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PubMed1976

Inflammatory cells in solid murine neoplasms. I. Tumor disaggregation and identification of constituent inflammatory cells.

Mechanical and enzymatic methods of disaggregating tumors were studied with the goals of (1) minimizing cell losses while (2) maintaining functional and surface membrane markers needed to objectively identify inflammatory cells (IC)1 in resultant suspensions. Application of the principles and methods described makes accurate estimation of the percentage of each IC type present in neoplasms possible for the first time. Compared to purely mechanical means of disaggregating tumors, all enzyme mixtures tested markedly increased yields of viable cells/g neoplasm. Best results were obtained with a combination of collagenase and a protease of broader substrate range (alpha chymotrypsin, papain, pronase or trypsin). The combination of enzymes that gave the highest yields with the least effect on inflammatory cell markers was trypsin, collagenase and DNAse (TCD). Because mechanical injury appeared to be the greatest single cause of cell loss (the enzymes themselves had little direct effect), potential sources were identified and either eliminated or minimized. With TCD, depending on the tumor system, cell recovery (measured as DNA recovered in cell suspensions) was as high as 50% and yields were as much as 6.9 X 10(8) viable cells/g tumor. Complete disaggregation was not required to obtain representative IC populations from tumor fragments. Neutrophils, eosinophils and mast cells from disaggregated neoplasms were counted in Giemsa stained cytocentrifuge preparations based on their unique morphologic appearances. Macrophages were identified by their capacity to phagocytose zymosan, a function which proved highly resistant to the effect of enzymes. Flourescent microscopic identification of brain associated thymus antigen (BATA) allowed quantification of T lymphocytes, since this marker was virtually unchanged by enzyme exposure. Surface immunoglobulin (Ig) was stripped from B lymphocytes most rapidly by pronase and chymotrypsin, slowly by trypsin and papain, and not at all by collagenase. Ig positive cells therefore could be quantified in suspensions generated by collagenase or very short (20 min) exposure of fragments to trypsin.

Animals↗

PubMed1989

Structure and expression of c-erbB-2 and EGF receptor genes in inflammatory and non-inflammatory breast cancer: prognostic significance.

C-erbB-2 and epidermal growth factor receptor (EGFR) genes were independently shown to be associated with breast cancer progression. In this report, we have analyzed the structure and expression of these 2 genes in the same tumor specimens of a large series of breast cancers. Two clinical types of tumor were studied: inflammatory (IBC) and non-inflammatory breast cancers (NBC) obtained from 221 untreated patients at different clinical stages. Amplification and over-expression of the c-erbB-2 proto-oncogene were observed in 27% and 47% of tumors, respectively, and were strongly associated with breast cancers of the most unfavorable prognosis, namely IBC and NBC with multiple positive axillary nodes. EGFR gene was neither amplified nor rearranged. A restriction fragment length polymorphism (RFLP) for HindIII endonuclease was observed. EGFR transcripts were detected in 46% of tumors and observed more frequently in IBC than in NBC (p less than 0.02). In NBC the presence of EGFR transcripts increased linearly with lymph-node involvement and was associated with estrogen-receptor-negative tumors (p = 0.01). Analysis of both genes from the same tumor samples indicated that genes are associated with cancer aggressiveness. Furthermore, in NBC these 2 genes were independently activated, in contrast to IBC in which activated genes were negatively correlated, suggesting that c-erbB-2 and EGFR genes play different roles in NBC and IBC.

Breast Neoplasms↗

PubMed1994

Association of c-erbB2-gene amplification with poor prognosis in non-inflammatory breast carcinomas but not in carcinomas of the inflammatory type.

It is now accepted that c-erbB2-gene amplification is correlated with poor clinical outcome for patients, mainly when axillary nodes are invaded. We have confirmed this result by multivariate analysis in 178 patients with non-inflammatory breast cancer followed up for a mean period of 6.8 years (SD, 1.6 years). In addition, we have shown that c-erbB2 amplification, found in 30 (17%) specimens, was associated with a high risk of multiple metastases developing simultaneously. In contrast, for the 67 patients with inflammatory breast carcinoma, the most aggressive type of breast carcinoma, the c-erbB2 amplification detected in 24 (36%) specimens was not found to be associated with a higher risk of death, suggesting that the c-erbB2 gene plays a different role in the progression of these 2 types of breast cancer. Furthermore, our data stress the importance of the methodological approach used to determine gene amplification. Although Southern blot hybridization is a tumour- and time-consuming method not easy to adopt in routine clinical practice, this method remains a reference quantitative method.

