Biomedical subjects

M Denis

Publications and source records attributed to M Denis.

At least 73 records · Page 4Linked to original sources

PubMed1994

H blood group antigen carried by CD44V modulates tumorigenicity of rat colon carcinoma cells.

Expression of carbohydrate ABH blood group antigens is oncodevelopmentally regulated and their presence on tumor cells constitutes a prognostic factor. However, it is not clear whether they directly affect tumor behavior. Using a rat model of colon carcinoma, we previously observed an association between the presence of H blood group antigens and tumorigenicity in syngeneic animals. In the present study, we show by immunoprecipitation experiments that cell surface H blood group antigens of a highly tumorigenic clone (PROb) are essentially carried by splice variants of the CD44 molecule containing exon V6. PROb cells were then transfected with an antisense fragment of the gene coding for a rat alpha (1-2)fucosyltransferase. This enzyme allows synthesis of H antigens from various beta-galactoside precursors. Transfected subclones of PROb cells were obtained which had significantly decreased enzymatic activity and H antigenic cell surface levels. In contrast, no such changes were observed in control cells transfected with either the empty vector or with a sense fragment of the gene. Compared to controls, the antisense-transfected cells were far less tumorigenic in syngeneic animals. These results show that H blood group antigens at the surface of PROb colon carcinoma cells contribute to tumor progression. The presence of the fucosylated structures on CD44 could modulate the functions of this adhesion molecule.

ABO Blood-Group System↗

PubMed1994

Tat protein from HIV-1 binds to Mycobacterium avium via a bacterial integrin. Effects on extracellular and intracellular growth.

We examined the interaction between HIV-1 Tat protein and the opportunistic pathogen Mycobacterium avium. AIDS-associated strains of M. avium were shown to bind Tat protein quite avidly in an attachment assay. The attachment of M. avium to Tat was shown to occur via the integrin alpha 5 beta 1 present on the mycobacterial cell surface. M. avium strains were shown to bind the viral Tat protein with high affinity in a specific fashion (600 binding sites with a Kd of 1 to 5 nM). M. avium coated with Tat protein were shown to be more infective for human alveolar macrophages than untreated M. avium. Other HIV-1 Ags had no such effects (e.g., p24, p17). Examination of the cytokine profile of infected macrophages showed that M. avium-Tat complexes induced higher levels of TGF beta-1 (TGF beta 1) than M. avium alone or M. avium that had been in contact with other viral proteins. Conditioned media from HIV-1-infected H9 cells released a factor that enhanced M. avium intramacrophage growth, and was partially neutralized by an anti-Tat Ab. Finally, Tat protein (purified or present in conditioned media from infected cells) moderately enhanced the growth of M. avium strains in extracellular media, and exposure of M. avium to Tat protein in the presence of IL-6 enhanced the growth of AIDS-associated strains. These data argue for an interaction between the Tat viral product and the opportunistic pathogen M. avium which may contribute to the exquisite susceptibility of AIDS subjects to this pathogen.

AIDS-Related Opportunistic Infections↗

PubMed1994

Human monocytes/macrophages: NO or no NO?

The production of nitric oxide (NO) and other reactive nitrogen intermediates by cytokine-activated rodent cells is an important component of antimicrobial and/or antineoplastic activity of these cells. This pathway involves the oxidation of arginine to citrulline, with the concomitant release of NO by an inducible form of NO synthase (iNOS). Numerous cell types express iNOS after stimulation with bacterial products and/or cytokines. The role of NO and its derivatives in host resistance is a subject of intense investigation in mouse models of infections or neoplasia. Although human cells such as hepatocytes and endothelial cells have been shown to express an inducible NO synthase, the presence of such a pathway in human monocytes/macrophages has been questioned by many investigators and is a subject of great controversy. In this short review, we discuss some salient points of this debate.

Animals↗

PubMed1994

Interleukin-12 (IL-12) augments cytolytic activity of natural killer cells toward Mycobacterium tuberculosis-infected human monocytes.

