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C Sorg

Publications and source records attributed to C Sorg.

At least 109 records · Page 6Linked to original sources
PubMed1993

Expression and complex assembly of calcium-binding proteins MRP8 and MRP14 during differentiation of murine myelomonocytic cells.

In the present study we analyzed expression and biochemical properties of the two recently cloned calcium-binding proteins MRP8 and MRP14, both members of the S-100 family, in murine myelomonocytic cells. Expression of MRPs was found to be restricted to granulocytes and distinct stages of macrophage differentiation when compared to the expression of other markers (Mac-1, F4/80) in transformed macrophage cell lines (M1, RMB.TG, WEHI.TG, J774A, P388D) and resident and exudate peritoneal and tissue macrophages. Similarly, mRNA and protein levels of MRP8/MRP14 in murine bone marrow cells decreased during culture in L cell-conditioned medium. Applying a cross-linking technique, the formation of noncovalently associated heteromeric MRP8/MRP14 complexes of 25, 35, and 48 kd was demonstrated. Our data suggest that MRP8/MRP14 expression and complexation are characteristic for granulocytes and distinct stages of macrophage differentiation in mice. Analysis of the MRP8/MRP14+ phenotype of macrophages may provide further insights into the mechanisms underlying macrophage differentiation.

Animals↗
PubMed1993

Immunohistochemical comparison of cutaneous histiocytoses and related skin disorders: diagnostic and histogenetic relevance of MS-1 high molecular weight protein expression.

Twenty-nine cases of Langerhans cell histiocytosis (LCH), non-Langerhans cell histiocytoses (N-LCH), non-infectious granulomas, and fibroblast-related lesions were examined with a panel of monoclonal and polyclonal antibodies on freshly frozen tissue sections to characterize the macrophage phenotype of N-LCH syndromes. MS-1 high molecular weight extracellular protein, specific for sinusoidal endothelial cells and dendritic perivascular macrophages in normal human organs, was expressed by N-LCH cells but was not found in LCH cells, epithelioid cells in sarcoidosis, or palisading histiocytes in granuloma annulare. The subcellular location of MS-1 protein, i.e., cytoplasmic vs. peripheral/extracellular, allowed discrimination of small and large (foamy or multinucleated) N-LCH cells. MS-1-positive cells, which were found intermingled in cellular dermatofibromas but not in fibrous dermatofibromas, differed from MS-1-positive N-LCH cells by their dendritic morphology, and thus rather resembled their normal dermal counterparts. A preserved functional relationship of these two MS-1-positive cell types was indicated by the fact that N-LCH and cellular dermatofibromas were the only lesions found to be highly vascularized. As expected, CD1a showed high specificity for LCH, while CD34 was predominantly expressed by fibroblast-related lesions; in cellular dermatofibromas, CD34 and MS-1 expression partially overlapped. The other antigens tested showed non-specific or overlapping patterns of expression. In conclusion, assessment of MS-1 protein expression (in addition to assessment of CD1a and CD34) promises to be of diagnostic value in the discrimination of N-LCH from related skin disorders, and it may indicate a common differentiative pathway for most N-LCH disease entities.

Antibodies, Monoclonal↗
PubMed1993

Phenotypic markers of alveolar macrophage maturation in pulmonary sarcoidosis.

The expression of maturation-associated antigens on alveolar macrophages (AMs) was studied in bronchoalveolar fluid of 30 patients with sarcoidosis and 11 control subjects. The percent of AMs expressing CD14 or CD11b (common for blood monocytes) was significantly increased in patients with active sarcoidosis compared to those with inactive disease, and control subjects. On the other hand, the mean expression of antigens characteristic for mature macrophages showed no significant difference (25F9), or was even increased in patients with sarcoidosis (CD71, KiM8). Since CD14 and CD11b molecules were also frequently expressed on large phagocytes morphologically similar to mature macrophages, and recent studies showed modulation of these glycoproteins by the activation of myeloid cells, our data indicate that the majority of AMs recovered by bronchoalveolar lavage in sarcoidosis are mature, activated cells.

Adult↗
PubMed1993

Inflammatory reaction in endometriotic tissue: an immunohistochemical study.

