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G Cozon

Publications and source records attributed to G Cozon.

36 records · Page 2Linked to original sources
PubMed1993

An improved assay for the detection of Toxoplasma gondii antibodies in human serum by flow cytometry.

The diagnosis of toxoplasmosis relies primarily on the demonstration of specific antibodies to Toxoplasma gondii. We describe a flow cytometry method for the determination of antibodies to whole fixed tachyzoites by indirect immunofluorescence. Fixed tachyzoites in suspension have characteristic light scattering properties. The amount of IgM, IgG, and IgA antibodies from patients' sera bound to the tachyzoites can be estimated from the mean fluorescence intensities observed using class-specific conjugates for different Ig heavy chains. Appropriate serum dilutions for the estimation of specific IgG titres and for the discrimination between sera positive and negative for IgA and IgM antibodies were established using 40 random sera from pregnant women. The method proved to be quantitative and highly sensitive as compared with currently used assays. Coefficients of variation between series ranged from 6.4% to 12.2% and could be controlled by the inclusion of positive and negative standard sera in the test series. The method might represent a major improvement in cost effectiveness as compared with routine immunofluorescence assay by fluorescent microscopy when the volume of testing is sufficient. It can be fully automated, and its large scale application is currently under investigation.

Animals↗
PubMed1992

Secretory immunoglobulins in serum from human immunodeficiency virus (HIV)-infected patients.

Infection by the human immunodeficiency virus is associated with polyclonal B cell activation and increased levels of serum IgA. In order to characterize the molecular species of serum IgA, we have measured total IgA, IgA1, and IgA2 in sera from 60 HIV-1-infected patients and 40 healthy controls. In addition, secretory IgA (S-IgA), secretory IgM (S-IgM), free immunoreactive secretory component (SC), and the distribution of monomeric and polymeric IgA were determined. The data confirm the elevation of total serum IgA levels in HIV-1-infected patients, and both IgA1 and IgA2 concentrations are elevated. Furthermore, the data show a substantial increase in serum levels of both monomeric and polymeric IgA. Serum S-IgA levels were significantly increased in CDC group II patients versus controls and more frequently elevated in CDC group IV patients. The highest S-IgA levels were found among patients with the lowest blood CD4+ cell counts. Serum S-IgA levels were not correlated with serum levels of either total IgA or polymeric IgA. Serum S-IgM levels were also increased in HIV-1-infected patients and positively correlated with serum S-IgA levels. Conversely, serum levels of free SC were not altered. An increase in serum S-IgA was not related to human hepatitis B virus infection and/or to hepatic dysfunction or to diarrhea or overt intestinal infection. The data indicate that secretory Ig (S-IgM and S-IgA), which are likely to be produced at mucosal sites, increase in the serum of HIV-1-infected patients.

Adult↗
PubMed1992

Cryptosporidium parvum sporozoite staining by propidium iodide.

Modified Ziehl-Neelsen (ZN) acid-fast stain is the usual method for detection of Cryptosporidium oocysts in feces. Propidium iodide permitted us to stain free or intra-oocyst sporozoites. With the ZN method only 3-5% of the oocysts purified from three human and one experimentally infected lamb dichromate-preserved feces were stained by carbol fuchsin. These fuchsin-stained oocysts were free of intact sporozoites as identified by propidium iodide staining. Treatment with 10% formalin or 0.5% sodium hypochlorite increased the percentage of acid-fast stained oocysts and thus the sensitivity of acid-fast staining. Treatment with sodium hypochlorite induced intra-oocyst sporozoite alterations as demonstrated by flow cytometric analysis of the oocysts' DNA content. Propidium iodide staining of fixed oocysts is a simple and rapid method to visualize sporozoites and to assess oocyst preservation after different treatments.

Animals↗
PubMed1992

Characterization of the lymphocytic alveolitis in visna-maedi virus-induced interstitial lung disease of sheep.

