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PubMed1993

Multiple defects of immune cell function in mice with disrupted interferon-gamma genes.

Interferon-gamma (IFN-gamma) is a pleiotrophic cytokine with immunomodulatory effects on a variety of immune cells. Mice with a targeted disruption of the IFN-gamma gene were generated. These mice developed normally and were healthy in the absence of pathogens. However, mice deficient in IFN-gamma had impaired production of macrophage antimicrobial products and reduced expression of macrophage major histocompatibility complex class II antigens. IFN-gamma-deficient mice were killed by a sublethal dose of the intracellular pathogen Mycobacterium bovis. Splenocytes exhibited uncontrolled proliferation in response to mitogen and alloantigen. After a mixed lymphocyte reaction, T cell cytolytic activity was enhanced against allogeneic target cells. Resting splenic natural killer cell activity was reduced in IFN-gamma-deficient mice. Thus, IFN-gamma is essential for the function of several cell types of the murine immune system.

Animals↗
PubMed1995

[Development of protective antituberculosis immunity after BCG vaccination in mice with silicon deficiency in water and feed].

An experimental mouse model of normal and deficient content of silicon in the diet in CBA strain has been developed. It is shown that after BCG vaccination silicon deficiency brought about a dramatic decrease of in vitro proliferation of splenic lymphocytes in the presence of mycobacterial antigens, ConA or in the absence of the stimuli. DTH response to tuberculin in silicon deficient mice was also reduced. The level of specific serum IgG did not depend upon silicon content in the diet. The addition of silicon into the diet of silicon-deficient mice beginning from BCG vaccination restored the level of immune reactions.

Animal Feed↗
PubMed1998

Vaccination with activated B cells pulsed with tumor-lysates can induce tumor-specific CD4+ T cells in vivo.

Activated B cells, pulsed with tumor-lysates, were examined for their potential to induce tumor-specific CD4+ T cells in vivo, MH2 cells, which are CD4+ T cells and can also recognize purified protein derivative from mycobacterium tuberculosis (PPD), showed a proliferative response in the presence of both syngeneic activated B cells and PPD in a major histocompatibility complex class II-restricted manner. For B cells to function as efficient antigen presenting cells, they need to be activated. Both irradiation and several inhibitors for antigen-processing were observed to block the antigen-presenting ability of activated B cells. Based in these findings, the possibility of anti-tumor vaccination with activated B cells was thus investigated. The spleen cells from mice, which were immunized with activated B cells pulsed with B16 melanoma-lysates, produced a higher level of interferon (IFN)-gamma than those from mice, which were immunized with either non-pulsed activated B cells or the tumor-lysates alone, after in vitro restimulation. This IFN-gamma production was also dependent on the CD4+ T cells. Moreover, the splenic CD4+ T cells in such mice were suggested to increase their ability to generate B16 melanoma-specific cytotoxic T lymphocytes after in vitro restimulation. Even more importantly, immunization with B16 melanoma lysate-pulsed activated B cells elicited a protective immunity against B16 melanoma at rechallenge. Collectively, these results indicate that an anti-tumor effect could be induced by immunization with activated B cells, pulsed with the tumor-lysates, by eliciting tumor-specific IFN-gamma producing CD4+ T cells in vivo.

Animals↗
PubMed1998

Natural resistance to intracellular parasites: a study by two-dimensional gel electrophoresis coupled with multivariate analysis.