A panel of monoclonal antibodies specific for macrophage subtypes appearing in early (27E10), down-regulatory (RM3/1) and late (25F9) stages of inflammation had been applied to 20 endometriotic implants of 14 women. Of those patients 9 were in the follicular phase of the cycle, two on danazol, one on LHRH-analogue (buserelin) and another two on oral contraceptives. Beside the macrophage subsets, antibodies against T4, T8 lymphocytes as well as proliferating cells (EN7/44 and Ki67) were examined. In all specimens immunologically competent cells could be detected to a varying degree and within the same implant different stages of inflammation were discernible. Endometriosis presented with signs of early inflammation indicated by 27E10+ macrophages and CD4+ lymphocytes (15 specimens) and with down-regulatory, late inflammatory reactions as shown by RM3/1+, 25F9+ macrophages and CD8+ lymphocytes (19 biopsies). Additionally, in 14 specimens cells of the EN7/44+ and Ki67+ type was detected. These preliminary results showed no significant correlation to either extension of endometriotic implants or adhesions or concomitant therapy and clearly indicate, that there is an immunological dynamic process within the lesion itself in addition to that one of the peritoneal fluid.

Adult↗
PubMed1993

Expression of intercellular adhesion molecule-1 by murine macrophages is up-regulated during differentiation and inflammatory activation.

Intercellular adhesion molecule-1 (ICAM-1, CD54) is a cell-surface glycoprotein which has been shown to play an important role for cell/cell interaction. Little is known about its occurrence in the murine monocyte/macrophage (M phi) lineage; hence, we analyzed ICAM-1 expression in cells and cell lines representing different stages of M phi maturation and studied its regulation during inflammatory activation. Flow cytometric analysis of bone marrow-derived M phi cultured in the presence of M-CSF, of thioglycollate-elicited peritoneal M phi and of M1 myeloblasts differentiated by lipopolysaccharide (LPS) treatment revealed that ICAM-1 is increasingly expressed during monocytic maturation. Accordingly, the myelomonocytic cell lines RMB.TG, WEHI.TG, J774A and P388D, which can be ordered in a linear differentiation sequence, showed increasing levels of ICAM-1 expression. Furthermore, ICAM-1 expression by bone marrow-derived M phi could be up-regulated by tumor necrosis factor-alpha, interferon-gamma and LPS. In two models of murine experimental inflammation, i.e. induction phase of contact hypersensitivity and cutaneous leishmaniasis, which are both dependent on M phi/T cell interaction, M phi expressing ICAM-1 were found to be highly abundant. In addition, it was demonstrated that co-culture of Leishmania maior parasites with bone marrow M phi led to up-regulation of ICAM-1 on these cells. In conclusion, our data clearly demonstrate that ICAM-1 is increasingly being expressed during maturation of murine M phi. Cytokines and inflammatory stimuli modulate M phi ICAM-1 expression as well thus referring to its considerable role during inflammation, e.g. providing accessory or costimulatory signals for T cell activation.

Animals↗
PubMed1993

Nickel chloride and cobalt chloride, two common contact sensitizers, directly induce expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and endothelial leukocyte adhesion molecule (ELAM-1) by endothelial cells.

Intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and endothelial leukocyte adhesion molecule-1 (ELAM-1, E-selectin) are endothelial surface molecules that play a role for leukocyte recruitment to sites of inflammation, e.g., during contact hypersensitivity. We studied the effects of sensitizing agents (2,4-dinitro-benzenesulfonic acid, metal salt haptens) and chemically related substances on endothelial adhesion molecule expression. Using flow cytometry and an enzyme-linked immunosorbent assay, NiCl2 and, to a lesser extent, CoCl2 were found to up-regulate ICAM-1, VCAM-1, and ELAM-1 expression on cultured human umbilical vein endothelium whereas the other substances tested showed no effects. Induction of adhesion molecules by NiCl2 required de novo mRNA and protein synthesis. Up-regulation could be blocked by kinase inhibitor H-7 but not staurosporine, suggesting involvement of phosphorylation events independent of protein kinase C activation. Concomitant application of NiCl2 and neutralizing antibodies to IL-1 did not block up-regulation by the hapten demonstrating that the latter did not act via an IL-1-dependent autocrine mechanism. Regarding ELAM-1 induction, pre-treatment for 24 h with NiCl2 produced hyporesponsiveness to IL-1 and TNF-alpha upon restimulation, suggesting that NiCl2 and these cytokines may partially share a common pathway of activation. In addition, analysis of cultured foreskin specimens revealed that NiCl2 may induce up-regulation of ELAM-1 on microvascular endothelium in vivo. Our data demonstrate that both Ni++ and Co++ to which simultaneous contact sensitivity is frequently observed have the ability to directly up-regulate endothelial adhesion molecules. This shared property may represent an adjuvant mechanism that promotes sensitization and elicitation events in contact hypersensitivity to these haptens.