In order to investigate the contribution of lymphocytes to interstitial lung disease in animals with visna-maedi infection, we studied in parallel bronchoalveolar cells and lung tissue from slaughter-house animals (n = 29) and from colostrum-deprived lambs transtracheally inoculated with field isolates of visna-maedi virus (n = 9) or saline (n = 6). Lymphocyte subpopulations were identified in bronchoalveolar lavage by immunofluorescence and flow cytometry analysis and in lung tissue using indirect immunohistochemistry. In infected animals a lymphocytic alveolitis containing CD4 and CD8 lymphocytes was observed. Peribronchovascular lymphoid nodules comprise mostly CD4 lymphocytes. Alveolar lymphocytes of both subsets displayed increased expression of MHC class II antigens in animals with naturally occurring maedi but not in experimentally infected ones. A sequential process of lymphocyte attraction and activation is likely to occur in vivo as part of the alveolitis.

Animals↗
PubMed1992

Oral administration of immunomodulators and the mucosal immune system.

Orally administered antigens reach the lymphoid tissue in Peyer's patches in the gut where they initiate an immune response with clonal expansion of antigen-specific T and B cells. Activated T cells migrate through lymph and blood to intestinal epithelium (intra-epithelial leukocytes) whereas activated B cells migrate to the lamina propria, other mucosae and exocrine glands where they differentiate into plasma cells secreting polymeric IgA1 or IgA2. These antibodies are transported across the epithelial cells after binding to a poly-Ig receptor, then excreted in the lumen as secretory IgA. Reciprocal interactions have been demonstrated between lymphoid and epithelial cells in the mucosae. Oral administration of antigens in different experimental models may induce the production of secretory antibodies and/or systemic unresponsiveness with suppression of delayed-type hypersensitivity or specific IgG and IgE antibody production or both. New strategies are currently being explored for the development of oral vaccines using recombinant antigens or viral vectors (e.g. pox-viruses, vaccinia virus, cholera toxin B subunit etc.). Conversely, immunomodulating compounds or procedures which could enhance specific oral tolerance in association with antigen would have considerable therapeutic applications in auto-immune diseases and allergy.

Adjuvants, Immunologic↗
PubMed1991

[Secondary deficiencies of humoral immunity].

Humoral immunity involves molecules in solution in biological fluids including effectors of non specific immunity (e.g. complement, cytokines) and specific immunity (antibodies) as well. Acquired humoral immunodeficiences are often multifactorial in origin and associated with defects of cell-mediated immunity. The most common etiologies are those of iatrogenic immunodeficiencies: surgery (especially splenectomy), radiotherapy, chemotherapy of leukemia and cancer, immunosuppressive treatments in organ transplanted patients. Protein-caloric malnutrition also induces cellular and humoral immunodeficiencies. Among other causes, three types of diseases may induce defective antibody production: 1/B cell neoplasias (e.g. multiple myeloma, chronic lymphocytic leukemia...) 2/renal diseases (nephrotic syndrome, renal insufficiency) and 3/various infectious diseases, including AIDS. Some principles of prevention and treatment of secondary humoral immunodeficiencies are given.

Hematologic Diseases↗
PubMed1991

Transient secretory IgA deficiency in mice after cyclophosphamide treatment.

Cyclophosphamide (Cy), an alkylating agent widely used in chemotherapy of leukemia and cancer, causes a well-documented toxicity on hematopoietic and lymphoid cells. Neutropenia is thought to be the main factor involved in infectious complications following antimitotic chemotherapy. Little is known on the effects of these therapies on the mucosal associated lymphoid system which is one of the main barriers against environmental pathogenic agents. The present study examined the effects of a single administration of Cy (200 mg/kg) on murine T and B cell populations of Peyer's patches (PPs), IgA secretion in the proximal part of the small intestine, and plasma cells of the lamina propria. Cy induced in mice a transient decrease in the T and B cell populations of the PPs with a drastic fall of B cell counts and a profound decrease of intestinal IgA secretion due to a reduction of lamina propria plasma cells. This transient secretory IgA deficiency may contribute to the infectious complications following antimitotic chemotherapy.

