PubMed Health⌕ Search

Biomedical subjects

M Aitani

Publications and source records attributed to M Aitani.

9 recordsLinked to original sources
PubMed1998

[Polymyositis-induced respiratory failure in the presence of antecedent pleural effusion].

Pulmonary involvement is generally recognized to be an important determinant of the clinical course in cases of polymyositis. A patient with bilateral pleural effusion as an initial symptom developed respiratory failure due to muscle weakness. Polymyositis was diagnosed on the basis of a muscle biopsy. A chemotherapy regimen consisting of methyl prednisolone (1 g/day for 3 days) followed by prednisolone (60 mg/day) alleviated, the pleural effusion and respiratory failure. Though pleural complications in polymyositis have been described mostly in association with concomitant interstitial lung disease, our patient exhibited only bilateral pleural effusion. Given that pleural effusion can be an initial symptom of polymyositis, it seems necessary that polymyositis be taken into consideration by differential diagnoses of pleural effusion of unknown etiology.

Aged↗
PubMed1998

[Severe pneumococcal pneumonia with acute respiratory failure and neutropenia].

Severe pneumococcal pneumonia may precipitate both respiratory failure and neutropenia. The prognoses are considered to be very poor in such cases. We encountered three patients with pneumococcal pneumonia presenting respiratory failure and neutropenia, and successfully treated two. All three patients showed disseminated intravascular coagulation, and respiratory failure requiring mechanical ventilation. Neutropenia was treated with granulyte-colony stimulating factor (G-CSF), with methylpredonisolone administered by pulse therapy for 3 days to treat severe respiratory failure during the clinical course. All 3 patients were relieved of their respiratory failure at least for a few days following treatment. As a result of treatment with antibiotics and G-CSF, pneumococci disappeared from the patients' sputum. However, it has been reported that disintegration of the bacterial cell walls can release inflammatory components capable of causing secondary inflammatory reactions in the lung tissue. This suggested that the worsening respiratory failure experienced by our patients during their clinical course was a result of such reactions, and that methylpredonisolone was effective as the treatment of inflammation.

Aged↗
PubMed1996

B cell-B cell interaction through intercellular adhesion molecule-1 and lymphocyte functional antigen-1 regulates immunoglobulin E synthesis by B cells stimulated with interleukin-4 and anti-CD40 antibody.

IgE synthesis by purified human B cells is induced by two signals: a class switching factor, most commonly interleukin (IL)-4, and the engagement of CD40, which is activated through its interaction with CD40 ligand (CD40L) expressed on activated T cells. Thus, the combination of IL-4 and anti-CD40 monoclonal antibody (mAb) has been shown to stimulate IgE production in vitro by highly purified B cells. In this T cell-independent system, strong homotypic aggregation of B cells is observed prior to the production of IgE. Flow cytometric analysis and cell binding assays showed that the stimulation of purified B cells with anti-CD40 mAb plus IL-4 resulted in a striking increase of intercellular adhesion molecule (ICAM)-1(CD54) expression, an induction of CD43 and an avidity change of lymphocyte functional antigen (LFA)-1(CD11a/CD18), with little augmentation of CD18 expression. Addition of anti-ICAM-1 mAb caused an inhibition of homotypic aggregation but augmented IgE synthesis by B cells stimulated with anti-CD40 mAb and IL-4, although it did not affect B cell proliferation or IL-6 production by the B cells. Among the mAb against counter-receptors for ICAM-1 tested, anti-CD11a mAb suppressed IgE synthesis, while anti-CD18 mAb and anti-CD43 mAb had little effect. The enhancing or inhibitory effect of anti-ICAM-1 mAb or anti-CD11a mAb on IgE production was achieved by the increased or decreased expression of germline C epsilon transcripts by B cells stimulated with anti-CD40 mAb and IL-4. These results indicate that B cell-B cell interaction through ICAM-1 and one of its counter receptors, LFA-1, regulates IgE synthesis by modulating C epsilon germ-line transcription.

