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Biomedical subjects

E Kita

Publications and source records attributed to E Kita.

At least 19 recordsLinked to original sources
PubMed1995

Murine tumorlytic factor, immunologically distinct from tumor necrosis factor-alpha and -beta, induced in the serum of mice treated with a T-cell mitogen of Corynebacterium kutscheri.

Murine tumorlytic factor (TF), immunologically distinct from murine tumor necrosis factor (TNF)-alpha and -beta, was purified to a homogeneity from the serum of mice injected with a T-cell mitogen of Corynebacterium kutscheri. The treated mouse serum was purified by Lentil lectin-Sepharose chromatography, DEAE-cellulose chromatography, preparative isoelectric focusing, and high-pressure liquid chromatography to the specific activity of 1.5 x 10(6) U/mg protein. TF was 42 kDa in its oligomeric form and 14 kDa in its monomeric form. TF activity was not impaired with hamster monoclonal antibody (mAb) to recombinant murine TNF-alpha and -beta and, reciprocally, rabbit antibody to TF neutralized the bioactivity of neither murine TNF-alpha nor -beta. TF was not precipitated with the mAb to murine TNF-alpha and -beta in Western blot analysis. The partial amino acid sequence of TF was at most 33% homologous to the 46-63 sequence of mouse TNF-beta. Thus, these results suggest that TF might be a novel tumorlytic factor which is immunologically distinct from mouse TNF-alpha and -beta.

Amino Acid Sequence↗
PubMed1995

Different sensitivity of complement to Salmonella typhimurium accounts for the difference in natural resistance to murine typhoid between A/J and C57BL/6 mice.

The difference in natural resistance to Salmonella typhimurium between S. typhimurium-resistant A/J mice and S. typhimurium-susceptible C57BL/6 mice was analyzed. In both strains, the growth of S. typhimurium was controlled in the spleen until 48 hr of infection, while serum C3b levels were increased in A/J mice immediately after infection but not in C57BL/6 mice. Incubation of A/J mouse serum with S. typhimurium or its lipopolysaccharide (LPS) generated sufficient amounts of C3b, but that of C57BL/6 mouse serum with them did not. A/J macrophages had higher intracellular killing activity in vitro than did C57BL/6 cells against S. typhimurium pre-opsonized with each corresponding fresh serum. However, the cells from both mice exhibited a similar level of killing activity against S. typhimurium pre-opsonized with fresh A/J serum or rabbit complement. The resistance of C57BL/6 mice was significantly increased by opsonizing S. typhimurium with fresh A/J serum or rabbit complement before inoculation. The serum level of interferon-gamma (IFN-gamma) in A/J mice was 2.7 times as high as in C57BL/6 mice at 48 hr post-infection. Recombinant murine IFN-gamma enhanced the intracellular killing activity of macrophages from both mice when S. typhimurium was pre-opsonized with fresh A/J serum but not with fresh C57BL/6 serum. These findings suggest that A/J macrophages exhibit maximal killing activity against A/J serum-opsonized S. typhimurium in vivo when the cells are activated with IFN-gamma. Therefore, the rapid and sufficient activation of complement by Salmonella LPS may render A/J mice more resistant against murine typhoid.

Animals↗
PubMed1995

Conversion of Salmonella typhimurium to L-forms contributes to the maintenance of acquired immunity against murine typhoid.

Conversion of Salmonella typhimurium to L-forms, both in vitro and in vivo, resulted in the expression of proteins cross-reacting to the mycobacterial 65,000 MW heat-shock protein (hsp). Immunization of C3H/HeJ mice with a protective dose of stable L-form S. typhimurium induced gamma delta T cells in the liver, in accordance with the multiplication of L-form Salmonella in Kupffer cells. The number of gamma delta T cells decreased after the intracellular growth of L-form Salmonella plateaued. Persistance of the L-forms in Kupffer cells, however, allowed hepatic gamma delta T cells to increase within 48 hr of infection with virulent S. typhimurium. Thus, the intrahepatic colonization of L-form Salmonella seems to keep gamma delta T cells on standby, but the emergence of these T cells does not correlate with the expression of L-form hsp. In addition, Kupffer cells colonized by L-forms constitutively synthesized mRNA for interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-alpha). These results suggest that conversion of S. typhimurium to L-forms in phagocytic cells builds up and maintains acquired resistance, conferred by live-cell vaccines of S. typhimurium, against murine typhoid.