Animals↗
PubMed1990

In vivo activation of alveolar macrophages in ovine lentivirus infection.

Sheep infected by visna-maedi virus, a lentivirus related to the human immunodeficiency virus, develop a chronic interstitial lung disease. Since monocyte/macrophages are known to be specifically infected by visna-maedi virus, we investigated the role of macrophages in the appearance of pulmonary lesions in animals with naturally occurring disease. Alveolitis in maedi leads to a doubling in bronchoalveolar lavage total cell counts and of macrophages as compared to normal sheep. A significant increase in the relative percentage of neutrophils was also observed, accompanied by an increased spontaneous release of neutrophil chemotactic activity by alveolar macrophages of diseased animals, suggesting that they may be activated. Macrophage activation is also demonstrated by the observation of a significant (x3) increase of spontaneous fibronectin release by alveolar macrophages from maedi lungs, and furthermore by the high level expression of major histocompatibility complex class II antigens on most of these cells. Thus viral infection, although restricted to a small population of macrophages, is able to modulate extensive activation of macrophages in the lung. Activated macrophages release mediators likely to play a role in the development of the alveolitis and the parenchymal desorganization. These findings may be relevant to our understanding of the mechanisms by which human immunodeficiency virus infection leads to pulmonary disease other than that caused by opportunistic infections.

Animals↗
PubMed1990

Experimental models and mechanisms of immune deficiencies of nutritional origin.

The complex interactions between nutrition, infection and immunity are still poorly understood and the precise role of each factor is difficult to ascertain. Infection itself induces profound metabolic alterations resulting in negative nitrogen balance. Protein energy malnutrition, whatever its origin, results in an immune deficiency characterized by impaired delayed cutaneous hypersensitivity, low production of lymphokines, low T cell counts, decreased T cell responses to specific or non specific mitogenic stimuli. Serum immunoglobulin levels are normal or elevated and antibody responses to most vaccines are normal or slightly altered. Secretory IgA levels, number of IgA plasma cells in jejunal mucosa and specific IgA antibody levels are depressed. Neutrophil chemotaxis and serum opsonic activity are normal but bacterial killing capacity is markedly reduced. C3 levels are usually reduced as a consequence of low hepatic synthesis and increased consumption but most other complement proteins remain within the normal range. Such alterations of immunological parameters can be induced by malnutrition itself but they are commonly observed in populations also exposed to a heavy load of infectious agents from birth. Various types of immunodeficiencies can be achieved by selective deficiencies of minerals trace elements and several vitamins. Several experimental and clinical studies showed that overnutrition could alter T cell immune responses and accelerate the development of spontaneous auto-immune diseases in selected strains. Conversely low calorie or low fat diets as well as supplementation in fish oil markedly enhanced survival in these models. Despite much controversy as regards the mechanisms of immune alterations of nutritional origin, the clinical and experimental data already available provide a framework for the design of further investigations and for prophylactic action.

Animals↗
PubMed1990

[Diffuse interstitial pneumopathies caused by lentivirus (HIV-1) in humans and animals].

Lentiviruses belong to the retroviruses family (ie RNA viruses with reverse transcriptase activity); they induce inflammatory and/or degenerative slowly progressive diseases, affecting various organs. Some lentiviruses preferentially infect lymphocytes (HIV-1 and HIV-2, SIV and FIV) and are associated with infectious and tumoral disorders. Most lentiviruses induce a pulmonary disease, typically diffuse interstitial pneumonia. The visna/maedi-virus of sheep infects monocyte macrophage cells and the pulmonary lesions are macrophagic and neutrophilic alveolitis, lymphoid infiltration, myomatosis and interstitial fibrosis. Such pulmonary lesions are also induced by the goat and equine lentiviruses. In humans infected by HIV-1 or HIV-2, a diffuse interstitial lung disease also occurs; the histological findings are of alveolitis associated with lymphoid peribronchovascular infiltrates. The mechanism of formation of the lesions involves complex cellular interactions (especially between macrophage and lymphocyte, via cytokine production). These interactions are well modelled by small ruminant lentivirus induction of interstitial pneumonia.