Capillaries↗
PubMed1993

Immuno-competent cells in the murine epididymis following infection with Escherichia coli.

Epididymitis was induced by retrograde injection of Escherichia coli into the vas deferens of 28 mice. A group of 28 saline-injected animals served as controls. On Days 1, 3, 7 and 28, groups of seven animals were killed. Bacterial culture was performed. Leucocyte numbers and distribution were determined in epididymides. In infected mice, E. coli were isolated from all epididymides on Days 1 and 3, but only from five of seven epididymides on Days 7 and 28. One week after infection, the total number of macrophages rose from about 10 to 28%. Significantly increased macrophage percentages were also found in animals killed 28 days after infection. A simultaneous increase in MHC class II positive cells was seen on Day 7. A total of 20% of the cells expressed MHC class II in infected epididymides (normal = 6%). A similar increase was found on Day 28 after infection. Most of the macrophages and MHC class II positive cells were located in the interstitium, fewer in the peritubular layer and nearly none in the epithelium. The main increase in these cells occurred in the interstitium and, to a lesser but significant extent, in the peritubular area. T-helper and T-suppressor/cytotoxic lymphocytes reached peak values on Day 28. The increase in T-lymphocytes and simultaneous appearance of plasma cells followed the increase in numbers of macrophages and MHC class II positive cells. They were located mainly in the interstitium. A sequential increase in leucocyte subsets and negative culture results for E. coli were observed on Days 7 and 28 (2/7 on each day). The inflammatory process was restricted to the interstitium.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Carcinoembryonic antigen and related glycoproteins in psoriasis.

Psoriasis is a benign but hyperproliferative skin disease. Psoriatic basal cells show a phenotype similar to that of normal skin, while psoriatic suprabasal cells exhibit a qualitatively altered keratinization pathway, resulting in the absence of the granular layer. These cells further show an abnormal expression of cellular differentiation antigens, which does not lead to tumor development. This immunohistological study demonstrates the appearance of carcinoembryonic antigen (CEA) in psoriatic suprabasal cells below the parakeratotic layer, while other markers such as CEA-related antigens, the nonspecific cross-reacting antigens and alpha-fetoprotein are not expressed. CEA is absent in normal skin, lichen planus, ichthyosis vulgaris and allergic dermatitis. Our data support the notion that dedifferentiation of psoriatic suprabasal keratinocytes is due to the reactivation of early developmental patterns of differentiation in this disease.

Antibodies, Monoclonal↗
PubMed1993

Changes in phenotypically distinct phagocyte subpopulations during nonspecific modulation of contact sensitization.

Environmental influences are increasingly recognized as nonspecific modulators triggering and aggravating allergic diseases. To obtain better insight into the pathomechanisms of these nonantigen-specific phenomena, we studied the augmenting and inhibitory effects of croton oil and glucocorticosteroid (GC) on the induction of murine allergic contact dermatitis. Application of the irritant croton oil simultaneously with the sensitization dose of the contact allergen oxazolone strongly amplified the inflammatory reaction (measured as ear swelling) during the effector phase. Immunohistologically, this effect correlated with an increased percentage of MRP8- and MRP14-positive phagocytes in the infiltrate of the early inflammatory reaction 8 h after sensitization with oxazolone plus croton oil as compared to oxazolone alone (62 vs. 27%; p < 0.05). Intravenously administered GC was used as an inhibitor of contact sensitization. The suppressive effect of GC on sensitization was dependent on the time of its application: suppression of the inflammatory reaction during the effector phase was clearly more pronounced when GC had been injected 1 day as compared to 1 h before sensitization. Correspondingly, the percentage of BM8-positive macrophages in the infiltrate of the early inflammatory reaction 8 h after sensitization was differentially decreased depending on the time of GC application: suppression of the percentage of BM8-positive macrophages was clearly more pronounced when GC had been injected 1 day as compared to 1 h before sensitization (17 vs. 25%; base value without GC 35%; p < 0.05). Furthermore, the percentage of BM8-positive macrophages in the inflammatory infiltrate of the effector phase was increased when sensitization had been enhanced by concomitant irritant contact dermatitis (47 vs. 59%; p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

The contact allergens nickel chloride and cobalt chloride directly induce expression of endothelial adhesion molecules.