Adenocarcinoma↗

PubMed2002

Inflammatory myofibroblastic tumour (inflammatory pseudotumour) of the breast. Clinicopathological and genetic analysis of a case with evidence for clonality.

Inflammatory myofibroblastic tumours (IMTs) were initially considered to be benign reactive processes, but cases with an unfavourable outcome have been reported. Moreover, clonal genetic alterations have recently been published in some cases, suggesting that IMT may represent a malignant neoplastic entity. This paper reports a case of IMT that developed in the mammary gland, an unusual site. The histological picture was characterized by a proliferation of spindle cells with little cellular atypia and rare mitoses, associated with a polymorphous inflammatory infiltrate. Their immunophenotype, characterized by the expression of vimentin, smooth muscle actin, and cytokeratins, corresponded to that of myofibroblasts. Cytogenetic analysis revealed the clonal nature of the lesion. The modal karyotype was 48, X, ins(2;X)(q34;p21.2p22.2), +7, del(9)(p23), +19. Including the present observation, a 9p deletion has now been found in three cases of IMT. These observations show that IMT may be a clonal neoplasm, even in sites different from deep soft tissues.

Breast Diseases↗

PubMed2004

Immunophenotypic analysis of inflammatory breast cancers: identification of an 'inflammatory signature'.

Inflammatory breast cancer (IBC) is a rare but very aggressive form of breast cancer. Its definition is based on clinical criteria, but a molecular definition could be useful when data are incomplete or features are missing. Recently, the identification of overexpression of E-cadherin in IBC has improved understanding of the molecular basis of this disease. Consequently, the aim of this study was to try to determine an immunophenotypic 'signature' of IBC. A series of 80 cases of IBC were compared with 552 non-IBC control cases and a model was elaborated to evaluate the probability of an inflammatory carcinoma being present in any clinical situation. Tissue microarrays (TMAs) were used to determine the immunohistochemical profile of eight proteins including E-cadherin, EGFR, oestrogen and progesterone receptor (ER and PR), MIB1, ERBB2, MUC1, and P53. All the parameters tested were differentially expressed between IBC and control cases in univariate analysis (p < 0.001). The five variables that were significantly associated with IBC in multivariate analysis were E-cadherin > or = 300 [HR = 5.64 (2.92-10.87)], ER negative [HR = 3.00 (1.67-5.51)], MIB1 > 20 [HR = 3.54 (1.87-6.71)], MUC1 cytoplasmic staining [HR = 2.72 (1.49-4.96)], and ERBB2 positive 2+ or 3+ [HR = 2.46 (1.26-4.78)]. The probability that a breast cancer with this full phenotype at diagnosis was an IBC was 90.5%. If any one of the five parameters was missing, this probability dropped to 75% and was less than 50% when one, two, or three parameters were present. The 5-year overall survival (OS) and 5-year disease-free survival (DFS) of patients with IBC were not significantly different from those of the non-IBC control group that expressed four or five parameters (nIBC-1), but this nIBC-1 control group had a significantly worse outcome than the non-IBC control group (nIBC-2) with only 0-3 parameters (p = 0.0049 for OS and p < 0.0001 for DFS). In conclusion, an immunophenotypic signature was suggested for IBC. This could help to determine the worst cases, independent of clinical criteria.

Adult↗

PubMed1999

Differential effects of IL-8, LIF (pro-inflammatory) and IL-11 (anti-inflammatory) on TNF-alpha-induced PGE(2)release and on signalling pathways in human OA synovial fibroblasts.

