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At least 595 records · Page 33Linked to original sources
PubMed1994

Activity of levofloxacin in a murine model of tuberculosis.

The activity of levofloxacin (LEV) was evaluated in a murine model of tuberculosis. Approximately 10(7) viable Mycobacterium tuberculosis ATCC 35801 were given intravenously to 4-week-old female outbred mice. In a dose-response study, treatment with LEV at 100, 200, and 400 mg/kg of body weight was started 1 day after infection and was given daily for 28 days. Viable cell counts were determined from homogenates of spleens and lungs. A dose-related reduction in organism cell counts in organs was noted for LEV. The activities of LEV at 100, 200, and 300 mg/kg were compared with those of first-line antituberculosis agents. Both isoniazid and rifampin were more active than LEV. There was no difference in activity between LEV and either ethambutol or pyrazinamide against splenic organisms. The activities of ethambutol and LEV at the two higher doses were comparable against lung organisms. LEV at 300 mg/kg was more active than pyrazinamide against lung organisms. The activity of LEV was compared with those of two other quinolones, ofloxacin and sparfloxacin. LEV at 200 mg/kg had more than twofold greater activity than ofloxacin at the same dose. Sparfloxacin at 100 mg/kg was more active than LEV at 200 mg/kg; however, the activities of sparfloxacin at 50 mg/kg and LEV at 200 mg/kg were comparable. The promising activity of LEV in M. tuberculosis-infected mice suggests that it is a good candidate for clinical development as a new antituberculosis agent.

Animals↗
PubMed1980

Augmented induction of tumor-specific resistance by priming with Mycobacterium tuberculosis (TBC) and subsequent immunization with PPD-coupled syngeneic tumor cells.

The present study investigates the augmenting effect of tuberculin- (PPD) reactive amplifier T cells on the induction of syngeneic tumor immunity. PPD-reactive helper (amplifier) T cell activity was generated in C3H/HeJ mice by appropriate immunization with heat-killed Mycobacterium (Tbc). Immunization of these Tbc-primed mice with PPD-coupled syngeneic X5563 tumor cells led to augmented generation of in vivo tumor-neutralizing activity contingent on the presence of PPD-reactive amplifier T cell activity. Splenic T cells from these mice exhibited potent tumor-neutralizing activity using Winn's assay, whereas spleen cells from mice not primed with Tbc before PPD-X5563 immunization failed to neutralize viable X5563 tumor cells. After establishing that the neutralizing activity was tumor specific and mediated by T cells, the applicability of this augmentation of tumor-specific immunity to an immunotherapy model was explored. Immunization with PPD-X5563 in the early stages of the tumor-bearing state induced potent anti-tumor activity sufficient to reject the growing tumor. Pretreatment of mice with cyclophosphamide or light x-irradiation (250 R), procedures that eliminate suppressor cell activity nonspecifically, before priming with Tbc further potentiated the anti-tumor activity under these conditions. Thus, the present study elucidates the augmenting effect of PPD-reactive amplifier T cells in the induction of tumor-specific immunity and provides an effective method of immunotherapy in tumor-bearing animals.

Animals↗
PubMedDate not supplied

[Decreased resistance of multiresistant mycobacteria to isoniazid during the treatment of experimental tuberculosis with ozone and isoniazid].

Mycobacteria (MB) of the clinical strain resistant to streptomycin, isoniazid (IN), rifampicin and kanamycin were injected intravenously into 68 BALB/c mice. The animals were divided into 5 groups: two control groups 0 and 1 (intact and infected without subsequent treatment), group 2 (treated with IN), group 3 (treated with IN and injected intraperitoneally with dissolved ozone, or dO3), group 4 (injected with dO3). The animals started to die by month 4 after the infection. By month 5 all mice died with the exception of intact mice and those treated with dO3). By month 4 the study of MB cultures isolated from the lungs revealed a decrease in their resistance to IN in the groups undergoing treatment with dO3. Hepatic and splenic lesions were observed after treatment with IN only were greater than in the absence of treatment. After the use of IN + dO3 such lesions were the least. The mechanism of a decrease in the medicinal resistance of MB under the action of dO3 and the expediency of the simultaneous use IN and dO3 in cases of the unknown medicinal resistance of MB are discussed.