Antibodies, Monoclonal↗
PubMed1996

Functional disturbance of naive T lymphocytes in very high IgE producers: depletion of interleukin-4-induced interleukin-4-producing cells.

We examined the capacity of T cells from normal individuals and allergic patients with very high IgE to differentiate into interleukin-4(IL-4)-producing cells in vitro. T cells incubated with anti-CD3 monoclonal antibody plus IL-4 or plus anti-IL-4 antibody in the presence of antigen-presenting cells for 7 days were restimulated and their capacity to express IL-4 mRNA was examined by RT-PCR. In T cells from normal individuals, there was a marked increase in the expression of IL-4 mRNA following the addition of IL-4. After fractionation of normal T cells into naive T (CD45RA+) and memory T (CD45RO+) cells, induction of the increase of IL-4 mRNA was restricted to the naive T cell population. In contrast, in T cells from allergic patients, the stimulation of whole or naive T cells with anti-CD 3 monoclonal antibody in the presence of IL-4 induced much less IL-4 mRNA. These findings suggest the presence of a functional abnormality in IL-4-dependent development of IL-4-producing T cells in the peripheral-blood naive T cells from allergic patients.

Adjuvants, Immunologic↗
PubMed1996

Peripheral blood T lymphocytes and basophils, freshly isolated from house-dust-mite-sensitive patients, produce interleukin-4 in response to allergen-specific stimulation.

We examined the capacity of interleukin-4 (IL) production from lymphocytes and basophils, isolated from the peripheral blood of allergic patients sensitive to house dust mite, after stimulation with mite extract. IL-4 production was measured by a sensitive bioassay based on coculture with CT.h4S (a human IL-4-responsive cell line). Lymphocytes and basophils from patients with elevated serum IgE specific to mite allergen [radioallergosorbent test (RAST) score > 3] could produce detectable levels of IL-4 in response to mite extract, whereas those from patients with a RAST score of less than 2 or normal volunteers could not. The sensitivity of basophils to mite extract was high, so that a lower concentration of mite extract (1-10 ng/ml) could induce maximal IL-4 production. On the other hand, a higher concentration (10 micrograms/ml) was required for maximal IL-4 production from the lymphocytes. These findings demonstrate that allergen-specific IL-4-producing cells, lymphocytes and basophils, are generated in vivo in allergic patients and also that there exist characteristic differences between lymphocytes and basophils related to the in vivo source of IL-4.

Allergens↗
PubMed1989

[Soluble interleukin-2 receptor levels in patients with pulmonary tuberculosis].

Utilizing an enzyme-linked immunosorbent assay, we detected markedly elevated serum levels of soluble interleukin-2 (IL-2) receptors in patients with untreated pulmonary tuberculosis. In these patients, we also found that serum levels of soluble IL-2 receptors were closely correlated with serum adenosine deaminase levels (r = 0.869, p less than 0.001). Therefore, serum soluble IL-2 receptors appear to reflect the existence of active cell-mediated immunity in pulmonary tuberculosis and may prove to be a useful immunological marker for pulmonary tuberculosis.

Adult↗
PubMedDate not supplied

Significance of soluble Fc epsilon receptor II (sFc epsilon RII/CD23) in serum and possible application of sFc epsilon RII for the prevention of allergic reactions.

The significance of sFc epsilon RII in IgE-mediated allergic disease was examined. sFc epsilon RII in serum was found to decrease following clinical improvement, suggesting sFc epsilon RII in serum may be an indicator of allergic diseases. Significant proportions of sFc epsilon RII in serum were present as complexes with IgE in normals as well as in atopic patients, and these complexes were more prominent in the former than in the latter group. From these observations, attempts were made to inhibit IgE-mediated allergic reactions in vitro employing recombinant sFc epsilon RII. sFc epsilon RII inhibited IgE-binding as well as IgE-mediated release of chemical mediators from Fc epsilon RI and Fc epsilon RII expressing cells. These results show the functional significance of sFc epsilon RII in the negative regulation of IgE-mediated allergic reactions.

Antigens, CD↗