Natural resistance to Mycobacterium bovis bacillus Calmette-Guérin (BCG) is determined by the Bcg gene (Nramp1), which is exclusively expressed by mature macrophages. The Nramp1 gene is a dominant autosomal gene that has two allelic forms; r confers resistance and s confers susceptibility to infection with intracellular pathogen. Although the wide range of pleiotropic immunological effects of the Nramp1 gene has been described, the exact mechanism of its action remains elusive. In this study we searched for differentially expressed proteins that might provide clues in the studies on Nramp1 gene function. We performed two-dimensional gel electrophoresis of cellular proteins prepared from a B10R macrophage line derived from mice carrying the r allele of the Nramp1 gene, B10S macrophages carrying the s allele, and B10R-Rb macrophages transfected with Nramp1-ribozyme. The classification of protein patterns and selection of distinct proteins characteristic of r or s allele-carrying macrophages was performed using the principal component analysis. We found differential expression of four proteins with the following isoelectric point/molecular weight (pI/Mr) in B10R macrophages compared to B10S and B10R-Rb macrophages: 6.6/25, 7.0/22, 9.1/31.5, and 5.3/8.5. The protein 7.0/22 has been identified as Mn-superoxide dismutase and the best candidate for protein p6.6/25 seems to be Bcl-2 according to the immunoblot analysis. When the splenic macrophages carrying the r or s allele were analyzed, the changes in relative abundance for proteins 6.6/25 and p7.0/22 were satisfactorily reproduced. Overall, the two identified proteins are important in the regulation of intracellular redox balance and the regulation of apoptosis in macrophages, respectively. Our findings may suggest their possible biological role in the innate immunity against intracellular pathogens.

Animals↗
PubMed1990

Lung cavities in patients with coeliac disease.

The clinical, radiological and pathological features of 7 patients with coeliac disease (CD) who developed lung abscesses or cavities are described. These patients were seen during a 20-year period during which time approximately 600 coeliacs were seen and 50 died. Six of the coeliac patients with lung abscess died. The patients were middle aged. Staphylococcal infection, Klebsiella pneumoniae, bronchial carcinoma and previous pulmonary tuberculosis accounted for the cavities in 4 patients. In the 3 other patients a definite cause could not be identified. Hyposplenism and malnutrition were common. Next to malignancy pulmonary abscess was the commonest cause of death in the coeliac population. The development of respiratory symptoms should be regarded as a potentially serious and a life-threatening event in the middle-aged coeliac patients. Lung abscess should be added to the list of respiratory diseases associated with coeliac disease.

Adult↗
PubMed1995

In vivo evidence for a non-T cell origin of interleukin-5.

Eosinophil myelopoiesis is to a great extent regulated by interleukin (IL)-5. Analysis of IL-5 mRNA in spleen cell preparations by reverse transcription-polymerase chain reaction (RT-PCR) revealed the presence of message for this cytokine in uninfected severe combined immunodeficiency (SCID) mice. This message was increased following Mycobacterium avium infection. Normal BALB/c mice had higher levels of expression of IL-5 but the expression of this cytokine was reduced during M. avium infection. Anti-IL-5 monoclonal antibody administration in vivo to SCID mice reduced the number of peritoneal and splenic eosinophils. Gamma interferon (IFN-gamma) had an inhibitory effect of eosinophilopoiesis during infection of SCID mice by M. avium since neutralization of this cytokine increased the number of eosinophils detected in the peritoneal cavity of infected animals. Our results suggest that IL-5 may be produced by cells other than T cells that are both able to respond to infection and are under the control of IFN-gamma.

Animals↗
PubMed1982

Peliosis of the spleen. Report of a case and review of the literature.

Peliotic lesions of the liver and spleen are rare and usually occur in patients with wasting diseases, such as tuberculosis and cancer, or in patients who have received treatment with anabolic-androgenic steroids. Peliosis appears grossly as blood-filled, cyst-like or nodular lesions, 1 to 5 mm in diameter, that are distributed throughout the parenchyma of the affected tissue but do not alter the size of the organ. Intraperitoneal rupture of a peliotic bleb can be fatal. Peliosis of the spleen usually occurs in conjunction with peliosis hepatis, but in this subject with myelofibrosis and myeloid metaplasia who underwent autopsy, the lesions were present only in the spleen.

Adolescent↗
PubMed2006

Lymphatic tracing and T cell responses following oral vaccination with live Mycobacterium bovis (BCG).

