The morphological characterization of alveolar macrophages of bronchoalveolar lavage fluid from 43 individuals, occupationally exposed to inorganic particles (asbestos 19, silica 10, coal 14) for long period, were studied by light and electron microscopy. Increased incidence of particle-laden macrophages and multinucleation were observed in cytospin preparations. Increased ruffling, filopodia, pinocytotic vesicles and subplasmalemmal linear densities were seen on the surfaces of alveolar macrophages. Interstitial macrophages also contained heterogeneous particles in the cytoplasm and revealed few filopodia, abundant cytoplasmic filaments and dilated endoplasmic reticulum. In vitro phagocytosis of particles using rat peritoneal macrophages revealed Ia antigen on the cytoplasmic and phagosome membranes. These observations are consistent with the concept of activation of alveolar macrophages by inhaled inorganic particles. Although the fate of particle-laden macrophages in the alveolar milieu remains to be clearly elucidated, the morphology of alveolar macrophages of the individuals with chronic exposure to inorganic particles must be an indicator for clearance mechanism in the lower respiratory tract.

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To elucidate the role of alveolar macrophages in inflammatory and fibrosing processes of lung, the paraquat-induced alveolitis in rats was investigated by the immunohistochemical method with especial references to the class II major histocompatibility antigen complex (MHC) expression. Two days after the peritoncal injection of paraquat, the class II MHC expression by type II alveolar epithelial cells was observed prior to obvious histological and immunohistochemical changes except for pulmonary edema. From four days after the injection, alveolar macrophages increased in number, and expressed class II MHC, which was not demonstrated in the normal control. The intensity of the expression was variable, and alveolar macrophages containing abundant dust particles were still absent for class II MHC. On the contrary, the class II MHC expression by alveolar epithelial cells turned obscure. Two weeks after the injection, alveolar fibrosis developed and inflammatory cell infiltration was almost disappeared. A small number of class II MHC negative foamy cells were observed in the alveolar spaces. Alveolar capillary endothelial cells and alveolar septal cells, which expressed class II MHC in the normal control, did not show significant changes in paraquat-induced alveolitis. These results suggest that resident alveolar macrophages with the active phagocytic activity are not the main component in inflammatory reactions in the lung. In contrast, type II alveolar epithelial cells participate invariably in inflammatory process of alveolitis.

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It has been thought that peripheral macrophages do not usually proliferate and that the population of macrophages is maintained by influx of monocytes or immature mononuclear phagocytes originating from bone marrow. However, several authors reported that in some normal or pathological conditions, such as inflammations or tumors, local proliferation of peripheral macrophages was observed. Growth of macrophages is known to be induced by protein factors, such as colony stimulating factors (CSFs). On the other hand, we recently demonstrated that lipoproteins, dead cells or cell debris can also induce growth of mouse macrophages and we elucidated that their active components are lipids. The active lipid species are cholesterol (esters), triglycerides and several negatively charged phospholipids. We now consider that it is an important system regulating number of peripheral macrophages in vivo and that this lipid-induced macrophage growth may exist in from lower animals to mammals because scavenging dead cells or denatured lipoproteins is the most fundamental function of macrophages.

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We have recently reported that the existence of a specific cell type, called the “Fibrohistiocytoid (FH) cell”, which was found in a variety of chronic inflammatory tissues. This FH cell includes a series of cell types from metamorphosized fibroblast to a certain cell type which resembles a histiocytic fibroblast. In this study, to examine whether cultured human dermal fibroblast (FB) was transformed into a FH cell, it was studied using morphological, immunocytochemical and enzyme-cytochemical techniques. Three different population doubling level (PDL), 2-4 PDL, 15-20 PDL and 30-35 PDL FBs were examined. Morphologically, FBs had a short spindle shaped or elliptical cell body, an irregular shaped nucleus, fragmented rough endoplasmic reticula distributed in a dendritic pattern and a few dense bodies, especially marked in 15-20 PDL and 30-35 PDL FBs, but did not have monocyte/macrophage-specific characteristics of pseudopodia, multivesicular bodies and phagosomes. Cytochemically, all three different PDL FBs showed the positive reaction to α₁-naphthyl butyrate esterase and acid phosphatase, and further only both of 15-20 PDL and 30-35 PDL FBs revealed the increasing immunoreactivity to α₁-antitrypsin, α₁-antichymotrypsin, lysozyme and ferritin. Moreover, the immunoreactivity to HLA-DR, HLA-DP and HLA-DQ was induced on 2-4 PDL and 15-20 PDL FBs treated with interferon-gamma. It has been considered that these immuno- and enzymecytochemical markers were found in FH cells as well as histiocytes in vivo, but never found in non-inflammatory fibroblasts in vivo. These data suggested that FBs under a certain condition in vitro expressed the analogous phenotype to FH cells. It seemed that FH cell might be a transformed fibroblast. Furtheremore, we also evaluated the similarity of FBs to MFH tumor cells in vivo and in vitro in the same way. MFH tumor cells revealed some similar phenotypes not only to FH cells but also FBs, suggesting that MFH might be originated from FH cells.

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The clinicopathological characteristics of 10 cases of non-Hodgkin lymphoma with lymph node infarction were reported.
Average ages of patients were 64 years; four patients were female and six were male. The site of lesions was cervical lymph node in four patients, axillary in two, submaxillary in two and each perigastric and retroperitoneal in one patient.
Initial lymph node biopsies showed complete infarction in 7 of 10 cases and the cases had malignant lymphoma on rebiopsy after periods ranging from 2 days to 1 year or in the primary lesions. In 3 cases, a narrow rim of viable subcapsular lymphoid tissue presented malignant lymphoma. The histology of the lymphoma was diffuse large cell type in 6, diffuse mixed type in 2 and each diffuse medium cell and small cell type in one patient.
Microscopically, the lymph nodes were characterized by extensive necrosis of medullary and cortical lymphoid cells, but the reticulin architecture was preserved. Antigens in infarcted lymphoid tissue were well preserved. The staining with antibodies for leukocyte-common antigen (CD45), T cell-associated antigens (UCHL-1, MT-1) and B cell-associated antigens (MxPan-B, MB-1) gave evidence of a malignant lymphoma of either T-or B-cell type; T-cell type in 4 and B-cell in six patients.
Follow-up study showed malignant nature of malignant lymphoma with lymph node infarction, dying for 2 months in 5 of 10 patients.

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We report histochemical and immunohistochemical studies of two cases of testicular malacoplakia from 54-year-old (case 1) and 45-year-old (case 2) men and an ultrastructural study of case 1 with review of the literature. The testes were enlarged and the cut surface showed a neoplasma-like appearance. The testicular architecture was destroyed due to replacing by granulomatous lesion consisting predominantly of macrophages with abundant eosinophilic granular cytoplasm (so-called von Hansemann cell) in both cases. In the cytoplasm of von Hansemann cells, PAS-positive inclusion bodies were frequently observed. There was no histochemical evidence of iron or calcium deposition in the inclusion bodies. Immunohistochemically, positive materials for anti-α1-antitrypsin, anti-α1-antichymotrypsin and anti-Escherichia coli (E. coli) antibodies were seen in the cytoplasm of von Hansemann cells in granulomatous lesion. Thus, we considered the inclusion body as Michaelis-Gutmann (M-G) body. Electron microscopically, various kinds of phagosomes, including M-G structures which do not seem to contain calcium, were observed in the cytoplasm of von Hansemann cells in case 1. Although, the pathogenesis of testicular malacoplakia is still unclear, bacterial infection, especially E. coli infection, may be play an important role for the pathogenesis of testicular malacoplakia.

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