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Results for “Cell Migration Inhibition”

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At least 19 recordsLinked to original sources
PubMed1975

In vitro evaluation of cell-mediated immunity to Epstein-Barr herpesvirus by cell migration inhibition tests.

Migration of peripheral leukocytes in samples from sensitized [Epstein-Barr virus (EBV) antibody-positive] humans was greatly inhibited when challenged by antigen prepared from EBV-producing P3HR-1 cells but not by antigen prepared from EBV-nonproducing RAJI cells, EBV-negative human fibroblasts, or epithelial cells. Such inhibition was not observed when peripheral leuocytes from subjects or neonates not sensitized to EBV were challenged. Similar results were obtained in a two-stage test when the same leukocyte samples were challenged in vitro by antigen prepared from P3HR-1 cells and the cell-free supernatant was assayed for migration inhibition factor (MIF) in the guinea pig macrophage migration inhibition test; migration of guinea pig peritoneal exudate cells was greatly inhibited by the supernatant filtrates of leukocyte cultures only from subjects positive for EBV-antibody. Furthermore, this inhibitory effect was not observed if supernatant filtrates from leukocyte cultures challenged by antigens prepared from RAJI cells, fibroblasts, or epithelial cells were used. The EBV antigen transformed peripheral leukocytes and induced early antigen production in RAJI cells; however, a "killed" preparation (by UV irradiation) was sufficient for eliciting MIF production.

Antibodies, Viral↗
PubMed1979

Mononuclear cell migration inhibition in children with nephrotic syndrome.

The relative number of T/B lymphocytes and the response of peripheral blood mononuclear cells to PHA in the migration inhibition test was studied in a group of patients with idiopathic nephrotic syndrome. It has been found that the level of T lymphocytes and the response to PHA was decreased in patients in particular those with frequent relapses. The possible implications of these finding for pathogenesis of idiopathic nephrotic syndrome is briefly discussed.

B-Lymphocytes↗
PubMed1977

In vitro correlate of tranplantation immunity: spleen cell migration inhibition in the lizard, Calotes Versicolor.

Sensitization to skin allografts in the lizard, Calotes versicolor, was assessed using the in vitro capillary migration inhibition (MI) assay. In the presence of the respective donor antigen, an appreciable degree of MI of sensitized spleen cells was observed as early as 4 days after grafting. A maximum level was attained on day 7 and this response was maintained as long as one month after grafting with only slight fluctuations in the level of MI. When the clinical manifestations of graft rejection culminated on day 35, the degree of MI was still at the maximum level. MI of allograft-sensitized spleen cells is an antigen specific event, and the same level of inhibition is observed whether the specific antigen is provided in the form of intact spleen cells or spleen extract.

Animals↗
PubMedDate not supplied

[Studies of cellular sensitization to BCG and PPD using leukocyte cell migration inhibition].

Leucocyte inhibition migration test (LMT) with BCG and PPD was applied in pulmonary tuberculosis, lung cancer and sarcoidosis. No significant differences were noticed in the results obtained with each of the two antigenic materials; nevertheless, one case lobectomized of lung cancer successively treated with chemiotherapie and immunostimulation with BCG presented LMT positivity with BCG and negativity with PPD. The unpublished results of the former investigations carried out with brute tuberculin (LMT) on patients with pulmonary tuberculosis are here reported no significant difference was noticed between the results obtained with brute tuberculin, and the results with PPD. The still unsettled problem presented by the lack of inhibition in the presence of PPD in leucocyte migration test in patients with areactive (AA) and intermediate areactive (AI) tuberculosis is also briefly discussed. Finally, the existence of a dissociation between the cutaneous delayed test and the in vitro test for the detection of cellular sensibilisation is confirmed even when LMT is applied either in the presence of BCG or of PPD.

Antibody Formation↗
PubMed1978

In vitro assessment of delayed hypersensitivity in the human. Inhibition of cell migration from agarose microdroplets.

The in vitro migration inhibition responses of peripheral blood leukocytes from tuberculin skin test positive and negative donors were tested to validate and determine optimal conditions for the agarose droplet method in the human. In vitro migration inhibition was observed in skin test positive donors in the presence of 25 microgram PPD/ml of medium using both unfractionated leukocytes and a mixture of immune lymphocytes with allogeneic polymorphonuclear leukocyte indicators. The supernatants of tuberculin positive lymphocytes cultured with PPD also inhibited the migration of human polymorphonuclear leukocytes and guinea pig peritoneal exudate cells but did not alter that of murine peritoneal exudate cells. These studies establish that the agarose droplet method is an efficient approach to the in vitro assessment of cell-mediated immunity in the human and define suitable indicator cell populations for assay of human lymphokines.