Activation of vascular endothelium is a key event in the initial phase of an inflammatory reaction e.g. to contact allergens. In the present study the effect of two common contact sensitizers, NiCl2 and CoCl2, on endothelial expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and endothelial leukocyte adhesion molecule-1 (ELAM-1, E-selectin) was studied. NiCl2 and CoCl2 were found to upregulate these adhesion molecules on human umbilical vein endothelial cells (HUVEC) in a dose- and time-dependent manner as could be demonstrated by flow cytometry and enzyme-linked immunosorbent assay. During organ culture of foreskin samples treatment with NiCl2 led to upregulation of ELAM-1 and ICAM-1 but not VCAM-1 on microvascular endothelium. Induction of adhesion molecules by NiCl2 was found to depend on de novo mRNA and protein synthesis and could be blocked by the protein kinase inhibitor H-7 in a dose-dependent manner but not by HA-1004 and staurosporine. An autocrine IL-1-dependent mechanism mediating NiCl2 effects could be excluded. Our data demonstrate that allergens as NiCl2 and CoCl2 are capable of directly activating endothelium which is an important step in evolving inflammatory reactions and may thus be of relevance for the pathogenesis of contact hypersensitivity.

Allergens↗
PubMed1993

The phenotype of alveolar macrophages and its correlation with immune cells in bronchoalveolar lavage.

The phenotype of alveolar macrophages (AMs) is known to be modulated during pathological immune reactions in the lung. In this study, we wanted to determine the relationship between the AM phenotype and changes in the proportions of the various immune cells in bronchoalveolar lavage (BAL). BAL was performed in 76 consecutive patients, including 32 with sarcoidosis, 8 with idiopathic pulmonary fibrosis, 9 with pneumoconiosis, 13 with other respiratory disorders, and 14 controls without evidence of interstitial lung disease. The phenotype of AMs was studied by a panel of 15 monoclonal antibodies against various myeloid antigens, and was correlated with the proportions of cells obtained by BAL. The percentage of BAL lymphocytes showed a relationship with the expression of macrophage antigens in 11 out of 15 antigens studied (all except adhesive molecules CD11a, CD11c, CD18 and the antigen 25F9 present on mature macrophages). Furthermore, the CD4/CD8 ratio of BAL T-lymphocytes correlated with the AM expression of CD54 (intercellular adhesion molecule-1 (ICAM-1)), RFD1 (marker of dendritic cells), and CD71 (transferrin receptor). In samples with an increased number of bronchoalveolar neutrophils, the subpopulation of 27E10 positive AMs (inflammatory acute phase macrophages) was increased. Eosinophils in BAL were not associated with a significant increase in AM membrane antigen expression. Prominent changes of the AM phenotype were found in active sarcoidosis showing lymphocytic alveolitis, with more frequent expression of CD54, KiM2, CD71, CD11b and RFD9. In conclusion, this study shows that the phenotype of AMs is related to the type and intensity of the immunopathological reaction in the lung, and correlates with the proportions of bronchoalveolar cells.

Antigen Presentation↗
PubMed1993

Function and "homing" of the lung macrophages. I. Evidence of functional heterogeneity of mobile cells of the murine lung parenchyma in the bronchoalveolar lavage (BAL).

