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Biomedical subjects

M Seitz

Publications and source records attributed to M Seitz.

At least 37 records · Page 2Linked to original sources
PubMed1985

Enhanced prostanoid release from monocytes of patients with rheumatoid arthritis and active systemic lupus erythematosus.

In patients with rheumatoid arthritis high levels of prostaglandin E1 have been found in the joint fluid, and its increased production by adherent synovial cells and macrophages clearly supports the notion that this arachidonic acid metabolite is involved in the pathology of the disease. Besides its known inflammatory qualities and the suppressive effects on various lymphocyte functions prostaglandin E2 has proved to be an essential cofactor in the secretion of the lymphokine osteoclast activating factor. In this study we have discovered an enhanced release of prostaglandin E1 and thromboxane B2 from a subpopulation of blood monocytes from patients with rheumatoid arthritis and active systemic lupus erythematosus. No correlation between prostanoid release from monocytes and inflammatory activity of the disease was found. However, even monocytes from patients with early stage or mild inflammatory activity displayed a 'stimulated' arachidonic acid metabolism. In contrast only patients with active systemic lupus erythematosus showed in this respect comparable secretory activity or monocytes. Our findings may point to a possible pathogenic role of prostanoids in rheumatoid arthritis, which may also have some implication for the early diagnosis of this disease and for its differentiation from other chronic inflammatory rheumatic conditions.

Arthritis↗
PubMed1984

Endogenous peroxidase in the nuclear envelope and endoplasmic reticulum of human monocytes in vitro: association with arachidonic acid metabolism.

The development of peroxidase (PO) reaction in the nuclear envelope (NE) and endoplasmic reticulum (ER) of monocytes differentiating in vitro and its relationship with arachidonic acid metabolism were studied. The PO, as visualized by the diaminobenzidine (DAB) technique, appeared in the NE and ER of the majority of monocytes within 24 hours of culture, with a substantial decrease thereafter. The influence of three major groups of agents--inhibitors of PO, of prostanoids, and of protein biosynthesis--upon the development of the PO reaction was examined. When aminotriazole, a PO inhibitor, was added to the culture medium, the appearance of PO was suppressed in the monocytes. The cyclooxygenase blocker, indomethacin, however, did not influence the development of PO. Also the blockers of protein synthesis, puromycin, cycloheximide, and actinomycin D, did not affect the appearance of PO. The prostanoids released from the monocytes, ie, prostaglandin E and thromboxane B2, were determined by radioimmunoassay and showed a time sequence of secretion that corresponded to the appearance of PO in the cells: a marked increase within the first 24 hours with a substantial decrease thereafter. The presence of the PO inhibitors aminotriazole and sodium azide in the culture medium produced a suppression of prostanoid release from the monocytes comparable with that of indomethacin. The data suggest that the PO in the NE and ER of differentiating monocytes in vitro (1) is associated with arachidonic acid metabolism, and (2) is not formed by de novo protein synthesis but rather by an activation process.

Adolescent↗
PubMed1984

Virus infection islet cell antibodies and islet cell function in type I diabetes mellitus.

The detection of islet cell antibodies has led to an increasing interest in autoimmune mechanisms in Type I diabetes mellitus. Other phenomena, such as insulitis in juvenile diabetics and in experimental animals, cellular immune reactions and concommitant antibodies against other endocrine organs, antinuclear antibodies and circulating immune complexes have supported such speculations. HLA-association and viral-infections could be predisposing and inducing factors. However, with one exception, the occurrence of ICA in a group of mumps infected children did not result in the development of diabetes mellitus over 3-4 years, nor could it be correlated with HLA-pattern. The islet cell antibodies block glucose stimulated insulin secretion in vitro without complement, while Type I diabetic sera with complement are beta cell cytotoxic irrespective of their ICA concentration. It is still not clear whether these mechanisms play any role in vivo. Therapeutic intervention before the clinical manifestation of the disease is as yet not possible due to the lack of markers indicating a subclinical autoimmune process.

Adolescent↗
PubMed1984

Macrophages release arachidonic acid, prostaglandin E2, and thromboxane in response to late complement components.