Animals↗
PubMed2026

Proteomic profiling reveals that DPP4 overexpression increases cell adhesion, inhibits cell migration, and restores androgen sensitivity in prostate cancer.

Dipeptidyl peptidase-4 (DPP4), a serine protease with both enzymatic and non-enzymatic roles, has emerged as a context-dependent modulator of tumor progression. In the present study, we investigated the expression and function of DPP4 in androgen-sensitive and castration-resistant prostate cancer (CRPC) models. Proteomic analysis of androgen-resistant prostate cells overexpressing DPP4 identified the involvement of the cellular adhesion molecules pathway. In prostate cells, lentiviral-mediated DPP4 overexpression restored androgen receptor signaling, inhibited epithelial-to-mesenchymal transition, and reduced cell migration, whereas DPP4 silencing produced the opposite effects. We demonstrate that DPP4 expression is down-regulated in CRPC cells and that treatment with capsaicin (CAP), a bioactive compound derived from red peppers, restores DPP4 expression. Moreover, DPP4 restoration by CAP suppresses prostate tumorigenesis in the TRAMP mice in vivo model of prostate cancer. Our results suggest that DPP4 could be a new target for CRPC.

Male↗
PubMed1975

Migration inhibition with various cell fractions in human colorectal cancer.

The unseparated leucocytes, separated mononuclear cells and granulocytes of six control subjects and nine patients with colorectal cancer have been studied by a direct cell migration inhibition technique. A migratory index was calculated from the migration in the presence and absence of a perchloric acid extract of large bowel tumours. In 10% homologous AB serum, no significant migration inhibition occurred with any of the cells from control subjects. Five of the nine cancer patients showed significant inhibition with their unseparated leucocytes, seven of seven with their mononuclear cells, and none of nine with their granulocytes. In 10% autologous serum, some controls exhibited migration inhibition with their unseparated leucocytes and their granulocyte fraction, but not with the mononuclear cell fraction. Migration inhibition was also now apparent in the granulocyte fraction of the cancer patients. It is concluded that, with a soluble tumour antigen preparation, a mononuclear cell population increases the sensitivity of the direct migration inhibition test and that autologous serum may interfere directly with the migration of granulocytes, by an action not dependent upon the release of inhibitory factors from sensitized lymphocytes. This could explain some of the inconsistencies of the assay when using an unseparated leucocyte population.

ABO Blood-Group System↗
PubMed1979

Migration of human vascular endothelial and smooth muscle cells.

Migration of endothelial and smooth muscle cells was studied in vitro by measuring the increase in surface area at specific time intervals of confluent cell colonies advancing under agarose gels that contained both Morgan's medium 199 and variuos types of sera. First passage cultures of endothelial cells or 3 to 6 passage smooth muscle cells were plated into wells punched in agarose gels, at a seeding density of 50,000 cells per well. At zero time the size of the cell colonies was 35.4 sq. mm. +/- standard error 0.1. Irradiation (1500 rads) did not affect the expansion of the cell colonies although 3H-thymidine uptake was inhibited. Endothelial cells migrated under the agarose gels concentrically as contiguous sheets. When exposed to either 20 per cent platelet-poor plasma serum, platelet-rich plasma serum, or whole blood serum, the average increase in surface area was approximately 9 sq. mm. per day. In contrast, arterial smooth muscle cell colonies expanded with an increment of approximately 9 sq. mm. per day when exposed to 10 per cent platelet-poor plasma serum but 12 sq. mm. per day when exposed to 10 per cent platelet-rich plasma serum (p less than 0.001). Platelet factors also had stimulatory effects on the migration of venous smooth muscle cells. Cytochalasin B, dibutyryl cyclic AMP, and theophylline inhibited the migration of both endothelial and smooth muscle cells, but the latter responded more to the inhibitory effects of all three agents. It is concluded that in contrast to vascular smooth muscle, endothelial cells do not require platelet factors for migration and are less responsive to specific inhibitors affecting cell movement.

Blood Platelets↗
PubMed1978

Assessment of cell-mediated hypersensitivity against coxsackievirus B3 viral-induced myocarditis utilizing hypertonic salt extracts of cardiac tissue.