Tumour necrosis factor alpha (TNF-alpha) inflammatory activity is mediated, at least in part, by prostaglandin E(2)(PGE(2)). In osteoarthritis (OA), other cytokines are believed to play a role by interacting with TNF-alpha. Using OA synovial fibroblasts, we investigated the effects of interleukin 8 (IL-8), leukaemia inhibitory factor (LIF) and IL-11 on the level of TNF-alpha-induced PGE(2), and their impact on the TNF-alpha-induced cellular signalling cascades including the TNF-receptor (TNF-R), soluble TNF-R (TNF-sR), cytoplasmic phospholipase A2 (cPLA2), cyclooxygenase 2 (COX-2), and the transcription factors NF-kappaB, C/EBP, CREB and AP-1.IL-8 increased in a synergistic manner (282% at 5 ng/ml) and LIF in an additive fashion (69% at 50 ng/ml) the TNF-alpha-induced PGE(2)release, while IL-11 reduced it (52% at 5 ng/ml). IL-8 (5 ng/ml) and LIF (50 ng/ml) alone upregulated (30%) the TNF-R binding level, but significantly downregulated the TNF-alpha-induced levels (P<0.007 and P<0.004, respectively) and the TNF-sR55 level. In contrast, IL-11 reduced the basal level by 18% (P<0.005) and the TNF-alpha-induced level of TNF-R by 51% (P<0.01) as well as decreasing both TNF-sR55 and TNF-sR75. The COX-2 synthesis level was increased by IL-8 and LIF under TNF-alpha treatment but downregulated by IL-11. IL-8 and LIF either alone or under TNF-alpha treatment increased the cPLA2 synthesis, while IL-11 decreased the level under both conditions. Interestingly, IL-8 induced in a synergistic manner and LIF in an additive fashion, the level of cPLA2 activity. IL-8 and LIF had no effect on the TNF-alpha-induced NF-kappaB accumulation, while IL-11 significantly decreased it (P<0. 02). All three cytokines inhibited TNF-alpha-induced C/EBP, but no true effect was noted for AP-1 and CREB in the presence of TNF-alpha. These results indicate that IL-8 synergizes and LIF potentiates the TNF-alpha PGE(2)effect which appears to be mediated mostly by increasing cPLA2 activity level. On the other hand, IL-11 alone had no effect on the PGE(2)release, but in conjunction with TNF-alpha, this cytokine showed anti-inflammatory properties. This study provides a rational foundation to develop therapeutic strategies for the treatment of OA by shedding light on the mechanisms of action of three prominent cytokines at work in articular joint tissues.

Dinoprostone↗

PubMed1996

Persistent production of inflammatory and anti-inflammatory cytokines and associated MHC and adhesion molecule expression at the site of infection and disease in experimental Trypanosoma cruzi infections.

Trypanosoma cruzi infection in humans and experimental animals often results in a chronic heart and gut inflammation and a dysfunction known as Chagas' disease. Previous studies have shown that the cellular infiltrate in the hearts of animals with chronic Chagas' disease consists mainly of CD8+ T cells. In this study, we have used immunohistochemical techniques to further characterize the immunological nature of chagasic heart lesions in three murine models of experimental Chagas' disease. Double-staining immunohistochemistry revealed that 10-30% of the infiltrating CD8+ T cells in the hearts of infected mice expressed the activation molecules, IL-2 receptor and CD44. In addition, large numbers of cells producing TNF-alpha, TGF-beta, IL-1 alpha, and IL-6 were consistently observed in the heart lesions, appearing during the acute infection and persisting throughout the chronic stage of infection (> 300 days). In contrast, IFN-gamma- and IL-10-producing cells were detected in relatively low numbers and only transiently between approximately 3 and 9 weeks postinfection. Cells producing IL-2, IL-4, and IL-5 were not observed in the hearts of mice at any point during the infection. The appearance of cytokine-producing cells in the hearts correlated with an increased local expression of class I and class II MHC molecules and adhesion molecules (ICAM-1, LFA-1, VLA-4, and VCAM-1). The results of this study suggest that the chronic inflammation in chagasic hearts is highly active and associated with a stable immunological pattern extending from the early acute stage of the infection through the late chronic stage. The pattern of cytokine production in heart is distinct from that observed in lymphoid organs and is not suggestive of an association between particular classes of cytokines and disease development. Instead it appears that both inflammatory and anti-inflammatory cytokines determine the pattern of the cellular response and the severity of disease in T. cruzi infection.

