and superoxide radicals, generated during the "oxidative burst" of activated cells. Presumably the drugs have an immunomodulating effect on rat peritoneal macrophages.     

Elimination of phagocytic cells in the spleen after intravenous injection of liposome-encapsulated dichloromethylene diphosphonate

Summary Dichloromethylene diphosphonate can be used for temporary elimination of macrophages in the spleen when administered after entrapment in liposomes. No comparable effect on the macrophages of the spleen was observed with free dichloromethylene diphosphonate or in the case of empty liposomes. Marginal metallophils on the boundary between white pulp and marginal zone as well as macrophages in the marginal zone and red pulp disappeared from the spleen within one day and remained largely absent for about a week. After this time cells reappeared slowly, and at approximately four weeks after injection their presence in the spleen did not differ from that in control animals. Marginal metallophils and macrophages in the spleen were demonstrated by use of enzyme-histochemical methods and by their capacity to ingest carbon particles.     

Growth regulation of transformed T cells by nonactivated macrophages: the role of Ia expression

We studied the influence of unactivated mouse peritoneal macrophages on the proliferative capacity of a spontaneously transformed MRL-lpr/lpr T cell clone. Macrophages, 25%, induced a reduction in proliferative rate from 20% to 95% measured by [3H]thymidine incorporation and microscopic cytometry. MHC-compatible (H-2k) macrophages caused growth inhibition reciprocal to the amount of Ia expression on the macrophage. Thus, with increasing preculture of the macrophages there was both decreasing Ia and increasing suppression. H-2-incompatible macrophages had maximal inhibitory capacity without preincubation. Macrophages derived from the peritoneum of MRL-lpr/lpr mice were less suppressive than macrophages from other H-2k mice. In contrast to the case of activated macrophages in other studies, in the present system there was no killing of T cells, only reduction in proliferation. The inhibitory effect of the macrophages correlated with the spontaneous formation of rosettes between the macrophages and the T cell clone. The number of rosettes forming a single layer of T cells around the macrophages, but not the number of rosettes with multiple layers of cells, was reciprocally related to the amount of Ia expression. The results suggest that macrophages bear a surface structure that influences and modulates the growth of T cells.     

Interaction of leishmania metacyclics with macrophages

Metacyclics of L. major and putative metacyclics of L. m. mexicana survived better in explanted murine macrophages than promastigotes from mid-log phase cultures. The latter forms, however, attached in greater numbers to macrophages and, in the case of L. major, also more became intracellular. Only a small percentage of the macrophages infected with amastigotes exhibited a respiratory burst (as detected by nitroblue tetrazolium (NBT) reduction), whereas this occurred with most of the macrophages infected with either metacyclic or non-infective promastigotes of L. major. Approximately half of the macrophages infected with L. m. mexicana promastigotes reduced NBT. The results suggest that avoidance of the oxygen metabolite arm of the host cell's microbicidal activity is not the main survival strategy for metacyclics entering macrophages. Metacyclics of L. major, however, were found to be less sensitive than mid-log phase promastigotes to hydrogen peroxide and also human serum; properties which may aid their survival.     

Effect of mouse genotype on interferon production

Upon induction with Newcastle disease virus, peritoneal macrophages derived from C57BL/6 mice produced ten times as much interferon as macrophages derived from BALB/c mice. This suggested that the alleles of theIf-1 locus are expressed in vitro by these cells. Further evidence for this was obtained by studying interferon production by peritoneal macrophages derived from seven recombinant inbred and one congenic line: in each case there was complete correlation between in vivo and in vitro phenotype: macrophages fromIf-1^l mice were low producers in vitro, and macrophages fromIf-1 ^h mice were high producers in vitro.     

Stimulation of erythrophagocytosis in mouse peritoneal macrophages by chondroitin sulfates: correlation with effect of phorbol esters

Resident macrophages which were harvested from the mouse peritoneal cavity showed the attachment activity to opsonized erythrocytes (OE) without the treatment of chondroitin sulfates (CSA) or phorbol esters. Phorbol ester (phorbol 12-myristate 13-acetate or phorbol 12,13-diacetate) rapidly activated an opsonin-dependent erythrophagocytosis in resident macrophages, whereas CSA slowly activated it in vivo and in vitro. An additive effect of phorbol esters was observed in macrophages which were cultured with CSA in vitro or stimulated by the intraperitoneal injection of CSA for 1 or 2 day(s). In the case of macrophages stimulated by the intraperitoneal injection of CSA for 3 or 4 days the erythrophagocytic activity was at very high level and the additive effect of phorbol esters vanished. These results indicate that CSA plays a role in the induction of opsonin-dependent ingestion activity of resident macrophages.     