Oral vaccination of mice with lipid-encapsulated Mycobacterium bovis bacille Calmette-Guérin (BCG) expands a subset of interferon-gamma (IFN-gamma)-secreting T cells and mediates protection against aerosol mycobacterial challenge. We have traced the movement of the live vaccine through the regional lymphatics of mice and monitored the resultant immune response. Six hours after oral vaccination BCG was detected in low numbers systemically and in draining lymphatic tissue. However, after 48 h, BCG was predominantly associated with alimentary tract lymphatic tissues, such as the cervical and mesenteric lymph nodes and Peyer's patches. Lymphocytes that produced IFN-gamma in response to PPD-B or BCG-pulsed dendritic cells predominated in the spleen and were almost exclusively CD4(+), CD44(+) and CD62L(-), thus resembling an effector memory T cell population. Despite the fact that an oral route was used for immunization, splenic IFN-gamma-secreting T cells in vaccinated mice did not express the mucosal homing antigens alpha(4)beta(7) integrin or alphaIEL (CD103). However, a proportion of BCG-specific CD4(+) T cells expressed the CD29 integrin (beta(1)) chain, potentially involved in lung homing function. Thus, oral priming with M. bovis BCG appears to induce a subset of spleen-resident CD4(+) T cells with the potential to provide protective immunity in the lung.

Administration, Oral↗
PubMed2006

[Clinical features and diagnosis of langerhans cell hyperplasia].

BACKGROUND & OBJECTIVE: The incidence rate of langerhans cell hyperplasia (LCH) is increasing. Its clinical manifestation is so diversified that it is easy to be misdiagnosed. This study was to analyze its clinical features for the sake of early diagnosis and treatment. METHODS: Clinical data of 44 LCH patients, treated from Jan. 1990 to Dec. 2003 in the First Affiliated Hospital of Sun Yat-sen University, were retrospectively analyzed. RESULTS: Of the 44 LCH patients, 32 (72.7%) were children, 12 (27.3%) were adults. Of the 32 children patients, 15 (46.9%) were less than 2 years old. The involved organs were bone (20/44, 45.5%), lymph nodes (20/44, 45.5%), skin (16/44, 36.4%), liver and spleen (16/44, 36.4%), lung (14/44, 31.8%), bone marrow (6/44, 13.6%), ear (4/44, 9.1%), eyes (2/44, 4.5%), pituitary gland (2/44, 4.5%), and thymus gland (1/44, 2.3%). Of the 44 patients, 10 had 1 organ involved, 11 had 2 organs involved, 9 had 3 organs involved, 7 had 4 organs involved, 7 had no less than 5 organs involved; 22 children patients and 4 adult patients had multiple organs (liver, lung, bone marrow, and so on) involved; 26 (59.1%) were misdiagnosed as dermatosis (6 cases), hemopathy (7 cases), bone or bone marrow diseases (7 cases), lung tuberculosis (2 cases), diabetes insipidus (2 cases), ear or eye disease (2 cases). Six children patients had bronchopneumonia, and 4 of them had septicemia. Six patients died with 5 cases below the age of 2. CONCLUSIONS: LCH is easy to be misdiagnosed. Children below 2 years old tend to complicate with multiple organ failure (MOF) and bronchopneumonia which have high death rate. Pathology examination is helpful for early diagnosis, treatment, and prevention of severe complications.

Adolescent↗
PubMed2004

Gastrointestinal infection in the immunocompromised (AIDS) patient.

In the past two decades acquired immunodeficiency syndrome (AIDS) has become one of the most devastating illnesses in human history. As the epidemic continues to spread increasingly, AIDS patients are no longer confined to a few specialized AIDS hospitals and are now seen in general hospitals and clinics everywhere. Radiologists need to recognize the appearances, to understand how-safely-to care for patients with this disease, and to know enough about the illness to be able to counsel their patients. This article presents a review of current knowledge about the wide range of gastrointestinal hepatic, splenic, biliary, and retroperitoneal manifestations in AIDS, and how the role of modern medical imaging techniques and diagnosis and treatment can be applied. The imaging aspects (conventional double-contrast gastrointestinal studies, ultrasound, CT, and MR) of the diseases of the luminal gastrointestinal tract, liver, spleen, biliary tract, and retroperitoneum will be systematically discussed. Candidiasis, herpes, cytomegalovirus, cryptosporidiosis, histoplasmosis, isosporiasis, salmonellosis, toxoplasmosis, unusual mycobacteria, and viral infections account for the majority of non-neoplastic disorders.