Administration, Oral↗
PubMed2005

Vascular involvement secondary to tuberculosis of the abdomen.

Although involvement of the abdomen is a common site of extrapulmonary tuberculosis, involvement of abdominal vessels with complications is rare after infections with Mycobacterium tuberculosis (M. tuberculosis). Vascular complications may result from direct involvement by M. tuberculosis of the vascular wall or may occur as a consequence of local spreading from a tuberculous mass. We describe the imaging findings in two patients with proven tuberculosis of the abdomen and significant vascular complications. In one patient, "dry plastic" peritonitis and tuberculous lymphadenopathy at the level of the porta hepatis with subsequent encasement and compression of the portal vein resulted in prestenotic dilatation and varicose formation in the upper abdomen. In the other patient, bulky necrotic tuberculous lymphadenopathy, located at the splenic hilum, resulted in encasement with stenosis of the splenic vessels and subsequent splenic infarction.

Adult↗
PubMed2000

IL-4 is required for defense against mycobacterial infection.

Although the involvement of T helper (Th1) cells is central to protection against intracellular bacteria, including Mycobacterium tuberculosis, the involvement of Th2 cells, characterized by potent interleukin (IL)-4 secretion in mycobacterial infection is still unclear. In order to clarify the role of IL-4 in murine tuberculosis, IL-4-deficient mutant mice, IL-4 knockout (IL-4 KO) mice, were utilized. The mice were infected with H37Rv, Kurono or BCG Pasteur via an airborne infection route by placing them in the exposure chamber of a Middlebrook airborne infection apparatus. Their capacity to control mycobacterial growth, granuloma formation, cytokine secretion, and nitric oxide (NO) production were examined. These mice developed large granulomas, but not necrotic lesions in the lungs, liver or spleen (P<0.05). This was consistent with a significant increase in lung colony-forming units (CFU). Compared with levels in wild-type mice, upon stimulation with mycobacteria, splenic IL-10 levels were low and IL-6 levels were intermediate, but interferon (IFN)-gamma and IL-12 levels were significantly higher. IL-18 levels were within the normal range. The level of NO production by alveolar macrophages of the IL-4 KO mice was similar to that of the wild-type mice. Granulomatous lesion development by IL-4 KO mice was inhibited significantly by treatment with exogenous recombinant IL-4. These findings were not specific to the IL-4 KO mice used. Our data show that IL-4 may play a protective role in defense against mycobacteria, although IFN-gamma and TNF-alpha play major roles in it. Our data do not rule out an IFN-gamma-independent function of IL-4 in controlling tuberculosis.

Animals↗
PubMed1986

Absence of lymphokine-enhanced macrophage migration in vitro in the Australian brush-tailed opossum, Trichosurus vulpecula.

The supernatants from cultures of either opossum or guinea pig splenic lymphocytes, stimulated with phytohaemagglutinin, significantly enhanced the in vitro migration of guinea pig peritoneal macrophages (P greater than 0.001) but not that of opossum peritoneal macrophages. Failure of opossum macrophages to respond to a putative macrophage chemotactic factor might account for the observed paucity of immune granulomas in these animals and help explain the species' susceptibility to tuberculosis.

Animals↗
PubMed1988

Primary B-cell lymphoma of salivary glands and its relationship to myoepithelial sialadenitis.