Cellular Aspects of the Resistance of Chickens to Eimeria tenella Infections*

SYNOPSIS. Sporozoites of Eimeria tenella were injected into the peritoneal cavity of normal chickens and chickens immunized against E. tenella. In some experiments normal scrum and serum from resistant chickens were injected prior to the injection of sporozoites. After 15 or 30 minute periods of intraperitoneal incubation, exudates were harvested and the occurrence of intracellular sporozoites was determined. Only macrophages and degranulated granulocytes were observed to contain sporozoites. There was no significant difference between the number of macrophages obtained from normal chickens (normal macrophages) which contained sporozoites and the number of macrophages obtained from immune chickens (immune macrophages) which contained sporozoites. Significantly fewer immune macrophages treated with immune serum contained sporozoites than untreated normal or immune cells, normal macrophages treated with either serum, or immune macrophages treated with normal scrum. Sporozoites in untreated normal macrophages did not appear to be harmed by the intracellular environment, based on structural observations. The majority of sporozoites in macrophages from all other groups were difficult to distinguish within the cytoplasm and were visibly distorted. It is hypothesized that the presence of fewer infected macrophages in exudates of immune chickens and serum-treated normal chickens was caused by an enhanced ability of these cells to destroy the parasite. Similar observations were noted in the case of sporozoites within degranulated granulocytes of experimental groups. The lack of understanding of the degranulation phenomenon makes it difficult to interpret these findings.     

The origin of chicken hematopoietic colonies as assayed in semisolid agar.

This investigation was undertaken to determine whether primitive stem cells and/or fully differentiated macrophages were the source of in vitro colonies derived from hematopoietic tissues. The chicken colony-forming cell (CFC) present in uncultured yolk sac was a nonadherent, presumably undifferentiated cell. The efficiency of colony formation in this case was approximately 0.08%. In contrast to uncultured yolk sac, the CFC present in one-week old yolk sac cultures was evidently a macrophage. Yolk sac cultures, which consisted of greater than 99% macrophages, produced colonies with an efficiency of 1-5% while cultures derived from peritoneal macrophages produced colonies with an efficiency of 10%. Silica selectively destroyed macrophages and reduced the colony forming efficiency of cells derived from yolk sac cultures.     

Cytotoxicity of lymphokine activated peritoneal macrophages against Trichomonas vaginalis]

Trichomonas vaginalis is a parasitic flagellate in the urogenital tract of human. Innate cytotoxicity of macrophages against T. vaginalis has been recognized, but any report on the cytotoxicity of lymphokine-activated macrophages to T. vaginalis is not yet available. The present study aimed to elucidate the lymphokine-activated cell mediated cytotoxic effect against T. vaginalis by mouse peritoneal macrophages. Cytotoxicity was measured by counting the release of 3H-thymidine from prelabeled protozoa, and tested in U-bottom microtiter plates. Nitrite concentration in culture supernatants was measured by standard Griess reaction. The results obtained are as follows: 1. The cytotoxicity of macrophages was increased by addition of rIL-2 or rIFN-gamma. 2. Cytotoxicity of macrophages was reduced by addition of rIL-4 to rGM-CSF, rIL-2 or rIFN-gamma. 3. Crude lymphokine mixed with anti-IL-2 decreased the cytotoxicity of macrophages. 4. In case of macrophages cultured with rIFN-gamma or rIL-4, the concentration of nitrite was related with cytotoxicity of macrophages against T. vaginalis, but the cytotoxicity of macrophages cultured with rIL-2 and rIFN-gamma was decreased in spite of its high production of nitrite. From the results obtained, it is assumed that rIL-2 and rIFN-gamma enhance the cytotoxicity of macrophages while rIL-4 inhibits the cytotoxicity against T. vaginalis, and that the production of nitrite does not relate with the cytotoxicity of macrophages, but nitric oxide may play a role as an inhibitory factor on the proliferation of T. vaginalis.