The object of the present investigation was to extend fundamental understanding of the composition, function and origin of bronchoalveolar lavage (BAL) cells, and to reduce the considerable gaps in our existing knowledge. BAL cells from the B10.D2 mouse were identified by morphological, enzyme cytochemical and immunocytochemical methods and a further functional characterisation of macrophages was undertaken in vitro using latex phagocytosis. The possible bone marrow origin of BAL cells was investigated with a radiation chimera. The bone marrow from H2k-positive F1 mice (B10.BR x B10.D2) was transplanted into the irradiated H2k-negative parent animals. At various time intervals after transplantation, BAL cells were tested immunocytochemically for the presence of H2k-positive cells. The principal finding was that BAL cells are functionally heterogeneous. It was possible by morphological, enzyme cytochemical and immunocytochemical techniques to subdivide the total BAL cell count into 89% macrophages, 8.5% lymphocytes and 2.5% granulocytes. Only 14.3% of the macrophages expressed the corresponding epitope, and this small population could be further subdivided immunocytochemically into mature and immature (7:1) macrophages. The ability to phagocytose, which is typical of active macrophages, could be induced in vitro in only one-third of all BAL macrophages. Three-quarters of the macrophages carried the H2d antigen and 9.5% of the BAL cells were natural killer cells showing a macrophage phenotype. Subdivision of the lymphocytes showed a significant majority of T-cells (75%) to B-cells (20%), and 5% Asialo GM1-positive cells. The CD4/CD8 ratio amounted to 1.3:1 and 38% of the lymphocytes expressed on the surface the H2d antigen.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Inducible expression of MS-1 high-molecular-weight protein by endothelial cells of continuous origin and by dendritic cells/macrophages in vivo and in vitro.

Recently, we have described a monoclonal antibody, named MS-1, which identifies a novel high-molecular-weight protein expressed by noncontinuous, sinusoidal endothelia and by interstitial dendritic cells in certain normal human organs (S Goerdt, LJ Walsh, GF Murphy, JS Pober, J Cell Biol 1991, 113:1425-1437; and LJ Walsh, S Goerdt, JS Pober, H Sueki, GF Murphy, Lab Invest 1991, 65: 732-741). In this report, we demonstrate in studying a variety of skin lesions that MS-1 antigen can also be expressed by endothelia of continuous origin under certain pathological conditions. Among the skin lesions tested, MS-1 antigen expression by endothelial cells of continuous origin is frequently observed in wound healing tissue, in cutaneous T-cell lymphoma, in psoriasis, and in melanoma metastasis, ie, in 100%, 80%, 71%, and 71% of cases, respectively. In contrast, endothelial MS-1 antigen expression rarely occurred in other skin lesions, including vascular tumors, six of which were Kaposi's sarcomas (13% and 0% of cases with vascular MS-1 expression, respectively). The percentage of cases with MS-1+ vessels is only marginally different in malignant versus benign lesions (55% versus 31%); when melanocytic nevi, primary melanomas, and melanoma metastases are compared, however, an increase in the percentage of cases with MS-1+ vessels is seen (31%, 50%, and 71%, respectively). Apart from wound healing, the relative number of MS-1+ vessels in a given lesion amounts to less than 5% compared with the number of continuous type vessels stained by monoclonal antibody 1F10 (S Goerdt, F Steckel, K Schulze-Osthoff, H-H Hagemeier, E Macher, C Sorg, Exp Cell Biol 1989, 57: 185-192). In addition, the occurrence of MS-1+ vessels is not related to the overall vascularity of a given lesion. Thus, the conditions for MS-1 antigen expression by endothelia of continuous origin cannot as yet be exactly defined. Furthermore, we have noticed that the number of MS-1+ dendritic cells varies considerably in skin lesions; in the early patch lesions of Kaposi's sarcoma and in juvenile xanthogranuloma MS-1+ cells even constitute the major cell type. This prompted us to investigate MS-1 antigen expression and its regulation in cultured human monocytes/macrophages. Expression of MS-1 antigen by these cells regularly starts at day 3 of culture and reaches its maximal value at day 9, after which it declines.(ABSTRACT TRUNCATED AT 400 WORDS)

Antibodies, Monoclonal↗
PubMed1992

A comparative study on the effects of tumor necrosis factor-alpha (TNF-alpha), human angiogenic factor (h-AF) and basic fibroblast growth factor (bFGF) on the chorioallantoic membrane of the chick embryo.