A detailed morphologic and immunohistochemical study has been carried out on salivary glands excised from 20 cases in which the initial histologic diagnosis was either myoepithelial sialadenitis (MESA) or salivary gland lymphoma (SGL). The results have shown that these cases, except one that had been diagnosed as MESA, showed a spectrum of changes ranging from focal lymphoid infiltrates, designated as early MESA, through established MESA with dense, extensive lymphoid infiltration, to lymphoma. The distribution of the lymphoid infiltrate in early MESA was related to ducts and mimicked Peyers patches. In established MESA, this infiltrate became confluent with the formation of prominent epimyoepithelial islands. The evolution of lymphoma was characterized by an expanded population of centrocyte-like (CCL) cells that showed light chain restriction. Like other lymphomas of mucosa-associated lymphoid tissue, to which they bear a striking resemblance, salivary gland lymphomas may remain localized for prolonged periods with a tendency to local recurrence rather than to distant spread. These properties may be explained by the histogenesis of these tumors from CCL cells that appear to be of similar lineage of splenic marginal zone cells.

Adult↗
PubMed1976

Effect of systemic BCG infection in syrian golden hamsters.

The response of Syrian golden hamsters to systemic infection with several doses of Mycobacterium bovis (strain BCG) was assessed. Large numbers of organisms (10(7)), injected intravenously, were lethal for hamsters, whereas all animals survived infection with 10(4) colony-forming units of BCG. Animals responded immunologically to purified protein derivative as assessed by increased footpad swelling and splenic lymphocyte proliferation. The immediate cause of death was a diffuse granulomatous interstitial pneumonia.

Animals↗
PubMed1994

[Sarcoidosis of the liver and spleen in Japan].

Although liver and/or spleen sarcoidosis usually shows no symptoms and subtle elevated levels of liver enzymes, diagnostic image scanning methods (abdominal ultrasonic scan, computed tomographic scan, magnetic resonance image, and Ga and Tc scintiscan) can easily detect the lesion. Laparoscopy unveils isolated scattered sarcoid nodules on the surface of the liver and/or spleen and biopsied specimen reveal a non-caseating epithelioid granuloma containing multinucleated giant cells especially in the portal area. Sometimes it is required to differentiate liver and/or spleen sarcoidosis from hepatic tuberculosis, primary biliary cirrhosis or malignant lymphoma. In severe cases, corticosteroid treatment is necessary. Prognosis is usually good, but may be poor in some cases.

Diagnosis, Differential↗
PubMedDate not supplied

[Liver and splenic sarcoidosis: diagnostic procedures].

INTRODUCTION: Clinical studies indicate involvement of the liver and spleen in approximately 20-30% of patients affected with sarcoidosis and their detection should be based on a standardized diagnostic procedure. DIAGNOSTIC PROCEDURES: Ultrasonography is a reliable and safe method to assess changes related to size and structure of the affected organs that are pathognomonic for sarcoidosis. Further evaluation may include computerized tomography or magnetic resonance, while percutaneous needle aspiration biopsy or laparoscopy may also be applied when indicated. The most important criterion used for final diagnosis is pathohistological evidence of epithelioid noncaseating granuloma in bioptic material along with already established sarcoidosis of the lungs or some other organ. MATERIAL AND METHODS: The study on the incidence of liver and spleen sarcoidosis included a group of 130 patients affected with sarcoidosis hospitalized at the Institute of Pulmonary Diseases and Tuberculosis, Clinical Center of Serbia, over the period 2002-2003. RESULTS: The analysis evidenced that 31.5% of sarcoidosis patients had pathognomonic echographic findings of abdominal organs: splenomegaly (13%), hepatomegaly (10.8%) and hepatosplenomegaly (7.7%). Three patients underwent surgical treatment of liver and spleen sarcoidosis. CONCLUSION: Pathognomonic findings of liver and spleen sarcoidosis were evidenced in approximately one third of sarcoidosis cases and they represented a significant parameter for further therapy, particularly in chronic patients.

Adult↗
PubMedDate not supplied

Prolongation of concomitant antitumor immunity in mice treated with Z-100, an arabinomannan extracted from Mycobacterium tuberculosis.