We tested the impact of interleukin-12 (IL-12) and of cytotoxic leukocytes (particularly natural killer (NK) cells) from normal and HIV-1-infected subjects on lysis of human monocytes infected with Mycobacterium tuberculosis. Nylon wool nonadherent cells stimulated with interleukin-2 (IL-2) or with IL-12 developed significant killing activity against infected monocytes, with IL-12 being a superior stimulant on a molar basis. Cells of the CD16+ phenotype mediated most of the cytotoxicity against infected monocytes and this lytic activity was associated with a significant decrease in mycobacterial numbers. When peripheral blood mononuclear cells (PBMC) from HIV-1-infected subjects were examined, it was also found that IL-12 very significantly increased lytic activity against M. tuberculosis-infected cells. Moreover, purified NK cells from normal volunteers or from HIV-1-infected subjects were shown to have elevated lytic activity against M. tuberculosis-infected monocytes after IL-2 or IL-12 stimulation. These data suggest an important involvement of NK cells and their activating stimuli (particularly IL-12) in host resistance to tuberculosis.

AIDS-Related Opportunistic Infections↗

PubMed1994

Interleukin-1 (IL-1) is an important cytokine in granulomatous alveolitis.

We examined the role of interleukin-1 (IL-1) in promoting an immune-induced lung fibrotic response in a mouse model of granulomatous alveolitis caused by exposure to heat-killed bacillus Calmette-Guérin. Instillation of the material induced an elevated production of IL-1 in the lungs of challenged mice. Lung homogenates from challenged mice contained high levels of antigenic IL-1, and alveolar macrophages from challenged mice released elevated levels of IL-1. Treatment of mice with a specific monoclonal antibody directed against type-1 IL-1 receptor quite significantly reduced the initial influx of cells, especially neutrophils into the bronchoalveolar lavage. Type-1 IL-1 receptor blockade did not directly alter the levels of tumor necrosis factor alpha in the lung homogenates, but it did lead to an interleukin-6 superinduction in the lungs. IL-1 receptor blockade quite significantly diminished lung tissue damage and granuloma formation, judging from morphometric index and lung hydroxyproline measurements. This diminished tissue damage was also evident on tissue sections stained with Masson's trichrome, as seen by fewer granulomas and less collagen deposition. These data suggest that IL-1 plays an important role in determining a lung granulomatous response.

Alveolitis, Extrinsic Allergic↗

PubMed1994

Release of monokines by pulmonary macrophages following antigen challenge in sensitized guinea pigs.

Guinea pigs were passively sensitized with immune serum to ovalbumin (OA), control serum, or saline. Twenty-four hours later, they inhaled aerosols of OA (2% in saline), saline, or lipopolysaccharide (LPS). Following anesthesia, bronchoalveolar lavage (BAL) was performed at 30, 60, 90 and 120 min postinhalation. Alveolar macrophages (AM) were isolated from the BAL fluid and incubated (18 h) in medium alone or with zymosan (1 mg/ml). Supernatants were collected and levels of interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) determined by bioassays. Unstimulated AM from animals that inhaled OA, saline, or LPS secreted similar amounts of IL-1 at 30, 60, and 90 min postinhalation. Zymosan (1 mg/ml) significantly increased IL-1 secretion by AM collected at 60 and 90 min from OA-sensitized animals that inhaled OA or saline. AM from guinea pigs sensitized to OA that inhaled OA or LPS secreted significantly increased amounts of IL-6 at 30, 60, 90, and 120 min postchallenge compared to saline sensitized controls. In all groups, AM from LPS-treated animals secreted large amounts of TNF-alpha at all sampling times postchallenge; AM from OA-sensitized and challenged animals secreted increasing amounts of TNF-alpha with time postchallenge, spontaneously and in response to zymosan. By contrast, AM from saline sensitized and challenged guinea pigs did not release detectable amounts of TNF-alpha spontaneously and secreted very low amounts in the presence of zymosan. These findings show that antigen challenge results in a rapid activation of AM isolated from BAL and suggest AM may initiate the development of inflammatory processes associated with antigen challenge.

Administration, Inhalation↗

PubMed1994

Quantitative assessment of the specific CD4+ T lymphocyte proliferative response in bovine herpesvirus 1 immune cattle.