AIDS-Related Opportunistic Infections↗
PubMed2002

Mycobacterial ESAT-6 protein enhances mouse IFN-gamma responses to Mycoplasma hyopneumoniae P71 protein.

Type 1 immune responses play an important role in the resolution of diseases with infectious or oncogenic etiologies. Vaccines for production animals frequently target humoral immune responses and are often ineffective in protecting against disease. In order to shift the immune response more toward cellular immunity (i.e., type 1 response), we tested the ability of a mycobacterial protein, early secretory antigenic target (ESAT-6), to enhance interferon-gamma (IFN-gamma) secretion during the recall response with a second antigen. The Mycoplasma hyopneumoniae membrane protein P71 was used as a test antigen in murine vaccination studies. The ESAT-6 open reading frame (ORF) was fused to DNA encoding P71 to produce a recombinant protein that was used to immunize BALB/c mice. Control mice immunized with P71 alone demonstrated a splenic response characterized by release of interleukin-10 (IL-10) and a balanced antigen-specific IgG1/IgG2a antibody response. The presence of ESAT-6 as a fusion partner with P71 during immunization, however, resulted in an enhanced P71-specific IFN-gamma response, decreased release of IL-10, and significantly greater (p < 0.05) IgG2a antibody levels in comparison to immunizing with P71 alone. These results demonstrate that ESAT-6 can modify the profile of an immunologic response to an accompanying immunogen.

Adjuvants, Immunologic↗
PubMed1998

Treatment with recombinant granulocyte colony-stimulating factor (Filgrastin) stimulates neutrophils and tissue macrophages and induces an effective non-specific response against Mycobacterium avium in mice.

A role of neutrophils in the host response against Mycobacterium avium (MAC) has recently been suggested. To investigate this matter further, we determined the effect of granulocyte colony-stimulating factor (G-CSF) on the outcome of MAC infection in mice. C57BL/6bg+/bg- black mice were intravenously infected with 1 x 10(7) MAC and then divided into four experimental groups to receive G-CSF as follows: (i) 10 micrograms/kg/day; (ii) 50 micrograms/kg/day; (iii) 100 micrograms/kg/day; (iv) placebo control. Mice were killed at 2 and 4 weeks of treatment to determine the bacterial load of liver and spleen. Treatment with G-CSF at both 10 and 50 micrograms/kg/day doses significantly decreased the number of viable bacteria in liver and spleen after 2 weeks (approximately 70.5% and 69.0%, respectively), and after 4 weeks (approximately 53% and 52%, respectively, P < 0.05 compared with placebo control). Treatment with 100 micrograms/kg/day did not result in decrease of bacterial colony-forming units in the liver and spleen after 4 weeks. Administration of G-CSF induced interleukin-10 (IL-10) and IL-12 production by splenocytes. To examine if the protective effect of G-CSF was accompanied by the activation of phagocytic cells, blood neutrophils and splenic macrophages were purified from mice receiving G-CSF and their ability to kill MAC was examined ex vivo. Neutrophils and macrophages from G-CSF-treated mice were able to inhibit the growth of or to kill MAC ex vivo, while phagocytic cells from untreated control mice had no anti-MAC effect. These results suggest that activation of neutrophils appears to induce an effective non-specific host defence against MAC, and further studies should aim for better understanding of the mechanisms of protection.

Animals↗
PubMed2004

Dietary soy phytoestrogens and ERalpha signalling modulate interferon gamma production in response to bacterial infection.