The effect of Z-100, a natural immunomodulator extracted from Mycobacterium tuberculosis strain Aoyama B, on concomitant antitumor immunity (CAI) was investigated in mice immunized with Meth-A tumor cells (primary inoculation) in combination with Corynebacterium parvum. CAI, which was observed in mice 10 days after immunization (I10 mice), disappeared in mice 20 days after immunization (I20 mice). However, no growth of secondary inoculated Meth-A tumors was demonstrated in I20 mice treated with Z-100 (IZ20 mice). CAI was demonstrated in tumor-bearing recipients when splenic mononuclear cells (SMNC) from I10 mice or IZ20 mice were transferred to recipients intralesionally. However, CAI was not detected when recipients received SMNC from I20 mice or a SMNC mixture from I10 and I20 mice. The SMNC mixture from I10 and IZ20 mice inhibited the growth of Meth-A solid tumors in the recipients. The activity of non-specific suppressor cells, which were characterized as CD8+ T cells, was demonstrated in SMNC from I20 mice, while SMNC from I10 and IZ20 mice did not show any suppressor cell activities. In addition, clear inhibition of tumor growth was demonstrated in recipient mice which received a SMNC mixture from I20 mice, previously treated with anti-Lyt-2+ MAb plus complement, and I10 mice. These results suggest that Z-100 might be able to prolong CAI observed in I10 mice through the inhibition of Lyt-2+ T suppressor cells detected in SMNC from I20 mice.

Adjuvants, Immunologic↗
PubMed2005

T cell expansion is regulated by activated Gr-1+ splenocytes.

CD4+ T cell proliferation depends on the balance between NO and extra-cellular superoxide (O2-). By reducing NO bio-availability, O2- promotes splenic T cell proliferation and immune response intensity. Here, we show that spleen cells from naïve mice produced neither NO nor O2- during T cell activation, but Gr-1+ splenocytes from primed mice regulated Ag-specific T cell expansion via production of both molecules. Purified splenic Gr-1+ cells included mostly granulocytes at various stages of maturation, as well as monocytes. Activation or recruitment of regulatory Gr-1+ cells was dependent on immunization with CFA. Importantly, these regulatory cells were not detected in draining lymph nodes. These data suggest that innate Gr-1+ splenic cells regulate adaptive immunity.

Animals↗
PubMed1982

Peliosis of the spleen with rupture.

A case of peliosis of the spleen without apparent involvement of the liver or other organs is presented. The peliosis was discovered following rupture of the spleen after minimal trauma and was successfully treated by surgery. None of the common associations of peliosis was present (i.e., tuberculosis or intake of steroid compounds). Drugs addiction and chronic alcoholism were the only coexisting debilitating conditions exhibited by this patient.

Alcoholism↗
PubMed2004

Cross-regulation of CD86 by CD80 differentially regulates T helper responses from Mycobacterium tuberculosis secretory antigen-activated dendritic cell subsets.

We report that stimulation of Mycobacterium tuberculosis secretory antigen- and tumor necrosis factor alpha-matured BALB/c mouse bone marrow dendritic cells (BMDCs) with anti-CD80 monoclonal antibody up-regulated CD86 levels on the cell surface. Coculture of these BMDCs with naïve, allogeneic T cells now down-regulated T helper cell type 1 (Th1) responses and up-regulated suppressor responses. Similar results were obtained with splenic CD11c(+)/CD8a(-) DCs but not to the same extent with CD11c(+)/CD8a(+) DCs. Following coculture with T cells, only BMDCs and CD11c(+)/CD8a(-) DCs and not CD11c(+)/CD8a(+) DCs displayed increased levels of surface CD86, and further, coculturing these DCs with a fresh set of T cells attenuated Th1 responses and increased suppressor responses. Not only naïve but even antigen-specific recall responses of the Th1-committed cells were modulated by DCs expressing up-regulated surface CD86. Further analyses showed that stimulation with anti-CD80 increased interleukin (IL)-10 and transforming growth factor-beta-1 levels with a concomitant reduction in IL-12p40 and interferon-gamma levels from BMDCs and CD11c(+)/CD8a(-) DCs and to a lesser extent, from CD11c(+)/CD8a(+) DCs. These results suggest that cross-talk between costimulatory molecules differentially regulates their relative surface densities leading to modulation of Th responses initiated from some DC subsets, and Th1-committed DCs such as CD11c(+)/CD8a(+) DCs may not allow for such modulation. Cognate antigen-presenting cell (APC):T cell interactions then impart a level of polarization on APCs mediated via cross-regulation of costimulatory molecules, which govern the nature of subsequent Th responses.