We quantified the CD4+ T cell proliferation specific for bovine herpesvirus 1 (BHV-1) in peripheral blood mononuclear cells from cattle. The stimulation index as detected in proliferative assays performed in the presence of BHV-1 antigen is highly variable in immune cattle. By using proliferative assays performed after negative selection we showed that, as expected, CD4+ T cells were the limiting cell type for antigen-induced proliferation. Neither B, gamma delta T nor CD8+ cells seemed to be involved. The limiting dilution method was established to obtain quantitative estimations, namely frequencies of specific T cells. When limiting dilution cultures were supplemented with interleukin-2 (IL-2), an IL-2 induced unspecific cell proliferation masked the specific T cell proliferation. Natural killer cells were not the major cell type involved, but CD4+ lymphocytes themselves seemed to respond to IL-2 irrespective of the presence of antigen. When cultures were performed without addition of IL-2, the frequency of BHV-1 specific proliferative T cells could be obtained by the difference between the frequency of proliferating cells calculated in the presence and absence of antigen. The method provides a sensitive and quantitative means to measure the T cell immune response to BHV-1 vaccine candidates.

Animals↗

PubMed1994

Dysregulation of interleukin 8, interleukin 10, and interleukin 12 release by alveolar macrophages from HIV type 1-infected subjects.

We examined the in vitro release of interleukin 8 (IL-8), interleukin 10 (IL-10), and interleukin 12 (IL-12) by alveolar macrophages from normal volunteers and HIV-1-infected subjects. Normal volunteers had very low levels of IL-8 and IL-10 and undetectable IL-12 in the cell-free bronchoalveolar lavage fluid (BALF). Asymptomatic HIV-1-infected subjects had elevated levels of IL-8 and IL-10 in their BALF, and HIV-1-infected subjects with nonspecific interstitial pneumonitis (NIP) or infected with Pneumocystis carinii had the highest BALF levels of IL-10 and IL-8. It was found that alveolar macrophages from asymptomatic HIV-1 subjects and from NIP subjects spontaneously released elevated IL-8, IL-10, and IL-12. However, AIDS subjects infected with P. carinii had cells that released elevated levels of IL-10 and IL-8, but low levels of IL-12. When alveolar macrophages were stimulated with Staphylococcus aureus Cowan (SAC), cells from normal volunteers responded with a considerably increased release of IL-8, IL-10, and IL-12; cells from HIV-1-infected subjects without P. carinii infection responded with a moderate increase in release of all three monokines. SAC stimulation did not enhance the release of monokines by cells from AIDS subjects with P. carinii infection, and IL-12 levels remained low. There was no strict relationship between spontaneous cytokine release and p24 HIV-1 antigen expression by alveolar macrophages. Finally, we showed that neutralizing IL-10 production by alveolar macrophages from AIDS subjects substantially increased IL-12 releasability.(ABSTRACT TRUNCATED AT 250 WORDS)

Acquired Immunodeficiency Syndrome↗

PubMed1994

Interleukin 13 and interleukin 4 protect bronchoalveolar macrophages from productive infection with human immunodeficiency virus type 1.

In this study, we examined the impact of the predominantly Th2-type lymphokines interleukin 13 (IL-13) and interleukin 4 (IL-4) on acute infection of human bronchoalveolar macrophages with a macrophage-tropic isolate of human immunodeficiency virus type 1 (HIV-1). Addition of 0.01-10 ng of IL-4 or IL-13 per milliliters significantly blocked HIV-1 replication in infected cells, judging from levels of reverse transcriptase and p24 antigen in the supernatants of infected cells. Both IL-4 and IL-13 were almost as efficient as interferon-gamma (IFN-gamma) in preventing HIV-1 replication, when given in equivalent amounts. Moreover, neither IL-13 nor IL-4 interfered with the IFN-gamma-mediated enhancement of anti-HIV-1 activity in alveolar macrophages. Both IL-4 and IL-13 interfered with enhanced replication of HIV-1 in macrophages pulsed with the growth factor granulocyte-macrophage colony-stimulating factor (GM-CSF). Interleukin 13 also prevented HIV-1 release from peripheral blood mononuclear cells in a cocultivation experiment with feeder cells from a seronegative subject. These data suggest that Th2-derived lymphokines have significant anti-HIV-1 activity in cells of the macrophage lineage, although they may enhance the susceptibility of HIV-1-infected subjects to some opportunistic pathogens.

Adult↗

PubMed1994

Prevention of acute rejection episodes with an anti-interleukin 2 receptor monoclonal antibody. I. Results after combined pancreas and kidney transplantation.