Animals↗
PubMed1994

Protective capacity of L-form Salmonella typhimurium against murine typhoid in C3H/HeJ mice.

L forms of Salmonella typhimurium LT2 conferred strong protection to a lethal challenge with its parental bacterium on innately hypersusceptible C3H/HeJ mice, and its minimal protective dose was approximately 150 L-forming units. Although L-form S. typhimurium was avirulent for C3H/HeJ mice, it multiplied slowly in both the liver and spleen with the maximal growth 2-3 weeks after immunization and thereafter it persisted in the liver until 24 weeks. Protective immunity began to work between 4 and 6 weeks after immunization, and it remained active as long as the L forms colonized the liver (until 24 weeks after immunization). Vaccination with the L form induced a population of T cells responding to L-form whole-cell lysate (WCL), while delayed-type hypersensitivity (DTH) to the extract of S. typhimurium was induced after the establishment of solid immunity. Moreover, neither T-cell responses nor DTH to heat-killed S. typhimurium was generated. In addition, antibody responses were elicited to WCL but not to heat-killed S. typhimurium. These results indicate that protection conferred by the L forms is attributable to the persistent colonization of the L forms rather than the presence of DTH, and also that Salmonella cytoplasmic antigens are involved in induction of immunological responses by vaccination with the L forms.

Animals↗
PubMed1994

Transfer of protection to murine typhoid conferred by L-form Salmonella typhimurium in dependence of cooperation between L form-adopted macrophages and L form-induced Lyt-2+ T cells.

The effector cells responsible for protection to Salmonella typhimurium in C3H/HeJ mice, conferred by L-form S. typhimurium, were determined by cell transfer test. Nonfractionated spleen cells from 6-week immune mice but not from 24-week immune animals transferred anti-S. typhimurium immunity. Treatment with anti-macrophage antiserum and complement most effectively abolished protective capacity in 6-week immune cells, while anti-T cell monoclonal antibody plus complement reduced it to a lesser extent. However, adoptive protection was achieved only by transfer of immune macrophages along with Lyt-2+ T cells selected from 6-week immune spleen cells. These Lyt-2+ T cells were cytotoxic to Kupffer cells from C3H/HeJ mice which had been infected 48 hr previously and from the mice which had been immunized 1 week previously, but not to the cells from 6-week immune mice and from normal animals. Moreover, protective capacity in immune macrophages seemed to be correlated to the degree of colonization by the L forms, and the inability to transfer immunity of 24-week immune spleen cells may be due to the decrease in the L form-colonization. These results suggest that cooperation between the L form-colonized macrophages and L form-induced cytotoxic Lyt-2+ T cells contributes to anti-S. typhimurium immunity, and might imply the immunological difference between the 6-week immune phagocytes and the cells at an early stage of infection or immunization.

Animals↗
PubMed1994

[Suppression of the Pseudomonas aeruginosa-induced biofilm formation on human epithelial cells by erythromycin].

In the present study, were examined the inhibitory effect of erythromycin on the biofilm formation by a temperature-sensitive mutant (Ts25) of Pseudomonas aeruginosa N-42 on the surface of Ishikawa cells which can produce a mucin-like glycoprotein physicochemically similar to mucoproteins produced in the human airway. Usually, 38-45 microcolonies (biofilms) were formed after 10 days of incubation in cultures of Ishikawa cells and P. aeruginosa Ts25. Erythromcin suppressed the adhesion to Ishikawsa cells of P. aeruginosa and its subsequent biofilm formation at doses as low as 0.2 microgram/ml. Erythromycin also exhibited the suppressive effect on the production of glycoproteins by Ishikawa cells at doses higher than 1 microgram/ml and the production of elastase and exoenxyme A from P. aeruginosa at doses higher than 2 micrograms/ml. These results suggest that erythromycin can inhibit the biofilm formation in culture of human epithelial cells and P. aeruginosa and the in-vivo bacterial biofilm formation may be attributed to host cell-derived factors rather than bacterial products.

Biofilms↗
PubMed1994

[A clinical study of Pseudomonas pneumonia diagnosed by transtracheal aspiration].

