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Biomedical subjects

J J Ballet

Publications and source records attributed to J J Ballet.

At least 55 records · Page 3Linked to original sources
PubMed1993

Assessment of candidate anticryptosporidial agents in an immunosuppressed rat model.

Cryptosporidium parvum causes life-threatening diarrhea in immunocompromised patients, especially those with AIDS. The efficiency of currently proposed anticryptosporidial therapies is limited or doubtful. In this report, molecular candidates for curative or preventive activity were investigated in an immunocompromised rat model that mimics severe human cryptosporidiosis. No significant anticryptosporidial activity was observed when using sulfadoxine-pyrimethamine, quinacrine, trimethoprim-sulfamethoxazole, bleomycin, elliptinium, daunorubicin, pentamidine, alpha-difluoro-methylornithine, diclazuril or N-methylglucamine. Vitamin A appeared to reduce oocyst shedding. Active agents included sinefungin (2-10 mg/kg/24 h), lasalocid A (2-10 mg/kg/24 h), metronidazole (25-50 mg/kg/24 h), and sulfadimethoxine (10-100 mg/kg/24 h). Sinefungin (10 mg/kg/24 h) and lasalocid A (10 mg/kg/24 h) displayed the highest anticryptosporidial activity.

Animals↗
PubMed1993

Curative and preventive anticryptosporidium activities of sinefungin in an immunosuppressed adult rat model.

An immunosuppressed rat model was used to investigate the anti-Cryptosporidium parvum activity of sinefungin. In infected animals, oral sinefungin therapy resulted in a dose-related suppression of oocyst shedding, which correlated with oocyst disappearance from ileal sections. When administered prior to or on the day of oocyst challenge, sinefungin successfully prevented infection. These data suggest that sinefungin could be considered as a candidate molecule in the treatment of human cryptosporidiosis, considered to be the most significant enteric opportunistic infection in AIDS.

Adenosine↗
PubMed1993

Virus recovery from stools of patients undergoing bone marrow transplantation.

Diarrhea in marrow transplant recipients is a frequent complication attributable to non-infectious events such as acute GVHD or infectious events such as viral gastroenteritis. Rotavirus and enteric adenovirus are the most frequent viral pathogens. To determine the frequency of these infections, we prospectively examined the stool specimens of 94 patients who underwent autologous BMT (34 cases) or allogeneic BMT (60 cases). Stool specimens were examined from patients twice weekly. Nineteen of the 94 patients were infected with viral pathogens. This study showed: (1) an incidence of viral gastroenteritis identical in autologous and allogeneic BMT (20%), (2) a persistent risk despite treatment in laminar air flow rooms, (3) a significant association with severe acute GVHD, and (4) a significant risk of multiple viral infections in autologous BMT recipients. Rotavirus and adenovirus are a cause of enteritis involvement in patients undergoing BMT and they may be underdiagnosed and confused with GVHD. Screening of stool specimens after BMT should be directed to prevention and treatment of these viral infections to decrease the morbidity and mortality associated with BMT.

Adenovirus Infections, Human↗
PubMed1992

[Leukocytic cytomegalic antigen. A new diagnostic method of cytomegalovirus infection after transplantation].

The occurrence of cytomegalovirus (CMV) viremia after transplantation is predictive of visceral lesions. Three-hundred and sixty blood samples were collected from 21 transplant recipients and examined. Direct CMV antigen detection was positive in 41 samples (11.4 percent), rapid viral isolation in 24 samples (6.7 percent) and conventional cell culture in 9 cases (2.5 percent). Direct detection of CMV antigen in blood leucocytes is as specific as, and more sensitive and rapid than isolation in culture. In 50 percent of secondary infections the antigenaemia assay and serology were equally sensitive, and antigenemia appeared earlier in 2 primary infections.

Antibodies, Monoclonal↗
PubMed1990

Responses of T cells from sensitized donors to recombinant and synthetic peptides corresponding to sequences of the Plasmodium falciparum SERP antigen.