A prospective, randomized trial was conducted to evaluate the short-term and long-term effects of induction immunosuppression with the rat IgG 2a monoclonal antibody 33B3.1, directed against the human alpha chain of the interleukin 2-receptor, following primary, cadaveric, combined pancreas and kidney transplantation. Forty patients were randomly assigned to receive 10 mg/day of 33B3.1 (n = 20) or 1.5 mg/kg/day of rabbit antithymocyte globulin (n = 20) for the first 10 postoperative days. Azathioprine, low-dose corticosteroids, and cyclosporine were given in association with either 33B3.1 or ATG. All 40 patients received the entire 10-day bioreagent course and no episode of rejection was observed during this period. Although the incidence of rejection did not significantly differ within the first, second, and third postoperative months (ten 33B3.1 and 6 ATG patients experienced, respectively, 10 and 6 rejection episodes within the first 3 months), the total number of 33B3.1 patients experiencing rejection throughout the follow-up was significantly higher than that of ATG (13 versus 6; P < 0.02). Immunological graft failure accounted for 2 pancreas and 2 kidney losses in the 33B3.1 group versus 1 in the ATG one (P = ns). The total number of infectious episodes was similar in both groups (21 versus 23). Two malignancies were observed in the ATG group (1 responsible for patient's death). One 33B3.1 patient died because of infectious pneumonia and 3 ATG patients died because of 2 cardiovascular diseases and 1 cancer. All patients had functioning grafts at the time of death. The 3-month and 36-month patient, pancreas, and kidney actuarial survival rates were, respectively, 100, 65, and 100%, and 95, 50, and 82% in the 33B3.1 group and 95, 80, and 90%, and 80, 70, and 80% in the ATG one (P = ns). These data suggest that, although a significantly higher rejection episode incidence was observed in patients treated with 33B3.1 monoclonal antibody as compared with ATG, similar long-term results can be obtained following primary cadaveric combined pancreas/kidney transplantation.

Acute Disease↗

PubMed1994

Prevention of acute rejection episodes with an anti-interleukin 2 receptor monoclonal antibody. II. Results after a second kidney transplantation.

The focus of progress in transplantation immunosuppression is to achieve more specific immunosuppression with monoclonal antibodies. We have already shown that the efficacy of 33B3.1, a rat monoclonal Ig2A directed against the human IL-2 receptor, was similar to that of rabbit antithymocyte globulin in the prevention of acute rejection in first kidney transplants. A similar comparative analysis has been made in 40-sec renal transplants. ATG (1 mg/kg/day) or 33B3.1 (10 mg/day) was administered during the first 10 days postgrafting in association with corticosteroids and azathioprine. Cyclosporine was introduced on day 9 and azathioprine/CsA constituted the patient's maintenance treatment after day 45. Rejection treatment consisted of equine antilymphocyte globulin in both cases and of steroid boluses when patients were under Cyclosporine. One patient in each group died. Graft survival was 90%, 85%, and 79% in the ATG group (n = 20) and 100%, 89%, and 89% in the 33B3.1 group (n = 20) at 3, 12, and 24 months, respectively. Of the ATG group patients, 45% and 40% in the 33B3.1 group had at least one rejection episode, half the episodes in the MoAb cohort occurring under 33B3.1, vs. none in the ATG group. Transplant function was similar in both groups. Viral infections appeared to be more frequent with ATG (60%) than with 33B3.1 (12%), with CMV accounting for half of these in the ATG group, and none in the MoAb group. Tolerance of both agents was good. Of the 33B3.1 recipients, 70% developed anti-33B3.1 antibodies. From these data, we conclude that this anti-IL-2 receptor MoAb seems less effective than rabbit ATG as induction treatment in second kidney transplant patients.

Acute Disease↗

PubMed1994

Alveolar macrophages from subjects infected with HIV-1 express macrophage inflammatory protein-1 alpha (MIP-1 alpha): contribution to the CD8+ alveolitis.