Animals↗

PubMed1984

The tissue architecture of synovial membranes in inflammatory and non-inflammatory joint diseases. II. The localization of mononuclear cells as detected by monoclonal antibodies directed against T-lymphocyte subsets and natural killer cells.

Tissue specimens of synovial membranes from patients with rheumatoid arthritis (RA) and non-inflammatory joint diseases were analyzed with a panel of monoclonal antibodies directed towards T-lymphocyte subsets and natural killer (NK) cells. In the RA group, mononuclear cell infiltrations in the synovium presented a distinguished pattern as compared to the non-RA group. Inflammatory synovial membranes displayed an increased level of cells recognized by the monoclonal antibodies OKT4 and OKT8, especially attributable to the broadened layer of synoviocytes and to the fibrous synovial tissue. No significant difference in the RA patients was observed with regard to the percentage of OKT4 and OKT8 positive cells in different investigated compartments of the synovium, e.g., diffuse inflamed synovial tissue, fibrous synovial tissue, and perivascular infiltrations. OKT4 and OKT8 positive staining was additionally observed on spindle-shaped cells present in the fibrous and diffuse inflamed synovium. OKT10 binding cells were located in the deeper layers of synoviocytes, in the inflamed synovial tissue, and in one case in perivascular areas, whereas HNK 1 positive cells were scattered in the fibrous synovial and perivascular cells, as well as in lymphocyte clusters of synovium in RA patients.

Antibodies, Monoclonal↗

PubMed1983

The tissue architecture of synovial membranes in inflammatory and non-inflammatory joint diseases. I. The localization of the major synovial cell populations as detected by monoclonal reagents directed towards Ia and monocyte-macrophage antigens.

Utilizing monoclonal reagents directed towards antigens of the monocyte-macrophage lineage and Ia antigens, the tissue architecture of synovial membranes obtained from patients with non-inflammatory joint diseases and patients with rheumatoid arthritis was studied. Emphasis was placed on the localization of the type I, type II and type III synoviocytes that previously had been defined by their cell surface phenotype with regard to the expression of monocyte-macrophage lineage (M theta) and Ia antigens as well as by their phagocytic capacity or the ability to produce glycosaminoglycans. In patients with non-inflammatory joint diseases, cells with the M theta + Ia+ (type I) phenotype constituted the majority of synoviocytes immediately adjacent to the joint cavity; cells with this phenotype were also scattered in the subsynovial tissue and in the perivascular regions. The fibroblastoid type III cells defined by the absence of both M theta and Ia antigens formed the major cell population in the subsynovial tissue in this patient group. In patients with rheumatoid arthritis, the Ia+ M theta + cells were present in a characteristic double configuration forming an intensely positive layer adjacent to the intra-articular space followed by an Ia- M theta - layer that again was succeeded by an intensely Ia+ M theta + layer. Large numbers of synoviocytes bearing M theta + Ia+ antigens were also demonstrated in the diffusely inflamed subsynovial tissue, in the perivascular regions as well as around and within lymphoid infiltrates.(ABSTRACT TRUNCATED AT 250 WORDS)

Antibodies, Monoclonal↗

PubMed1982

Studies on the ability of inflammatory exudate obtained from acute and chronic phases of the inflammatory process to promote leukocyte locomotion in vitro.

Using a modified Boyden chamber system, inflammatory exudates taken from the acute carrageenan pleural model and the chronic carrageenan air-pouch model were tested for their ability to promote leukocyte locomotion in vitro. Both exudates were able to induce polymorphonuclear leukocyte (PMN) and mononuclear leukocyte (MN) migration, suggesting that cell-specific chemoattractants are not responsible for the progression of the inflammatory process from the acute to the chronic phase. Checkerboard assay were used to establish whether the observed migration was in response to chemotactic stimulation and/or chemokinetic stimulation. Both acute and chronic exudates were able to induce MN chemotaxis and chemokinesis. Acute exudate was able to induce PMN chemotaxis and chemokinesis. Acute exudate was able to induce PMN chemotaxis and chemokinesis, but chronic exudate was only able to induce PMN chemokinesis. This may partly explain the predominance of MNs in chronic inflammation. However, our present in vitro results have failed to demonstrate that cell-specific chemoattractants are responsible for the in vivo observation that migration of polymorphonuclear leukocytes precedes the migration of mononuclear cells.