We performed a clinical study of 16 cases (18 episodes) of Pseudomonas pneumonia by transtracheal aspiration (TTA) from April 1983 to March 1993. The isolation rate of Pseudomonas aeruginosa (P. aeruginosa) among 235 episodes of pneumonias with positive microorganism by TTA was 7.7%. All patients had one or more underlying disease. The most frequent underlying disease was chronic lower respiratory tract infection, followed by lung epidermoid cell carcinoma. More than half of the cases had been given antibiotics prior to the occurrence of pneumonia, and administration of adrenal corticosteroid, heavy smoking habit, and aspiration were seen as other predisposing factors concerning the onset of pneumonias. Monomicrobial infection of P. aeruginosa was 61.1%, and polymicrobial infection containing P. aeruginosa was 38.9%. Community-acquired pneumonia was 61.1% and hospital-acquired pneumonia was 38.9%; the rates of polymicrobial infections and prior administration of antibiotics were higher in the latter group. Mortality due to Pseudomonas pneumonia was 27.8% and the levels of serum albumin and total protein at the onset of pneumonia were significantly lower in the fatal cases than in the recovered cases. It was considered that not only general underlying disease which weaken the immunological resistance of the host, but local bronchial lesion was also important to the onset of the Pseudomonas pneumonia. Also, nutrition is an important prognostic factor on the host's side.

Adult↗
PubMed1993

Isolation of a cytotoxin from L-form Salmonella typhimurium.

A cytotoxic protein was isolated from the sodium dodecyl sulphate (SDS)-solubilized extract of the stable L forms of Salmonella typhimurium by ion-retardation chromatography, ion-exchange chromatography, isoelectric focusing and gel filtration. The purified toxin, with a molecular mass of 32 kDa and with isoelectric point of 6.4, was thermolabile and trypsin-sensitive. Against mouse macrophages, its cytolytic effect was detectable in vitro at concentrations higher than 0.7 micrograms/ml, with a complete lysis obtained at 5 micrograms/ml. In contrast, it stimulated C3H/HeJ macrophages in the dose range of 0.1-0.5 micrograms/ml to allow the cell to respond to endotoxin, resulting in the significant production of tumor necrosis factor alpha. By Northern blot analysis, this effect was detectable at a dose as low as 0.01 micrograms/ml. These findings suggest that the transformation of bacillary S. typhimurium into L forms in vivo may induce alterations in host resistance against murine typhoid.

Animals↗
PubMed1993

Restoration of the acute phase response after infection in cyclophosphamide-treated mice by granulocyte colony-stimulating factor.

The therapeutic effect of granulocyte colony-stimulating factor (G-CSF) against intramuscular infection with Pseudomonas aeruginosa in cyclophosphamide (CY)-treated mice was analyzed by measuring plasma levels of amyloid P-component (APC) and proinflammatory cytokine levels. CY (100 mg/kg) treatment of mice significantly suppressed plasma concentrations of APC and tumor-necrosis factor-alpha (TNF-alpha) following infection with P. aeruginosa, in associated with enhanced susceptibility of the treated mice to this bacterium. A 4-day treatment of CY-treated mice with recombinant human G-CSF (rhG-CSF) increased resistance of CY-treated mice, together with the marked restoration of APC and TNF-alpha productions. The capacity to produce interleukin 1-beta and TNF-alpha of peritoneal macrophages and also that to produce IL-6 of spleen cells were significantly enhanced by the in vivo administration of rhG-CSF in CY-treated mice. These results indicate that G-CSF may increase the functions of monocytes/macrophages directly or indirectly in vivo. Therefore, the therapeutic effect of rhG-CSF seems to consist of not only increases in the number and functions of neutrophils but also enhancement of monocyte/macrophage functions.

Acute-Phase Reaction↗
PubMed1993

Induction of hypersensitivity to endotoxin in C3H/HeJ mice by immunization with L-form Salmonella typhimurium.

When endotoxin low-responder C3H/HeJ mice were immunized with L-form Salmonella typhimurium, the mice were more susceptible to a lethal challenge with S. typhimurium 1 week after immunization (1-week mice) than were the unimmunized controls. One-week immune mice produced overwhelming amounts of tumor necrosis factor-alpha (TNF-alpha) in the blood after infection, while 4-week immune mice produced lesser amounts of this cytokine with a 75% survival rate at 60 days postinfection. Pretreatment with anti-TNF-alpha antibody prevented 1-week immune mice from succumbing to acute illness. Endotoxin-stimulated peritoneal macrophages from 1-week immune mice produced higher amounts of TNF-alpha in vitro than did those from 4-week immune mice and they expressed larger amounts of TNF-alpha mRNA on Northern blot. The capacity of macrophages to produce TNF-alpha in vitro was correlated with the degree of colonization by the L form in the cells. These results suggest that the colonization by L-form S. typhimurium in macrophages alters the susceptibility to S. typhimurium of C3H/HeJ mice and that TNF-alpha might play a major role in this alteration of host resistance.