We examined the synthesis and release of MIP-1 alpha in alveolar macrophages obtained from normal subjects or subjects infected with HIV-1, at different stages of the disease. HIV-1-infected subjects in groups II, III and IV all had significant interstitial pneumonitis, featuring a significant infiltration of CD8+ lymphocytes in the bronchoalveolar lavage. Alveolar macrophages from HIV-1-infected subjects were shown to express significant levels of MIP-1 alpha via immunohistochemistry, both spontaneously and in response to lipopolysaccharide (LPS), whereas cells from normal subjects expressed very low levels of the cytokine. Supernatants of alveolar macrophages from HIV-1-infected subjects exerted strong chemotactic activity for purified activated blood CD8+ T lymphocytes, which was strongly inhibited by neutralizing MIP-1 alpha. Studies of patients with HIV-1 infection at different stages of the disease showed that MIP-1 alpha secretion increased as viral infection developed. There was a significant positive correlation between MIP-1 alpha secretion and the CD8+ alveolitis in HIV-1-infected subjects. Infection of alveolar macrophages in vitro with three distinct strains of HIV-1 which replicated profusely in macrophages did not induce the expression of MIP-1 alpha. Collectively, these data suggest that HIV-1 infection in vivo induces MIP-1 alpha expression and release in alveolar macrophages, and this appears to contribute significantly to the alveolar lymphocytosis seen in HIV-1-infected subjects.

Adult↗

PubMed1994

Mycobacterium avium infection in HIV-1-infected subjects increases monokine secretion and is associated with enhanced viral load and diminished immune response to viral antigens.

The complex interaction between HIV-1 infection and Mycobacterium avium was studied. Viral burden was assessed, as well as immune response to HIV-1 in the context of Myco. avium infections. We also examined serum cytokine levels and cytokine release by blood mononuclear cells in HIV-1-infected subjects, infected or not with Myco. avium. Undetectable serum levels of IL-1, tumour necrosis factor-alpha (TNF-alpha) and IL-6 were found in normal controls and in groups I, II and III of HIV-1-infected subjects. Moderate levels of TNF-alpha, IL-1 and IL-6 were found in the sera of group IV patients. When group IV was subdivided into subjects with and without Myco. avium infections, subjects with Myco, avium infections were shown to have higher serum levels of TNF-alpha, IL-1 beta and IL-6 than those with other infections. Blood mononuclear cells from controls and HIV subjects were stimulated with bacterial lipopolysaccharide, and cytokine levels assessed. Cells from group II patients were shown to secrete normal levels of TNF-alpha and IL-6, and lower levels of IL-1 beta; group III subjects released higher levels of IL-6. Patients in group IV had blood cells that released elevated levels of IL-6 and TNF-alpha, and lower levels of IL-1 beta. Group IV subjects with Myco. avium infections had blood cells that released higher levels of TNF-alpha, IL-6 and IL-1 than group IV subjects with other infections. Assessment of viral burden in cells of HIV-1-infected subjects revealed that Myco. avium-infected subjects had a higher level of virus burden and a lower level of lymphoproliferative response to an inactivated gp120-depleted HIV-1 antigen than AIDS subjects with other infections. These data suggest that Myco. avium infections in HIV-1-infected subjects hasten the progression of viral disease, enhance cytokine release and contribute to the anergy to viral antigens.

AIDS-Related Opportunistic Infections↗

PubMed1994

Envelope glycoprotein (gp120) from HIV-1 enhances Mycobacterium avium growth in human bronchoalveolar macrophages; an effect mediated by enhanced prostaglandin synthesis.

Human bronchoalveolar lavage (BAL) macrophages were obtained from normal human volunteers and infected with an AIDS-associated strain of Mycobacterium avium. Infected cells were exposed to purified envelope glycoprotein (gp120) from HIV-1 or to the recombinant non-glycosylated gp120 fragments PBI-RF and PBI-IIIB. Native gp120 increased Myco. avium growth in human cells from six separate donors, whereas the non-glycosylated fragments of gp120 had no such effect. Moreover, gp120 induced a substantial secretion of prostaglandin E2 (PGE2) from macrophages; inclusion of indomethacin blocked the enhanced permissiveness of infected cells treated with gp120. Soluble CD4 also neutralized the effect of gp120. Overall, these results indicate a role for gp120 in the susceptibility of AIDS patients to Myco. avium infections, mediated by an enhanced PGE2 release.

Bronchoalveolar Lavage Fluid↗

PubMed1994

Experimental allergic bronchopulmonary aspergillosis in the mouse: immunological and histological features.