In the present work, we intend to determine the capacity of human lymphocytes to recognize subfragments of the serine-stretch protein SERP, a blood-stage antigen from Plasmodium falciparum. Individuals sensitized by a previous P. falciparum infection were studied. Some recombinant proteins (RP) including RP7 and RP10 (amino acids 631-684 and 631-892 of SERP, respectively), were recognized in proliferation assays by lymphocytes from 28 sensitized individuals and not by lymphocytes from control, non-sensitized, donors. Synthetic peptides covering predefined zones of particular interest were tested and appeared to induce proliferative responses of lymphocytes from sensitized donors, allowing identification of putative T cell epitopes.

Amino Acid Sequence↗
PubMed1990

Impairment of Plasmodium falciparum-specific antibody response in severe malaria.

Serum antibody response to plasmodial antigens was investigated in 97 Thai patients with Plasmodium falciparum malaria. No difference in immunoglobulin G (IgG) antibody levels was detected between groups without or with cerebral manifestations of malaria (n = 40). In patients with the most severe form of the disease, i.e., those who died despite adequate therapy (n = 12), antibody detected in the immunofluorescent-antibody test was found at lower levels than in those who recovered (geometric means: IgG = 1/420 versus 1/3,800; IgM = 1/15 versus 1/70); similarly, precipitating malarial antibodies were present in only 1 of these 12 patients, while they were detectable in 65 of the remaining 85 patients (76.5%). In contrast, anticytomegalovirus antibody levels were similar in the different groups of patients. Results show that depression of antibody response may extend to antiplasmodial responses during severe malaria. The link between fatality and a low level of antibody production suggests that an appropriate immune response to malarial antigens may be required to achieve recovery with drug treatment and provides a new direction for malaria therapy research.

Adolescent↗
PubMed1989

Interactions of CD4+ and CD8+ human T lymphocytes from malaria-unprimed donors with Plasmodium falciparum schizont stage.

During Plasmodium falciparum malaria, a wide spectrum of parasite-encoded blood-stage proteins is presented to the immune system of the host. To explore their multiple interactions with T cells from donors who have had no previous exposure to the parasite, whole schizont extract was used in vitro. Both CD4+ and CD8+ lymphocytes from all individuals tested were stimulated to proliferate. The responses were dependent on the presence of accessory cells and were only partially replaced by recombinant interleukin-1. Responses were inhibited by monoclonal antibodies to CD3, the alpha beta-chain T-cell receptor, or CD4 molecules but not to CD2. P. falciparum schizont extract-specific T-cell clones were generated and maintained by using sole stimulation by P. falciparum extract with autologous accessory cells or recombinant interleukin-2. Monoclonal antibodies to CD3 (or the alpha beta-chain T-cell receptor) blocked cloned T-cell responses to the schizont extract, and although the responses of the majority of the CD4+ or CD8+ T-cell clones were restricted by autologous accessory cells and inhibited by monoclonal antibodies to either CD4 or CD8, other clones responded to P. falciparum in the absence of accessory cells and were not regulated by the same monoclonal antibodies. The last category of clones consisted of autoreactive T cells. These data suggest that at the first contact with P. falciparum, requirements are met for significant T-cell stimulation.

Animals↗
PubMed1989

Impaired in vitro lymphocyte response to toxoplasma antigen in HIV1 infected patients.

The containment of Toxoplasma gondii infection is largely dependent of T cell mediated immunity. In this study, in vitro lymphocyte responsiveness to T. gondii antigen was examined in 59 HIV1 infected individuals and in 58 HIV non-infected controls. Of the 45 patients with serological evidence of past Toxoplasma infection, a significant proliferative response was found in only 18, whereas responses were present in 48 out of 51 controls with anti-Toxoplasma antibodies. In the 27 non-responder patients, the lack of proliferative response to T. gondii antigen was correlated with the loss of CD4+ cells, and the impairment of proliferative responses to other microbial antigens, whereas responsiveness to phytohaemagglutinin and concanavalin A were not significantly diminished. Results are consistent with impairment of cell mediated immunity to T. gondii in patients at risk for reactivation of chronic Toxoplasma infection. Of note, in the one year clinical following, 2 of the 27 non-responder patients developed toxoplasmic encephalitis compared to 0 of 18 with a Toxoplasma specific proliferative response.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Plasmodium falciparum exoprotein stimulation of human T-lymphocytes unsensitized to malaria.