Animals↗
PubMed1993

Alterations of host response by a long-term treatment of roxithromycin.

Roxithromycin (10 mg/kg) was administered once-daily for seven or 28 days to mice intragastrically and its effects on cytokine synthesis were studied. Administration of roxithromycin for 28 days resulted in increased synthesis of interleukin (IL)-1 and tumour necrosis factor (TNF-alpha) production by macrophages, and the production of IL-2, IL-4 and interferon gamma by splenocytes. In contrast, 7 day administration of roxithromycin did not affect these parameters. Furthermore, clindamycin treatment did not significantly increase the capacity of host cells to produce cytokines, irrespective of the duration of treatment, when compared with the solvent control receiving 0.9% ethanol solution or the untreated controls. In addition, the supernatant of a 7 day culture of splenocytes with roxithromycin showed suppression of the production of TNF-alpha and prostaglandin E2 by mitogen-stimulated macrophages, and this suppressive activity was impaired by a monoclonal antibody to murine IL-4. Thus, this data suggests that roxithromycin may not only enhance the host defence system through increased cytokine synthesis by host cells, but also exhibit anti-inflammatory activity by including an anti-inflammatory cytokine, IL-4.

Adjuvants, Immunologic↗
PubMed1993

[A clinical study of chronic lower respiratory tract infections with Pseudomonas aeruginosa by transtracheal aspiration].

We investigated the yearly changes of the incidence of Pseudomonas aeruginosa (P. aeruginosa) isolated from chronic lower respiratory tract infections (CLRTI), and also performed a clinical study on CLRTI with P. aeruginosa by transtracheal aspiration (TTA) to clarify the recent trend of P. aeruginosa infection in CLRTI and the predisposing clinical factors to the acute exacerbation. The isolation rate of P. aeruginosa among the total isolated bacteria in CLRTI between December 1978 and March 1983 was 8.4%, but it increased to 23.1% between April 1988 and March 1993. In 69 episodes (40 cases) of P. aeruginosa isolated from CLRTI between April 1983 and March 1993, monomicrobial infections of P. aeruginosa were 42 episodes (60.9%) and polymicrobial infections were 27 episodes (39.1%). When the diseases were classified into acute exacerbated and non-exacerbated phases, polymicrobial infections were seen more in the former phase, and the principal organisms detected with P. aeruginosa were Haemophilus influenzae and Streptococcus pneumoniae. In the acute exacerbated cases, predisposing conditions concerning the exacerbation were divided into four patterns: 1. polymicrobial infections with H. influenzae or S. pneumoniae, 2. after acute upper respiratory tract infections due to viral superinfection, 3. early phase from bacterial replacement by P. aeruginosa, 4. immunocompromised states such as adrenal corticosteroid administration or systemic underlying diseases. These results suggest that the importance of P. aeruginosa in CLRTI is increasing year by year and we must pay attention to the fact that P. aeruginosa alone may also cause acute exacerbation in the latter 2 patterns of the condition.

Adult↗
PubMed1993

[Effect of erythromycin on production of cytotoxin and attachment factors of bacteria].

We studied the effect of erythromycin (EM) on the attachment of Pseudomonas aeruginosa and Neisseria gonorrhoeae to HeLa and HT-177 cell and on cytotoxin production of P. aeruginosa. 1. EM inhibited attachment of these bacteria. 2. EM inhibited manifestation of the pili of these bacteria. 3. EM inhibited production of protein II, the second attachment factor of N. gonorrhoeae. 4. EM inhibited production of 66 K cytotoxin of P. aeruginosa. On the basis of these findings, it was suggested that EM might inhibit infection by repressing manifestation of the attachment factor and production of cytotoxin of the bacteria.

Bacterial Adhesion↗
PubMed1993

[Determination of neutrophil function in the respiratory infection by chemiluminescence (CL). I: Change in neutrophil's CL by chemotherapy against the bacterial pneumonia].