Animals↗

PubMed1975

Inflammatory pseudotumors (inflammatory fibrous polyps) of the esophagus. A clinicopathologic study.

When they involve the gastrointestinal tract, inflammatory pseudotumors, composed of inflamed fibrous and granulation tissue, produce localized, frequently polypoid, masses. These rare lesions have been described in the stomach, small intestine, and colon. Only two have been previously reported in the esophagus. In this paper, 4 cases of inflammatory pseudotumor involving the esophagus are presented. These lesions usually occur in the esophagus as raised, occasionally pedunculated, masses and may be mistaken on radiologic examination and in the operating room for a neoplasm, usually a leiomyoma. Theories concerning pathogenesis of these lesions are considered and the differential diagnostic criteria are discussed.

Aged↗

PubMed1990

Inflammatory abdominal aortic aneurysms: a disease entity? Histological analysis of 60 cases of inflammatory aortic aneurysms of unknown aetiology.

Sixty inflammatory aortic aneurysms of unknown aetiology were examined by serial sections. The histological findings failed to reveal significant differences in either thoracic or abdominal aneurysms with or without marked adventitial fibrosis. Their identical morphology does not favour the existence of a special disease entity of so-called inflammatory abdominal aortic aneurysms (IAAA). Absence or existence of giant cells of any type, occurrence of plasma cells, eosinophils, granulomas, fibrinoid necrosis and adventitial fibrotic thickening cannot be considered as variables which help in differentiation. IAAA are characterized by a marked predominance of male patients and a rather benign clinical course. They usually affect the age group around 60 years. They are not rare and do not seem to be restricted to certain races. Their aetiology, like that of the cases affecting the thoracic aorta (Takayasu's disease, non-specific aortitis) remains unknown, although autoimmune diseases, the retroperitoneal fibrosis of Ormond and arteriosclerosis may be related. However, on the basis of the present evidence we cannot consider them to be one of these diseases. There are no morphological findings which would justify the separation of IAAA from Takaysu's disease.

Adult↗

PubMed2005

Plasma levels of the anti-inflammatory cytokine IL-10 and inflammatory cytokine IL-6 in patients with unstable angina.

The plasma levels of inflammatory cytokine interleukin-6 (IL-6) and anti-inflammatory cytokine interleukin-10 (IL-10) in the patients with unstable angina or stable angina were determined and compared. In 30 patients with unstable angina and 22 patients with stable angina, plasma levels of IL-10 and IL-6 were detected by ELISA and plasma lipid parameters by lipid research clinical methods respectively. The results showed plasma levels of IL-10 were significantly lower in unstable angina group than in stable angina group (P = 0.005), while those of IL-6 were significantly increased in unstable angina group as compared with those in stable angina group (P = 0.039). There was a significantly negative correlation between IL-10 and IL-6 in patients with unstable angina (r = -0.41, P = 0.003). In the unstable angina group, IL-6 levels were obviously positively correlated with TC (r = 0.314, P = 0.023), but not with TG and HDL. There were no significant correlations between IL-10 and plasma lipid parameters. It was suggested that the decreased IL-10 and increased IL-6 might be associated with the atheromatous plaque stability and progression of coronary heart diseases. IL-10 may play an important role in preventing coronary vascular lesions.

Angina, Unstable↗

PubMed1998

[Tissue eosinophilia and local deposition of eosinophil-specific granule proteins. Regulation and significance for inflammatory response in atopic dermatitis and other inflammatory dermatoses].

