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Biomedical subjects

G Milon

Publications and source records attributed to G Milon.

90 records · Page 5Linked to original sources
PubMed1981

Decreased erythropoiesis: the origin of the BCG induced anaemia in mice.

Transient anaemia follows a high dose of viable BCG given intravenously to mice. The anaemia was dependent upon the dose, viability and the route of injection of the BCG. The evidence of an absolute anemia was based on red cell mass decrease. Serum iron concentration and red cell life span were unchanged in the first 14 d after BCG infection. The erythropoietin level increased 20-fold. Despite the high level of this hormone and the appearance of increased erythropoiesis in the spleen, the production of erythrocytes was decreased presumably because of a decrease in numbers of erythropoietin-responsive cells.

Anemia↗
PubMed1980

Altered circulation of lymphocytes mediating delayed-type hypersensitivity when primed in Wf/Wf mice.

When mice were homozygous for the Wf allele at W locus, the delayed-type hypersensitivity (DTH) reaction observed in mice primed i.v. or s.c. with optimal doses of sheep red blood cells was greatly decreased. The number of sensitized splenic cells able to transfer a delayed-type hypersensitivity reaction was identical in +/+ and Wf/Wf primed mice. At site of local transfer of +/+ sensitized cells and antigen, the recruitment of monocytes was identical in +/+ and Wf/Wf mice. In contrast, the number of blood cells able to transfer a DTH reaction was decreased by a factor 40 in Wf/Wf primed mice compared to +/+ ones. This decreased number of sensitized cells in blood of Wf/Wf mice revealed a specific defective circulation of Wf/Wf DTH mediating cells whatever the genotypes (+/+ or Wf/Wf) of recipients used to measure this property of circulation.

Animals↗
PubMed1979

High radiosensitivity of induction in contrast to radioresistance of expression of cells mediating delayed-type hypersensitivity during response to sheep red blood cells in mice.

The delayed-type hypersensitivity DTH) reaction observed in mice primed i.v. with low doses of sheep red blood cells was greatly decreased when mice were irradiated with 300 rad before priming. An estimation of the radiosensitivity of DTH-mediating cells (DTH-C) was performed using a titration assay after local adoptive transfer of these cells mixed with antigen into the footpad of unprimed mice. A high radiosensitivity of the induction of DTH-C was observed with a D37 of approximately 50 rad. In contrast, the expression of DTH-C appeared radioresistant, as the D37 was approximately 2000 rad.

Animals↗
PubMed1978

Titration and circulation of cells mediating delayed type hypersensitivity in normal and cyclophosphamide treated mice during response to sheep red blood cells.

The delayed-type-hypersensitivity (DTH) reaction observed in mice primed i.v. with low doses of sheep red blood cells is not detectable after priming with large doses. Estimation of the number of DTH mediating cells (DTH-C) was performed by titration (D50 determination) using local adoptive transfer of these cells mixed with antigen into footpads of unprimed mice. In opposition to the absence of peripheral DTH-C, splenic DTH-C were more numberous after large doses than after low doses of antigen. The ability of cyclophosphamide to restore DTH responsiveness in mice primed with large doses appeared to be related to an increased cirulation of DTH-C. These cell circulated only in mice without any detectable B-cell response or in which this response was depressed. Thus a B-cell dependent splenic retention process of DTH-C is discussed as the origin of DTH unresponsiveness observed after priming with large doses of antigen.

Animals↗
PubMed1978

Increased infiltration by monocytes in delayed type hypersensitivity site following cyclophosphamide treatment.

Sensitized lymphocytes transferred locally with antigens into footpads of unprinted mice can elicit a delayed-type-hypersensitivity (DTH) reaction. Treatment of recipients with cyclophosphamide (CY) increased the infiltration observed at the DTH site. The enlargement of footpads was detected with low doses of DTH mediating cells as with large ones. An enumeration of circulating monocytes performed on the test days and the preceding days has shown a three to ten fold increase of number of monocytes. During the recovery following CY treatment (20 mg/kg and 200 mg/kg) a rebound effect at level of precursors of monocytes was observed. Thus a dual mechanism is proposed to explain the effect of CY on DTH reaction: a liberation of DTH cells by inhibition of B response as previously described; an increased number of monocytes which can be recruited by DTH-cells in site of antigen injection.

Animals↗
PubMed1977

[Preferential differentiation of hematopoietic stem cells transferred to mice previously infected by BCG].

Following injection of bone marrow cells in lethally irradiated mice, previously infected with BCG regenerating hemopoietic cell populations differentiate along the leucocyte pathway to the detriment of erythroid lineage. Such a phenomenon persisting even if anemia of infected mice is increased by bleeding just before irradiation and reconstitution supports the hypothesis of preferential differentiation of stem cells.