Animals↗
PubMed1995

Problems in the treatment of kala-azar: case report.

Frequent relapses after treatment for visceral leishmaniasis and apparent parasitological cure is not commonly reported. Seven year old boy who relapsed four times with clinical and parasitological evidence of the disease at each two months follow-up period is presented. He had Leishimania donovani Kenya strain. After treatment, review would be after two months, six months and twelve months periods. Splenic aspirates were routinely done weekly and on the last day of each treatment. The drugs administered for varying periods included intravenous sodium stibogluconate 20 mg/kg daily, P20 in combination with allopurinol 21 mg/kg three times daily, and Pentamidine 4 mg/kg three times weekly and antituberculous drugs. The presence of abundant extra cellular leishmania donovani bodies in the bone marrow and possible pulmonary tuberculosis might have precipitated the frequent relapses. It is not clear which of the drugs effected the cure. It was observed that inspite of prolonged antileishmanial drug administration no side effects were noted.

Allopurinol↗
PubMed2002

Improved tuberculosis DNA vaccines by formulation in cationic lipids.

Mice were vaccinated with plasmid DNA (pDNA) encoding antigen 85A (Ag85A), Ag85B, or PstS-3 from Mycobacterium tuberculosis either in saline or formulated for intramuscular injections in VC1052:DPyPE (aminopropyl-dimethyl-myristoleyloxy-propanaminium bromide-diphytanoylphosphatidyl-ethanolamine) (Vaxfectin; Vical, Inc., San Diego, Calif.) or for intranasal instillations in GAP-DLRIE:DOPE (aminopropyl-dimethyl-bis-dodecyloxy-propanaminium bromide-dioleoylphosphatidyl-ethanolamine). These two novel cationic and neutral colipid formulations were previously reported to be effective adjuvants for pDNA-induced antibody responses. The levels of Ag85-specific total immunoglobulin G (IgG) and IgG isotypes were all increased 3- to 10-fold by formulation of pDNA in Vaxfectin. The level of production of splenic T-cell-derived Th1-type cytokines (interleukin-2 and gamma interferon) in response to purified Ag85 and to synthetic peptides spanning the entire Ag85A protein was also significantly higher in animals vaccinated with pDNA formulated in Vaxfectin. Cytolytic T-lymphocyte responses generated by pDNA encoding phosphate-binding protein PstS-3 in Vaxfectin were better sustained over time than were those generated by PstS-3 DNA in saline. Intranasal immunization with Ag85A DNA in saline was completely ineffective, whereas administration in GAP-DLRIE:DOPE induced a positive Th1-type cytokine response; however, the extent of the latter response was clearly lower than that obtained following intramuscular immunization with the same DNA dose. Combined intramuscular and intranasal administrations in cationic lipids resulted in stronger immune responses in the spleen and, more importantly, in the lungs as well. Finally, formulation in Vaxfectin increased the protective efficacy of the Ag85B DNA vaccine, as measured by reduced relative light unit counts and CFU counts in the spleen and lungs from mice challenged with bioluminescent M. tuberculosis H37Rv. These results may be of importance for future clinical use of DNA vaccines in humans.

ATP-Binding Cassette Transporters↗
PubMed1999

An immunomodulatory arabinomannan extracted from Mycobacterium tuberculosis, Z-100, restores the balance of Th1/Th2 cell responses in tumor bearing mice.