Diets rich in soy phytoestrogens have many potential health benefits but isoflavones such as genistein may suppress cell mediated immune function. The effect of dietary phytoestrogens on the host response to infection has not been extensively examined. Mice were fed a diet containing soy phytoestrogens and infected with Mycobacterium avium to establish a chronic infection and inflammatory response. As phytoestrogens may act through classical oestrogen receptors (ER), mice deficient in ERalpha signalling and wild type mice were evaluated for a panel of Type 1-associated cytokines (IFNgamma, IL-12 and IL-18) in the spleen. IFNgamma production in the spleen was increased approximately 4-fold in ERalpha-deficient mice fed a casein-based diet over wild type mice fed a casein-based diet (P < 0.05), suggesting a role for ERalpha in suppressing IFNgamma production. IL-18 levels in spleens of wild type mice were decreased compared to ERalpha-deficient mice on a casein diet. Splenic IL-12 and IL-18 levels were not affected in wild type and ERalpha-deficient mice on the phytoestrogen containing diets, with the exception that whole soy increased IL-12 levels in the tissues of ERalpha deficient mice. We conclude that ERalpha and dietary phytoestrogens can influence production of key regulatory cytokines in response to chronic bacterial infection.

Animals↗
PubMed1995

Production of TNF-alpha, IL-6 and TGF-beta, and expression of receptors for TNF-alpha and IL-6, during murine Mycobacterium avium infection.

The Mycobacterium avium complex comprises intracellular bacteria associated with disseminated infection in patients with acquired immune deficiency syndrome (AIDS). Immune defects that lead to infection are unknown but cytokines appear to play an important role in the immunomodulation of host defence mechanisms. We evaluated the cytokine profiles seen temporally after murine M. avium infection. Spleen cells were obtained from M. avium-infected C57BL/6 mice and uninfected mice at weeks 1, 2, 3, 4 and 5. Cells were cultured in vitro and subsequently pulsed with killed M. avium. Supernatants were collected from the cultured splenic cells and the concentrations of interleukin-6 (IL-6), transforming growth factor-beta 1 (TGF-beta 1) and tumour necrosis factor-alpha (TNF-alpha) were measured. TGF-beta 1 was detected at week 1, followed by IL-6 production at week 2. Elevated TNF-alpha levels were observed at week 3. The addition of polyclonal anti-TGF-beta 1 antibody to M. avium-infected peritoneal macrophages in the presence of splenic cell supernatants from weeks 1, 3 and 5 led to decreased bacterial counts compared to controls. Anti-IL-6 antibody did not have any effect on macrophage anti-mycobacterial activity. Concurrently, we observed decreased expression of TNF-alpha receptors on infected macrophages. We propose that the early elevated levels of TGF-beta 1, a known suppressor of macrophage function, in conjunction with down-regulation of TNF-alpha receptors may help explain the suboptimal macrophage response to TNF-alpha, leading to impaired anti-mycobacterial activity.

Animals↗
PubMed1984

In vivo and in vitro administration of interleukin 2-containing preparation reverses T-cell unresponsiveness in Mycobacterium bovis BCG-infected mice.

Mice infected with high doses of Mycobacterium bovis BCG (3 X 10(7)) showed a marked impairment of delayed-type hypersensitivity to PPD in vivo, and their splenic T cells failed to proliferate when cultured in vitro with concanavalin A or PPD. However, this state of unresponsiveness could be reversed both in vitro and in vivo by the administration of an interleukin 2 (IL-2)-containing preparation. IL-2 produced spontaneously by the gibbon lymphosarcoma T-cell line MLA-144 and T-cell-conditioned medium from a mixed lymphocyte reaction were able to increase DNA synthesis of splenic T lymphocytes from BCG-immunosuppressed mice cultured with concanavalin A or PPD. Furthermore, BCG-infected mice treated in vivo with at least 100 U of IL-2 showed a positive skin reaction to PPD, and their spleen cells were fully responsive in vitro. The reversal of BCG-induced immunosuppression was not observed when infected mice were injected with IL-2 preparations previously incubated with blast cells, a procedure known to remove IL-2 activity. These results indicate that the basis of BCG-induced unresponsiveness is a deficiency in the production of IL-2 rather than a lack of reactive T cells.

Animals↗
PubMed1988

Induction by an immunogenic immunomodulating agent of nonspecific T cell suppression of lymphocyte responsiveness in MLR but not of antibody production.