Animals↗
PubMedDate not supplied

Assay for quantitation of mature monocytes in murine haemopoietic tissues.

We propose a new assay which allows the extent of production of mature monocytes in murine haemopoietic tissues to be monitored with precision. To develop such a quantitative assay, we chose a T-cell function easily detectable in vivo, namely the ability of T lymphocytes to locally transfer a delayed-type hypersensitivity (DTH) reaction. T cells co-transferred with antigen into footpads of syngeneic mice are mediators of DTH through their ability to recruit phagocytes recently produced in haemopoietic tissues. Therefore, if recipients of DTH-mediating T cells (DTH-T cells) are depleted of phagocytes by lethal irradiation given 36 to 48 h before local transfer of these DTH-T cells mixed with antigen, they no longer respond by a DTH reaction, measured as an increase in footpad thickness, unless they receive i.v. bone marrow cells as a source of recruitable phagocytes. In such conditions, the footpad thickness increase is linearly related to the number of cells injected i.v. Pretreatment of bone marrow cells with the rat IgG2b F4/80 monoclonal antibody abolishes their ability to restore expression of DTH, indicating that monocytes (F4/80+ cells) are the phagocytes to be measured. This assay system thus provides a means of measuring levels of recruitable mature monocytes present in haemopoietic tissues. One illustration of the assay is given by the study of the recovery of recruitable phagocytes in bone marrow following a single treatment with cyclophosphamide.

Animals↗
PubMedDate not supplied

Numeration of DTH-mediating T lymphocytes in mice under optimal titration conditions.

The magnitude of the delayed-type hypersensitivity (DTH) reaction observed in appropriately immunized mice appears to be dependent on an early non-specific inflammatory reaction. The volume of injection and dose of antigen are two major components of this early reaction. The determination of optimal conditions for revealing the DTH reaction enabled definition of a titration method for DTH-mediating T lymphocytes. Injection of a subinflammatory dose of antigen led to conditions of limiting dilution analysis. Thereafter, the initiation of DTH reaction by local injection of a minute number of sensitized cells mixed with an optimal dose of antigen allowed in vivo titration of sensitized T lymphocytes. Single-hit linear curves were obtained when the percentages of negative transfers were plotted against the number of transferred cells in the classical semi-log plot of Poisson's distribution. Initiation of reaction by a quantal mechanism and results giving a linear plot (a single cell type being diluted out) served as an indication that a numeration of sensitized T cells had been performed for the more diluted concentrations of cells assayed.

Animals↗
PubMedDate not supplied

BCG-induced anaemia in mice: no direct effect of the growth of bacilli.

Mice receiving viable BCG intravenously (i. v.) rapidly and transiently develop anaemia, the origin of which is a decrease in erythropoietic progenitor cells. BCG-induced anaemia appears to be related to conditions which allow the development of a protective immune response against BCG infection. An increased number of blood phagocytes is strictly associated with the development of the anaemia and is dependent on the presence of T lymphocytes. Anaemia does not occur in some strains of mice: C3H/He Past strain was chosen as a typical non-responding strain and the opposite C57BL/6 strain as a responding one. Enumerations of BCG particles were performed in haemopoietic tissues, spleen and bone marrow of mice of the two strains in order to appreciate an eventual direct effect of bacilli growth on erythropoiesis. We never observed the particular growth of bacilli in mice which developed anaemia. On the contrary, the number of BCG viable units decreased progressively in responding strain C57BL/6 when numerations were performed after the 2nd month of the infection. This ability of C57BL/6 mice to control the infection contrasted with a relapse of bacilli growth in C3H.

Anemia↗
PubMedDate not supplied

Cyclosporin A inhibits the delayed-type hypersensitivity effector function of T lymphocytes without affecting their clonal expansion.

The effect of an immunosuppressor, cyclosporin A (CsA), on the induction by sheep erythrocytes of T cells mediating the delayed-type hypersensitivity (DTH) reaction was investigated using a quantitative assay of DTH-mediating T lymphocytes. CsA administration did not affect their clonal expansion following immunization. The frequency of the DTH-mediating T cells was not significantly different in mice sensitized by antigens in the presence or absence of CsA. However, CsA interfered with expression of effector function of DTH-mediating T lymphocytes by impairing the production of pro-inflammatory factor(s). Resting T cells as well as blast T cells were sensitive to this inhibitory effect of CsA.

Animals↗
PubMedDate not supplied

Fertile dominant spotting in the house mouse.