The regulatory effect of Z-100 on the balance of Th1/Th2 cell responses in BALB/c mice bearing Meth-A fibrosarcoma was investigated. In tumor bearing mice, Th1 cytokine production (IL-2, IFN-gamma) are suppressed and Th2 cytokine production (IL-4, IL-10) are increased, as compared with those of normal mice. The administration of Z-100 (10 mg/kg) to tumor bearing mice restored the balance of Th1/Th2 cell responses from Th2 dominant state to the normal state. This regulatory effect of Z-100 was eliminated by depletion of adherent cells from splenocytes derived from tumor bearing mice, and by the treatment with 2-ClAdo (a macrophage inhibitor). Similarly, this regulatory effect was diminished by the treatment with anti-IL-12 mAb and anti-IFN-gamma mAb. In addition, the IL-12 p40 mRNA expression in splenic adherent cells and IFN-gamma mRNA expression in CD4+ T cells were increased by the administration of Z-100 to tumor bearing mice. These results suggested that Z-100 restored the balance of Th1/Th2 cell responses to the normal one in tumor bearing mice through the activation of macrophages and up-regulation of IL-12 production from macrophages and IFN-gamma production from CD4+ T cells.

Adjuvants, Immunologic↗
PubMed1995

Gradual loss of T-helper 1 populations in spleen of mice during progressive tumor growth.

BACKGROUND: The carefully orchestrated events that result in a protective immune response are coordinated to a large extent by cytokines produced by T helper 1 (Th1) and T helper 2 (Th2) T-cell subsets, which are two arms of the immune system. Th1 cells preferentially produce interleukin 2 (IL-2), interferon gamma (IFN gamma), and tumor necrosis factor (TNF), resulting in a cellular response that helps to eliminate infected cells. In contrast, Th2 cells produce IL-4, IL-5, IL-6, and IL-10 and stimulate an antibody response that helps to prevent the cells from becoming infected. The clinical progression of several infectious diseases, including human immunodeficiency virus, some types of parasitoses, and tuberculosis, is thought to be associated with the predominance of a Th2-type T-cell response. Recent reports have demonstrated the presence of T cells producing Th2 lymphokines (IL-4, IL-6, and IL-10) in tumor-infiltrating lymphocytes of renal cell carcinoma. PURPOSE: The purpose of this study was to investigate at the molecular level whether there was any change in the splenic T cells of mice with progressively growing tumors from a Th1 to a Th2 DNA-binding pattern or phenotype. METHODS: Splenic T cells from mice bearing renal cell carcinoma or MCA-38 colon carcinoma were tested for cytokine production after in vitro activation. Nuclear extracts of splenic T cells were used for the DNA-binding assay using IFN-gamma core promoter region, the kappa B (kappa B) site from immunoglobulin gene, and the nuclear factor of activated T-cell (NFAT) site from IL-2 gene. RESULTS: Splenic T cells from mice bearing renal cell carcinoma or MCA-38 colon carcinoma preferentially produced Th2 cytokines (i.e., IL-4) upon activation and showed a marked decrease in Th1 cytokine (particularly IFN gamma) production compared with the production observed in normal splenic T cells. The DNA-binding assay with the IFN-gamma core promoter region confirmed the gradual decline in the nuclear transcription factors associated with the Th1 phenotype during tumor progression in both tumor models. Renal cell carcinoma-bearing mice, successfully treated with flavone-8-acetic acid and recombinant human IL-2, showed a reversion to a Th1-like pattern. In addition, nuclear extracts of T cells from tumor-bearing animals showed a Th2-type kappa B-binding pattern. Moreover, the NFAT complex present in the normal splenic T cells was lost at the later stages of tumor progression; instead, a new complex was present in mice bearing long-term tumors. CONCLUSION: T cells from tumor-bearing mice lose the Th1 phenotype with progressive tumor growth.

Animals↗