Hypertonic KCl extracts prepared from heart tissues of adolescent CD-1 mice inoculated with coxsackievirus B3 (CVB3) were tested for antigenicity in evaluating cell-mediated sensitivity to CVB3 virus utilizing the agarose droplet cell-migration-inhibition assay. Immune mouse peritoneal exudate cells (IMPEC) from mice immunized against CVB3 virus and Freund's complete adjuvant were specifically inhibited in the cell-migration-inhibition assay with graded doses of KCl-extracted antigen and purified protein derivative (PPD). Unimmunized for "normal" mouse peritoneal exudate cells (NMPEC) were not inhibited in the presence of the CVB3 KCl extracts. KCl heart extracts from mice inoculated with a cardiotropic strain of antigenically distinct mengovirus failed to inhibit CVB3 IMPEC, and noncardiac KCl extracts of liver and spleen from CVB3-inoculated mice also failed to inhibit cellular migration of CVB3 IMPEC. Reciprocal specificity experiments utilizing KCl-extracted antigens from mice infected with antigenically distinct cardiotropic mengovirus failed to inhibit cellular migration of IMPEC from mice immunized against the mengovirus. Serum-blocking power experiments indicate the antigenic KCl extracts failed to bind virus-neutralizing antibodies, indicating absence of detectable quantities of virion antigens. The results indicate that inoculation of mice with CVB3 virus results in the appearance of a new antigen(s) in cardiac tissue reacting with CVB3-IMPEC, but not with mengovirus IMPEC.

Animals↗
PubMed1975

Mastocytoma cell migration in vitro: inhibition by MIF-containing supernatants.

Supernatants with macrophage migration inhibition factor (MIF) activity were obtained from cultures of antigen-stimulated guinea pig and human lymphocytes, and from SV40-infected monkey kidney cells. The monkey and human but not guinea pig preparations were effective in inhibiting migration of mastocytoma cells as well as macrophages. This inhibition of migration was not associated with cytotoxicity and was reversible.

Animals↗
PubMed1978

Human colostral macrophages as indicator cells in migration inhibition test.

The macrophage inhibition test was carried out using colostral macrophages obtained from PPD sensitive and measles and mycoplasma pneumoniae antigen insensitive woman. The macrophage migration was inhibited by PPD but neither by measles nor by mycoplasma pneumoniae antigen. Human colostral macrophages can be used as indicator cells in migration inhibition tests.

Antigens, Bacterial↗
PubMed2026

Furmonertinib inhibits non-small cell lung cancer progression through ANGPT1-mediated regulation of cell migration and apoptosis.

BACKGROUND: Lung cancer remains one of the leading causes of cancer-related mortality worldwide, highlighting the urgent need for effective therapeutic agents. This study investigates the antitumor effects and underlying mechanisms of furmonertinib (FUR) in lung cancer cells. METHODS: Transcriptomic and clinical data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases were utilized to identify FUR target genes, followed by functional enrichment, survival, and protein-protein interaction (PPI) network analyses. Human lung cancer cell line A549 was treated with FUR and/or ANGPT1-specific siRNA. Cell migration, apoptosis, and protein expression were assessed by wound healing, flow cytometry, and Western blotting. Cellular thermal shift assay (CETSA) and drug affinity response target stability (DARTS) assays were used to assess FUR-induced stabilization of angiopoietin-1 (ANGPT1) protein. RESULTS: FUR treatment significantly inhibited cell migration and increased apoptosis in NSCLC cells. Bioinformatics analysis revealed 12 overlapping target genes of FUR from the PharmMapper and SwissTargetPrediction databases, with ANGPT1 emerging as a key candidate. ANGPT1 expression was downregulated in tumor tissues and positively correlated with patient survival. Western blotting confirmed that FUR upregulated ANGPT1 protein levels in a dose-dependent manner. Knockdown of ANGPT1 enhanced migration and suppressed apoptosis, while FUR reversed these effects. FUR treatment enhanced the stability of ANGPT1 under high-temperature conditions while reducing its sensitivity to protease. ANGPT1 may have affected tumor cell migration through cell adhesion and extracellular matrix (ECM) pathways. CONCLUSIONS: FUR suppresses lung cancer progression by upregulating ANGPT1, thereby inhibiting cell migration and promoting apoptosis. ANGPT1 is a potential therapeutic target and provides new insights into the anti-tumor mechanism of FUR in lung cancer.

Lung cancer↗
PubMed1977

[Influence of autologous serum on leucocyte-migration-inhibition-test in melanomalignoma (author's transl)].

Influence of autologous serum on cellular immunological reactivity to melanomalignoma (MM)-associated antigens was examined on 20 patients have MM at different clinical stages, using the Leucocyte-Migration-Inhibition-Test (MIT). These 20 patients were referring to this till now not investigated. When heterologous serum (horse serum) was supplemented, an inhibition of cell-migration could be established in 15/20 cases, whereas a cell-migration inhibition in 14/20 cases was absent if autologous serum was added to culture medium. No correlation could be found between our test results and the clinical stage of the disease. Our results suggests urgently that blocking factors are present in serum of MM-patients. There is reason to believe that this factors will be active in lymphocyte level.

Adult↗