Recognition of a new allele (Wf) at the W locus of the mouse is based on genetic analysis and demonstration of defective hair pigmentation, macrocytic anemia, and defects in pluripotent hemopoietic stem cells. Unlike other alleles of the W series, this one does not result in sterility.

Alleles↗
PubMedDate not supplied

Selective suppression of tumour-immune cytolytic T lymphocytes in mice with chronic Trypanosoma cruzi infections.

Trypanosoma cruzi is the causative agent of Chagas' disease in man, often leading to suppression of T lymphocyte functions; the present study thus considered the effects of infection by T. cruzi on T-dependent immune responses in a murine model, namely, the immune resistance to a syngeneic tumour and a delayed-type hypersensitivity reaction to sheep red blood cells (SRBC). In BALB.B mice infected with T. cruzi, the graft of syngeneic Gross murine leukaemia virus-induced tumour cells leads to an increased incidence of progressive subcutaneous tumours and development of lymphatic leukaemia. This decreased resistance to tumours correlates with a suppression of the generation of tumour-specific cytolytic T lymphocytes (CTL) from the pre-CTL stage. In contrast, clonal expansion and circulation of T cells detected through their ability to locally transfer a delayed-type hypersensitivity (DTH) reaction to SRBC remained normal in T. cruzi-infected mice. However, at the site of the DTH reaction, a decreased availability of phagocytes was observed in T. cruzi-infected mice.

Animals↗
PubMedDate not supplied

Enumeration of haemopoietic progenitors (CFU-C and BFU-E) in liquid microculture using a limiting dilution analysis.

In order to overcome the difficulty of scoring multicentric colonies of haemopoietic progenitor cells, cultures in 10 microliter of liquid medium were grown. Plated at three different cell concentrations, progenitor cells (CFU-C or BFU-E) are not present in all wells. Their presence is easily scored in each well of microculture 7 days after incubation. A limiting dilution analysis allows one to obtain accurate quantification.

Animals↗
PubMedDate not supplied

[Anaemia following BCG infection in mice: need for presence of thymodependent lymphocytes (author's transl)].

An anaemia and a decreased number of erythroid bone marrow cells were observed on the first weeks following the intravenous injection of 1 mg of BCG into normal mice. No such modification of erythropoiesis was detected in Nude mice. The graft of thymus from new born mice to Nude adults before BCG infection allowed to obtain a drop of packed-cell volume. In previously infected Nude mice, the injection of spleen cells providing from infected normal mice also modified the erythropoiesis. This effect was lost by pretreatment of injected spleen cells with anti-theta serum and complement. Thus, the conditions necessary to the development of the anaemia during BCG infection correlated with the conditions which allowed an immune response against infection.

Anemia↗
PubMedDate not supplied

TNF-induced microvascular pathology: active role for platelets and importance of the LFA-1/ICAM-1 interaction.

Pathogenic mechanisms of brain microvascular injury were studied in an experimental model of cerebral malaria (CM). The lesion, leading to perivascular microhemorrhages, is due to cytokine overproduction, and is associated with the sequestration of macrophages and parasitized erythrocytes in cerebral venules. In this in vivo model, we demonstrate that platelets are critical effectors of the neurovascular injury. First, electron microscopy indicated that during CM platelets adhere to and probably damage brain endothelial cells. Second, radiolabelled platelet distribution studies indicated that platelets sequestered in the brain and lung vasculature during CM. Non-cerebral malaria was not associated with cerebral sequestration of platelets. Third, in vivo treatment with a mAb to LFA-1 (which is expressed on platelets) selectively abrogated the cerebral sequestration of platelets, and this correlated with prevention of CM. Fourth, malaria-infected animals rendered thrombocytopenic were significantly protected against CM, further indicating that platelets are central to the pathogenesis of CM. Thus, a CD11a-dependent interaction between platelets and endothelial cells appears pivotal to microvascular damage. These data suggest a novel mechanism of action for anti-LFA-1 mAb in vivo and illustrate an unexpected role of platelets, in addition to monocytes, in vascular pathology.

Animals↗
PubMedDate not supplied

[Immunological responsiveness in C57BL/6 mice during the growth of a tumoural graft: the Lewis' lung carcinoma (author's transl)].

Using antibody and delayed type hypersensitivity responses to sheep red blood cells, immunological responsiveness was studied during the course of 3LL tumor growth. Acquired specific resistance to Listeria monocytogenes of tumor bearing mice was also investigated. Experimental results obtained, showed that the ability of 3LL bearing mice to establish a specific immune response is not markedly impaired.

Animals↗