The chorioallantoic membrane (CAM) assay is a widely used bioassay for testing angiogenic activities. In the present study we compared the gross and micromorphological effects of three angiogenic factors applied in Elvax carriers on the CAM: Tumor necrosis factor-alpha (TNF-alpha), human angiogenic factor (h-AF), and basic fibroblast growth factor (bFGF). Our question was whether the CAM responds to these factors which have very different actions with a stereotype or with a factor specific reaction. By microangiography and light microscopy, all positive reactions appeared as a spoke-wheel vascular pattern with a bundle of small capillary blood vessels in the center. These vessels were predominantly of a distended type in h-AF and TNF experiments, while narrower capillary vessels followed bFGF application. Chorioallantoic ectoderm and endoderm were thickened by cell accumulation and the mesenchymal stroma of the CAM was edematous and infiltrated with leucocytes in all three reactions. Additionally, bFGF experiments showed areas of densely arranged fibroblasts. Observations in vivo showed chorioallantoic tissue movements as a possible mechanism for the spokewheel vascular pattern. As compared with our results from studies of cytokinetics with bromodeoxyuridine, these current findings indicate that chemotaxis is responsible for the chorioallantoic angiogenic reaction rather than cellular proliferation.

Allantois↗
PubMed1992

The calcium-binding proteins MRP8 and MRP14 form a membrane-associated heterodimer in a subset of monocytes/macrophages present in acute but absent in chronic inflammatory lesions.

Monocytes/macrophages expressing an epitope recognized by a monoclonal antibody 27E10 are present in acute but are absent in chronic inflammatory disorders. This report shows that the 27E10 antigen is formed by noncovalent association of the two Ca(2+)-binding proteins MRP8 and MRP14 which belong to the S100 protein family. Identification has been confirmed immunochemically, by matrix-assisted UV-laser desorption/ionization spectrometry and by partial amino acid sequencing. Surface expression of the MRP8/MRP14 complex on a subset of monocytes is reported for the first time and shown to be up-regulated in a Ca(2+)-dependent manner. The 27E10 surface-positive monocytes isolated by cell separation techniques release high amounts of tumor necrosis factor-alpha and interleukin-1 beta in contrast to their 27E10 surface-negative counterparts thus emphasizing their role in inflammation.

Acute Disease↗
PubMed1992

Restin: a novel intermediate filament-associated protein highly expressed in the Reed-Sternberg cells of Hodgkin's disease.

We have identified a cDNA coding for a protein of 160 kDa which is expressed in in vitro cultured human peripheral blood monocytes. The predicted amino acid sequence contains an alpha-helical rod domain possessing features characteristic of intermediate filament proteins. However, the immunocytochemical staining pattern, abundance and solubility in Triton X-100/high salt buffers suggest that this protein is probably only associated with the intermediate filament network and represents a new type of intermediate filament associated protein. In a survey of normal, inflammatory and human tumour tissue samples, this protein, which we have named restin, was found to be highly expressed in Reed-Sternberg cells, the tumoral cells diagnostic for Hodgkin's disease. We suggest that restin overexpression may be a contributing factor in the progression of Hodgkin's disease.

Amino Acid Sequence↗
PubMed1992

Differences in the onset of the inflammatory response to cutaneous leishmaniasis in resistant and susceptible mice.

Sites of cutaneous infection with Leishmania major in genetically susceptible (BALB/c) and resistant (C57B1/6) mice were investigated for the early inflammatory response (6 h to 12 days) by electron microscopy combined with enzyme-histochemical methods. Susceptible BALB/c mice spontaneously recruited only polymorphonuclear leukocytes (PMNs) at the site of infection. Infiltrating mononuclear phagocytes (and eosinophils) were first observed at day 1 in a ratio equal to the influx of PMNs (about 40%). This pattern persisted during the following 11 days of infection. In the resistant C57/B16 mice, the first cellular infiltrate at the infected site contained mononuclear phagocytes (25%) and eosinophils (15%) besides PMNs (60%). Within 3 days after infection, mononuclear phagocytes became the dominant population of cells in cutaneous lesions (up to 80%). It was found in situ that L. major accumulated and replicated in immature macrophages, that is, intermediate stages between monocytes and resident macrophages, which were found in lesions of both strains. The burden of parasites was, however, degraded more rapidly by the infiltrating cells of the resistant mice than by those of the susceptible ones. Within the first 4 days of infection, the parasites were found in PMNs, mononuclear phagocytes, and extracellular spaces in both strains. In susceptible mice this distribution pattern persisted up to 12 days after infection; in resistant C57B1/6 mice parasites accumulated inside mononuclear phagocytes within this period. It is concluded that the features of acute inflammation during leishmaniasis in BALB/c mice are sustained over a prolonged period that is ineffective in the elimination of L. major.

Animals↗