We measured neutrophil's CL (CL-index) in 12 patients of the bacterial pneumonia three times per each case: before, during and after chemotherapy. Before the initiation of chemotherapy. CL-index in the six patients remained higher than that in healthy controls, while the remaining six showed lower levels of CL-index compared to the controls. In the 11 cases, their CL-indexes fell to levels lower than those obtained before treatment. Additionally, in the 11 cases their CL-indexes increased after the termination of chemotherapy. Furthermore, in the nine cases the product of the neutrophil number and CL-index was decreased by chemotherapy, and the decrease in the product correlated with improvement in their clinical conditions.

Adolescent↗
PubMed1992

Contribution of interferon gamma and membrane-associated interleukin 1 to the resistance to murine typhoid of Ityr mice.

Resistance of mice to Salmonella typhimurium in the early phase of infection is known to be controlled by the expression of chromosome 1 locus Ity. To clarify the mechanism by which the genetically resistant (Ityr) mice can overcome the first phase of salmonellosis, the early response in DBA/2 (Ityr) and BALB/c (Itys) mice was compared after a subcutaneous injection of S. typhimurium. In both strains, the growth of S. typhimurium was controlled in livers and Kupffer cells until day 3, but thereafter the bacteria multiplied rapidly in BALB/c mice. Over the first 2 days nonspecific responses (changes in levels of blood leukocytes, plasma iron, and alpha 1-antitrypsin) were not significantly different between the strains, and the capacity of Kupffer cells isolated from infected mice of both strains to produce interleukin 1 (IL-1) and tumor necrosis factor alpha (TNF-alpha) was of the same degree. Thereafter, only DBA/2 Kupffer cells were able to produce membrane-associated IL-1 (ma IL-1) as well as TNF-alpha. Moreover, only DBA/2 splenocytes were able to produce interferon gamma (IFN-gamma) upon stimulation with Salmonella antigens, although concanavalin A-stimulated splenocytes of both strains produced the same level of interleukin 2. Furthermore, administration of recombinant murine IFN-gamma and DBA/2 Kupffer cells of day 6 to BALB/c mice 3 days after infection resulted in a significant level of protection, whereas neither of these materials alone induced protection. Injection of anti-TNF-alpha antibodies did not affect the resistance of DBA/2 mice. Thus, these findings suggest that the early resistance of Ityr mice is partly attributable to their capacity to produce IFN-gamma and ma IL-1 after infection.

Animals↗
PubMed1992

The anti-inflammatory effect of erythromycin in zymosan-induced peritonitis of mice.

The anti-inflammatory effect of erythromycin was investigated using zymosan-induced peritonitis in mice. When mice were given erythromycin 10 mg/kg/day po for 28 days, a marked suppression of inflammatory responses, including the reduced influx of leucocytes, plasma exudation and prostaglandin E2 synthesis, was observed. However, neither a 7-day treatment with erythromycin nor a 28-day treatment with clindamycin suppressed the response. The anti-inflammatory activity induced after a 28-day treatment with erythromycin was comparable to the anti-inflammatory effect conferred by a 2-day treatment with dexamethasone 40 microgram/mouse/day. Thus, these data confirm previous studies which show that erythromycin can exert an anti-inflammatory effect when used over long periods of time.

Animals↗
PubMed1992

Mononuclear cell response in the liver of mice infected with hepatotoxigenic Campylobacter jejuni.

Intragastric inoculation with hepatotoxigenic strains of Campylobacter jejuni led to the death of mice during the late phase of infection. Histological study disclosed a massive infiltration of mononuclear cells in the liver, mimicking intrahepatic hypersensitivity. Neither enterotoxigenic nor enteroinvasive Escherichia coli induced such a lesion. However, the same histopathological change was induced by injecting the hepatotoxic factor of hepatotoxigenic C. jejuni intravenously on two occasions separated by 14 days. Neither a single injection of an increased dose of the hepatotoxic factor nor two injections, the second of which was heat-inactivated, induced this change. Pre-treatment with rabbit antibody to the hepatotoxic factor inhibited the development of the hepatic lesion. These results suggest that C. jejuni-induced hepatic lesions in mice may be caused, at least in part, by the active moiety of the hepatotoxic factor. The possible mechanisms by which the toxic factor induces hepatitis as a consequence of hypersensitivity are discussed in relation to Guillain-Barré syndrome and Reiter's syndrome associated with C. jejuni enteritis.

Animals↗