Acquired Immunodeficiency Syndrome↗
PubMed1989

[Karyotype study of blood lymphocytes in sarcoidosis].

Among 31 patients presenting with pulmonary sarcoidosis, two had abnormalities of their blood lymphocyte karyotypes. The karyotype of the first patient showed an initially high percentage of non-specifically broken chromosomes. The second patient, who had been treated with azathioprine (AZ) one year previously, had an apparently balanced translocation 46 XX, t (11; 11) (p 12, p 14) in blood T lymphocytes but not in skin fibroblast culture. Various hypotheses can be discussed to explain this translocation: a direct toxic effect of AZ or a genomic abnormality depending upon sarcoidosis and possibly revealed by AZ. It is important to note that this translocation concerned a region of the short arm of chromosome 11, where Harvey ras I and parathormone genes have been located.

Adolescent↗
PubMedDate not supplied

Visna-maedi virus-induced expression of interleukin-8 gene in sheep alveolar cells following experimental in vitro and in vivo infection.

Visna-maedi virus is a lentivirus which causes inflammatory disorders in sheep, including a chronic interstitial lung disease resembling that observed in human immunodeficiency virus type 1 (HIV 1) infection. In view of our previous demonstration of the production of neutrophil chemotactic activity by alveolar macrophages, and given the lymphocytic and neutrophilic nature of the alveolar cell infiltrate in both naturally and experimentally infected animals, we hypothesized that interleukin-8 (IL8) could be a candidate for at least part of the chemotactic activity we described. In this study, we investigated IL8 mRNA expression following visna-maedi virus infection. Northern analysis of total RNA using an ovine IL8-specific probe demonstrated that the IL8 gene is upregulated in alveolar macrophages as a consequence of in vitro infection and in alveolar cells from experimentally infected animals. Using a semi-quantitative RT-PCR method, we showed that various levels of IL8 mRNA are expressed by alveolar cells from infected animals and that they correlate with the intensity of the lesions. In conclusion, visna-maedi virus is able to induce IL8 mRNA expression in sheep alveolar cells. Results from in vivo infected animals suggest that IL8 could play a role in the early build-up of visna-maedi virus-induced lesions.

Animals↗
PubMedDate not supplied

Detection of activated basophils using flow cytometry for diagnosis in atopic patients.

BACKGROUND: human basophils release mediators of allergy after cross-linking of IgE receptors by allergens. Specific activation of basophils is detectable through flow cytometry (FCM) using an anti-CD63 fluorescein-conjugated monoclonal antibody. OBJECTIVES: this study evaluate the detection of activated basophils by FCM in routine diagnosis of atopic diseases as regard to skin prick tests and specific immunoglobulin E antibodies. METHODS AND RESULTS: whole blood from twenty patients suspected of atopy was preincubated with interleukin-3 (IL-3), then incubated with specific allergens. After staining using anti-CD63 antibodies, activated basophils were detected through FCM. IL-3-preincubation increases the spontaneous expression of CD63 even at low concentrations (0.1 ng/ml) on the basophils of 2 patients out of 20. The sensitivity and specificity of FCM were respectively 0.56 +/- 0.17 (m +/- SD) and 1.0 +/- 0.0 for the detection of dust mite-activated basophils without IL-3 preincubation, and 0.73 +/- 0.13 and 1.0 +/- 0.0 for the detention of grass pollen-activated basophils. IL-3-preincubation increased the sensitivity in a dose-dependent manner but decreased the specificity fo FCM for detecting dust mite hypersensitivity. CONCLUSION: this method allow for rapid and easy detection of activated basophils from whole blood, and could be of interest for detecting allergies to non-conventional allergens such as pharmaceutical drugs.

Allergens↗