The effects of Plasmodium falciparum proteins released in asexual blood stage culture supernatants on human T-lymphocytes from malaria non-immune donors were examined. Supernatants from several plasmodial strains stimulated both CD+4 and CD+8 T-lymphocytes to proliferate and secrete interferon gamma in vitro. Active moieties were predominantly released during the final stages of the parasite cycle. They were enriched by gel filtration and were further purified by anion-exchange and Superose 12 column fast protein liquid chromatography. Three active fractions of apparent 250, 70 and 18 kilodaltons were identified. The parasitic origin of the predominant 70-kilodaltons protein(s) was shown by biosynthesis experiments with radioactive amino acid precursors and was also demonstrated by in vitro translation of parasitic mRNA species. Interestingly, antibodies to the 70-kilodalton exoprotein(s) also reacted to a schizont protein of similar molecular weight.

Animals↗
PubMed1988

Impaired T-lymphocyte-dependent immune responses to microbial antigens in patients with HIV-1-associated persistent generalized lymphadenopathy.

T-cell mediated and humoral responses directed to microbial antigens were investigated, at the time of the initial visit, in a group of 139 patients with HIV-1-related persistent generalized lymphadenopathy (PGL) enrolled in a longitudinal study. In vivo and in vitro cell-mediated responses to tuberculin were lower in patients than in controls. Differences were not significant for candidin and streptococcal antigen in vitro, whereas higher responses were observed in the patient group for cytomegalovirus antigen. Following immunization, a subgroup of patients did not have a significantly raised serum antitetanus antibody level, whereas in vitro lymphocyte proliferative responses to tetanus toxoid were lower than in controls. No association was found between these abnormalities and other immunological parameters, including the blood level of CD4+ lymphocytes. Lower responses to most microbial antigens were observed in patients with HIV-1-related symptoms in addition to lymphadenopathy, or the patients who progressed to AIDS in the 2 years following the study. Moreover, intravenous drug users showed higher responses than homosexual patients, possibly because of the influence of previous infections on immunological responses to microbial antigens.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Rat model for human cryptosporidiosis.

Effective treatment for Cryptosporidium infection in immunocompromised patients has yet to be found. We report a rodent model of persistent Cryptosporidium infection. Sprague-Dawley rats were injected subcutaneously twice a week for 8 weeks with 25 mg of hydrocortisone acetate. Fed a regular low-protein diet for 9 weeks, they were challenged once with 10(5) calf Cryptosporidium oocysts 5 weeks after the start of the hydrocortisone acetate regimen. Oocyst shedding was evaluated in feces daily by using a carbolfuchsin-staining method. Rats shed oocysts from days 2 to 9 after ingestion and developed a persistent infection for more than 38 days. Excretion was lower after subsequent parasite challenges, suggesting that a degree of protection developed progressively. The results suggest that this experimental model provides a procedure for screening candidate therapeutic agents.

Animals↗
PubMed1988

[Humoral immunity, 5 years after anti-tetanus vaccination, in a group of malaria-infected and malnourished African children].

In 1978 a campaign of vaccination against tetanus was conducted in a savannah biotope of Burkina Faso (Garango). The effects of 1 or 2 tetanus toxoid injections and of concomitant malnutrition and malaria infection were assessed by measurements of specific antibody and cell-mediated responses. None of these 2 variables did interfere with the development of anti-tetanus immunity. In 1983, 5 years later, similar results were obtained, giving evidence that in spite of malnutrition and malaria, factors known for their immunosuppressive action, a good degree of specific protection was acquired. This local survey revealed also that multiple schemes of vaccination, 1 to 5 injections of vaccine over 5 years, had been performed by unidentified operators. The issues raised by such incongrous, costly and possibly detrimental practices are discussed within the frame of national vaccination policies.