Spleen cells derived from BALB/c mice that had been repeatedly immunized with the methanol extraction residue (MER) fraction of tubercle bacilli exhibited a depressed capacity to act as responder cells in allogeneic and syngeneic mixed lymphocyte reactions (MLR). Previously reported studies revealed that such spleen cells are also defective in the in vitro generation of antibodies. In order to determine the nature of the cells responsible for the depressed MLR reactivity, purified populations of splenic macrophages, B lymphocytes, T lymphocytes originating from normal and from MER-immunized mice, and cell culture supernatants were added to MLR mixtures consisting of normal mouse splenocytes. Macrophages originating from MER-immunized mice and their culture supernatants exerted a significantly higher suppressive effect on MLR than that of corresponding preparations from normal mice. Splenic T cells originating from MER-immunized mice and their supernatants also significantly suppressed the MLR response. However, the same T cell populations that were inhibitory in MLR failed to suppress the in vitro generation of antibodies against sheep red blood cells in the presence of either MER or 2-mercaptoethanol. These and previously reported findings indicate that a nonspecific immunomodulating agent, MER, can, under certain conditions of treatment, elicit the induction of nonspecific suppressor T cells for MLR but not for antibody production, and, accordingly, can inhibit cellular and humoral immunological responsiveness by different mechanisms.

Adjuvants, Immunologic↗
PubMed1989

Mechanisms of recrudescence of Mycobacterium bovis BCG infection in mice.

The capacity of various immunosuppressive agents to cause a recrudescence of the replication of Mycobacterium bovis BCG in the spleens of chronically infected mice was investigated. The actions of three corticosteroid preparations, cyclosporin A, and anti-T-cell subset monoclonal antibodies were compared. Treatment of mice with hydrocortisone acetate, which depressed the number of splenic lymphocytes and suppressed T-cell responses, most effectively exacerbated the stationary BCG counts, at 4 to 6 months after infection. The magnitude of reactivation was more pronounced in innately resistant CBA/Ca mice than in the susceptible C57BL/6 strain of mice. Splenic bacterial counts were also amplified by anti-L3T4 antibody when the antibody was injected at the chronic phase, whereas cyclosporin A had an effect only during the initial 6 weeks after BCG infection. Cultures of spleen cells from chronically infected mice showed a significant increase in the numbers of viable BCG recovered after 7 days of incubation in the presence of dexamethasone but not with cyclosporin A. The observed differences between the tested immunosuppressive agents indicate that the stationary bacterial counts during chronic BCG infection are maintained by discrete T-cell actions on the infected macrophages.

Animals↗
PubMed1995

Cytokine-mediated activation of macrophages from Mycobacterium bovis BCG-resistant and -susceptible mice: differential effects of corticosterone on antimycobacterial activity and expression of the Bcg gene (Candidate Nramp).

Previous work in our laboratory has shown that corticosterone increases the susceptibility of macrophages from Bcgs mice to the growth of Mycobacterium avium. The innate antimycobacterial activity of macrophages from Bcgr mice was not affected by corticosterone. In contrast to the differential effect of corticosterone on the antimycobacterial activity of the macrophages, corticosterone suppressed the production of tumor necrosis factor alpha and nitric oxide by macrophages from both Bcgr and Bcgs mice. The purpose of this investigation was to compare the effects of corticosterone on the antimycobacterial activity of macrophages from Bcgr and Bcgs mice that have been activated in vitro with recombinant gamma interferon or granulocyte-macrophage colony-stimulating factor. We found that macrophages from both strains of congenic mice responded equally to the activation stimuli. The capacity of the activated macrophages from Bcgs mice to suppress the growth of M. avium was inhibited by the addition of corticosterone to the cultures. The addition of NG-monomethyl-L-arginine to the cultures did not affect the capacity of resident splenic macrophages from Bcgr mice to limit the growth of M. avium. However, NG-monomethyl-L-arginine reduced the capacity of gamma interferon-activated, but not granulocyte-macrophage colony-stimulating factor-activated, macrophages to limit the growth of M. avium by macrophages from both Bcgr and Bcgs mice. The addition of corticosterone suppressed Nramp expression by macrophages from Bcgs mice. Nramp expression by macrophages from Bcgr mice was not affected by corticosterone.

Animals↗