Recent in vitro-studies have substantially increased our knowledge of eosinophil activation, the regulation of eosinophilia in the peripheral blood and the role of cytokines in that process. Accordingly, chemoattraction and activation of eosinophils by cytokines results in the local release of reactive oxygen species and toxic cationic granule proteins followed by local propagation of the inflammatory reaction and tissue damage. This extracellular tissue deposition of toxic granule proteins as an expression of complete activation of eosinophils, rather than only the presence of intact eosinophil granulocytes, is crucial for their functional effect in situ. Semi-quantitative studies of local eosinophil granula deposition so far have been done only in atopic dermatitis and a limited number of other inflammatory skin diseases as summarized in this review. Evaluation of the pathogenetic role of eosinophils may be of potential therapeutic importance.

Blood Proteins↗

PubMed1995

[Colon carcinoma simulating retroperitoneal inflammatory pseudotumor. Case report of so-called abdominal inflammatory fibrosarcoma].

Resection of a stenosing colon tumor in an 89-year-old male patient led to the diagnosis, unusual at this age, of an inflammatory pseudotumor (synonym: plasma cell granuloma) of the retroperitoneum and mesentery, which invaded the large bowel and showed infiltration of one regional lymph node. Histology and immunohistochemistry (demonstrating a myofibroblastic phenotype of the proliferating spindle cells and polyclonality of abundantly present plasma cells) of the specimen resembled previously reported lesions in various locations. The etiology and exact nosological classification of inflammatory pseudotumors are not yet unequivocally settled. The recently published conjecture that such lesions of the retroperitoneum represent a separate entity with features of a malignant neoplasm is discussed.

Aged↗

PubMed1999

Inflammatory myofibroblastic tumor of the lung (inflammatory pseudotumor): uncommon cause of solitary pulmonary nodule.

Lung inflammatory myofibroblastic tumor is an uncommon cause of solitary lung nodule (0.7 % of lung tumors). The principal site of inflammatory pseudotumor is the lung, but it can also occur elsewhere in various organs. Although benign, they may be locally very aggressive. Recurrent and multifocal forms have been described. Since they are likely to mimic malignant neoplasms, accurate histopathologic diagnosis is necessary in order to guide appropriate surgical excision and avoid aggressive treatments. We report a case of lung involvement in a young adult with radiologic and pathologic correlations.

Adult↗

PubMed2006

Pancreatic malignant fibrous histiocytoma, inflammatory myofibroblastic tumor, and inflammatory pseudotumor related to autoimmune pancreatitis: characterization and differential diagnosis.

Malignant fibrous histiocytoma (MFH) and inflammatory myofibroblastic tumor (IMT) are uncommon primary non-epithelial cell tumors of the pancreas. In addition, there are inflammatory pseudotumors (IPT) that may arise in the course of autoimmune pancreatitis (AIP). In the English language literature, only 24 cases of IMT and nine cases of MFH in the pancreas have been reported to date. We investigated three individual spindle cell tumors of the pancreas that were identified as MFH, IMT, and IPT, respectively, using immunohistochemical and molecular analysis. Both the MFH and the IMT, but not the IPT, showed nuclear p53 expression and mutations of the p53 gene. The MFH and the IMT also had higher mitotic and Ki-67 (MIB-1) indexes than the IPT. The IPT was found to be a tumor-like case of AIP. Many IgG4-positive plasma cells, which are considered to be a feature of AIP, were found in all three tumors. It is concluded that in this series of spindle cell tumors of the pancreas, apart from immunohistochemical features, the demonstration of p53 mutations may be helpful in distinguishing true neoplastic tumors from pseudotumors such as IPTs arising in the context of AIP.

Adult↗

PubMed1991

Late-stage mediators of the inflammatory response: identification of interleukin-1 and a casein-degrading enzyme in equine acute inflammatory exudates.

Interleukin-1 and a casein-degrading enzyme have been identified in an experimental system for studying acute inflammation in the horse. The levels of both the cytokine and the proteinase increased over the first 24 hours following initiation of the inflammatory response, and remained at high levels through to the last sample collected at 48 hours. This is in marked contrast to prostaglandin E2 concentrations which were low initially, peaked at four to eight hours and had returned to low levels by 12 to 24 hours. It is likely that interleukin-1 and various proteinases are involved in the later stages of the inflammatory response, such as the tissue remodelling associated with wound repair, and control of this cytokine may be important in the progression from acute to chronic inflammation.

Animals↗