C57BL/6 mice treated with intranasal instillation of 100 micrograms of Aspergillus antigen three times a week developed a pulmonary eosinophilia, observed in the bronchoalveolar lavage (BAL) and on histopathological examination. At week 3, the instillation of Aspergillus antigen provoked a 10-fold increase in the BAL cell number and eosinophils were the predominant inflammatory cells (66.4%). Histopathological findings showed focal alveolar lesions with peribronchial and perivascular infiltration of lymphoid cells, numerous eosinophils, epithelioid cells, and granulomas with giant cells. Increases in total IgE and IgG1 levels in BAL fluid (33-fold and 14-fold) and serum (67-fold and 8-fold) were observed also (P < 0.05). IgG1 specific to Aspergillus fumigatus (Af) was detected only in the antigen-treated mice. At 12 weeks, there was a persistent but less intense eosinophilia both in BAL and on histopathological examination accompanied by steadily elevated total IgE and total IgG1 and a higher level of specific IgG1-Af in BAL fluids and sera. No bronchocentric granulomatosis, mucoid impaction nor bronchiectasis could be observed. Data from the study described here showed that in mice repeated exposure to Aspergillus antigen leads to a strong inflammatory pulmonary response, characterized by remarkable pulmonary eosinophilia and elevations of total IgE, total IgG1 and specific IgG1-Af in both BAL and serum, which are the hallmarks of human allergic bronchopulmonary aspergillosis also. However, this inflammation did not induce the chronic histological features of the human disease.

Animals↗

PubMed1994

Interleukin-1 is involved in mouse resistance to Mycobacterium avium.

In this study, we examined the contribution of the monokine interleukin-1 (IL-1) in mouse resistance to the intracellular pathogen Mycobacterium avium. The effect of neutralizing endogenous IL-1 in mouse macrophage resistance to M. avium infection was investigated. Infection of mouse peritoneal macrophages with M. avium B101 was shown to result in significant IL-1 beta release by cells at 4 and 7 days postinfection. Addition of IL-1 receptor antagonist (IL-1ra) at doses of 5 micrograms daily, which neutralized endogenous IL-1, failed to significantly modify the intracellular growth of M. avium. Mice were injected with M. avium B101 by the intravenous route, and the growth of the mycobacteria was monitored in the organs of intact mice and in those of mice that received repeated high doses of IL-1ra. The infection with M. avium elicited the production of large amounts of IL-1 in the lungs, livers, and spleens. Repeated injections of IL-1ra into M. avium-infected mice resulted in moderately enhanced growth of the bacilli in the livers and spleens but in much enhanced growth in the lungs. The enhanced growth of M. avium in the lungs correlated with a diminished inflammatory influx of cells (particularly neutrophils) in the bronchoalveolar space. These data argue for a role for IL-1 in host resistance to M. avium infections.

Animals↗

PubMed1994

Usefulness of PCR for detection of Pneumocystis carinii DNA.

Diagnosis of Pneumocystis carinii pneumonia is based on the identification of the various stages of the parasite in lung samples by standard staining techniques. We therefore assessed the value of the PCR for detection of P. carinii in bronchoalveolar lavage, induced sputum, and blood samples relative to that of standard staining techniques.

AIDS-Related Opportunistic Infections↗

PubMed1994

Results of chemotherapy in 30 AIDS patients with symptomatic pulmonary Kaposi's sarcoma.

BACKGROUND: The aim of this study was to report the effects of a three-drug chemotherapy regimen in patients with symptomatic AIDS-related pulmonary Kaposi's sarcoma and to analyse prognostic factors for survival. METHODS: Thirty consecutive HIV seropositive patients with respiratory symptoms and proven pulmonary Kaposi's sarcoma were treated with the same therapeutic regimen comprising adriamycin (30 mg/m2), bleomycin (10 mg/m2), and vincristine (2 mg) administered intravenously once every four weeks. RESULTS: Two patients died during the first course of chemotherapy. In the other 28 cases dyspnoea improved and Pao2 rose despite minimal (n = 17) or no (n = 11) improvement in the chest radiographic appearance. The median survival from the beginning of chemotherapy was 6.5 months. Poor prognostic factors for survival were: (1) absence of cutaneous Kaposi's sarcoma; (2) previous opportunistic infection; (3) CD4 cell count < 100/microliters; (4) leucocytes < 3500/microliters; (5) haemoglobin < 10 g/dl; and (6) absence of radiological response. Of the 28 patients 24 experienced at least one episode of neutropenia which was associated with bacterial infection in 16 cases. CONCLUSIONS: Chemotherapy may improve respiratory impairment in patients with extensive pulmonary Kaposi's sarcoma but the outcome remains poor. The efficacy of chemotherapy may be limited by neutropenia.

Acquired Immunodeficiency Syndrome↗