Antibody Formation↗
PubMed1987

Sequential determination of IgG subclasses and IgA specific antibodies in primary and reactivating toxoplasmosis.

During the course of T. gondii infection, we have analysed serum IgG and IgA antibodies responses in 50 immunocompetent with acquired infection and 19 immunocompromised patients with evidence of reactivated toxoplasmosis. Using an ELISA, IgG1, IgG2, IgG3 and IgA antibodies were found in sera of all patients, whereas IgG4 antibodies were usually not detectable. In immunocompetent patients, the predominant antibody isotype was IgG1 at the different stages of infection, presumably in relation with a T-cell control of humoral response during toxoplasmosis. In immunocompromised hosts (kidney or bone marrow transplanted and HIV infected patients), a sequential study was performed on serum samples taken before and after reactivation had occurred. The isotypic distribution of antibodies was similar to that observed in immunocompetent patients, but differences between groups of immunocompromised patients were detected when the kinetics of the antibody response was considered. The IgG and IgA antibody rise was lower in HIV1 infected patients with clinical toxoplasmosis; whatever was the peak antibody value, clinical symptoms appeared earlier in patients with a slower antibody response. This presumably reveals a functional T-cell abnormality, which may rely to the defective containment of the parasite in these patients.

Acquired Immunodeficiency Syndrome↗
PubMed1987

Impaired anti-pneumococcal antibody response in patients with AIDS-related persistent generalized lymphadenopathy.

Pre- and post-immunization serum antibodies to pneumococcal polysaccharides (PPS) and tetanus toxoid (TT) were measured in 25 patients with persistent generalized lymphadenopathy and serum antibodies to the human immunodeficiency virus (HIV). The increase in post-immunization anti-PPS antibodies was lower than 40% in 16/25 patients. Isotype analysis indicated that the IgM, IgA, IgG2, but not the IgG1 antibody responses were lower in patients that in healthy controls, whereas pre-immunization values were similar. For TT, no difference was found between the patients and the healthy group in total and IgG1 antibody response whereas IgG4 response was lower in patients. No significant association was found between the defect in anti-PPS antibody response and associated thrush or constitutional symptoms or other immunological parameters. These findings suggest that defective response to a thymo-independent polysaccharide antigen is a distinctive consequence of HIV infection.

AIDS-Related Complex↗
PubMed1986

Influence of circulating malarial antigens on cell mediated immunity in acute Plasmodium falciparum malaria.

In a group of Thai patients with P. falciparum acute malaria, circulating malarial antigens (CMA) were detected in 27/33 cerebral malaria (CM) cases and 31/43 noncerebral cases. Delayed cutaneous responses to phytohemagglutinin and candidin were found frequently negative in patients with CMA, especially in the CM group. Mean in vitro lymphocyte proliferative responses to lectins were lower in the group of patients with CMA. An inhibitory activity on proliferative responses to phytohemagglutinin of lymphocytes from healthy individuals was exerted by sera containing CMA. Data suggest that CMA from P. falciparum may suppress in vivo and in vitro cell mediated immune reactions.

Acute Disease↗
PubMed1985

Human lymphocyte responses to Plasmodium falciparum merozoite antigens. A functional assay of protective immunity?

Merozoites obtained from cutaneous cultures of Plasmodium falciparum were used as antigen for an in vitro lymphocyte assay. Antigen specific proliferative responses were observed with lymphocytes from individuals with long-standing immunity to P. falciparum. Donors whose last P. falciparum challenge occurred within the year preceding the assay exhibited lymphocyte responses significantly higher than those from donors whose infection was more remote. This suggests that a lymphocyte dependent assay may relate to the protective status of the donor.

Adult↗