Rat peritoneal macrophages released arachidonic acid, prostaglandin E2, and thromboxane B2 when treated with normal rabbit or C6-deficient rabbit complement in vitro. Normal rabbit complement, however, was more efficient, which indicates that late complement components, in addition to the known effects of C3a and C3b, were responsible for an enhanced arachidonic acid turnover. Indeed, in the absence of the C3 cleavage products, the purified late complement components C5b6, C7, C8, and C9 stimulated the arachidonic acid, as well as the prostaglandin E2 and thromboxane B2 release. Incubation of C5b6, C7, C8, and C9 for 1 hr at 37 degrees C before addition to the macrophages abolished the stimulatory activity, being in complete agreement with the fact that a fluid phase-formed complex of C5-9 loses its membrane-binding capacity. Although the mechanism by which C5b-9-membrane interaction affects the arachidonic acid metabolism remains unclear, the data describe a new function of the late complement components.

Animals↗
PubMed1983

Characterization of blood mononuclear cells of rheumatoid arthritis patients. II. Depressed PPD presentation by monocytes to T lymphocytes.

Purified blood monocytes from patients with rheumatoid arthritis (RA) were significantly less capable of presenting purified protein derivative of tuberculin (PPD) to autologous lymphocytes than monocytes from patients with osteoarthritis, degenerative spine diseases, or healthy controls. Since lymphocytes from RA patients exhibited a normal response to soluble PPD or concanavalin A, the lowered T-cell reactivity had to be attributed to a diminished antigen-presenting capacity of monocytes. Several reasons may be responsible for this altered monocyte function in rheumatoid arthritis: a shift of monocytes to subpopulations expressing less Ia-like antigens, an inherent monocyte disorder, or a "preactivation" of monocytes associated with a reduced antigen-presenting capacity.

Adult↗
PubMed1983

[Autoimmune phenomena in diabetes mellitus. On the pathogenetic and diagnostic significance].

The detection of islet cell antibodies lead to an increasing interest in autoimmune mechanisms in Typ I diabetes mellitus. Other phenomena such as insulitis in juvenile diabetics and in experimental animals, cellular immune reactions and concomitant antibodies against other endocrine organs, antinuclear antibodies and circulating immune complexes supported these suggestions. HLA-association and viral infections could be predisposing and inducing factors, although there are no clear correlations to any viral infection in a larger number of patients so far. For clinical and therapeutic purposes there are not enough sufficient criteria to demonstrate a pathologic autoimmune process in patients before developing diabetes. Up to now there is no realistic possibility and justification for starting an early immunosuppressive therapy.

Animals↗
PubMed1981

The influence of synovial fluid from patients with rheumatoid arthritis on the proliferation of peripheral blood lymphocytes and the prostanoid release from monocytes.

The present study was designed to characterize leukocytes of patients with rheumatoid arthritis (RA) with regard to proliferation of peripheral blood lymphocytes (PBL) and prostanoid release from circulating monocytes (M phi. Compared to cells of healthy individuals, PBL from RA patients exhibited a reduced mitogenic response to concanavalin A (Con A) which was associated with an increased capacity of circulating M phi to synthesize PGE and thromboxane B2 (TXB2). Addition of synovial fluid exudates of RA patients (RA-SFE) to peripheral blood leucocyte cultures produced three effects: A spontaneous proliferation of normal and RA-PBL, a reduction of the Con A response of normal and RA-PBL, a reduction of the Con A response of normal and RA-PBL, and an enhanced release of PGE and TXB2 from RA-M phi only. To elucidate the cellular origin of these activities, normal and RA-PBL were incubated with supernatants (SNT) os synovial cell cultures from RA patients and patients with non-RA joint diseases. SNT from Con A-stimulated synovial lymphocytes of both RA and control patients induced a spontaneous proliferation of normal and RA-PBL. In contrast, SNT from non-lymphoid adherent synovial cells of RA and control patients reduced the Con A response of normal and RA-PBL but a striking difference was noted in that an enhanced PGE and TXB2 release occurred only from M phi of RA patients.

Arthritis, Rheumatoid↗
PubMed1979

Depressed prostaglandin release from peritoneal cells induced by a T cell adjuvant, lentinan.

PGE and PGF release from peritoneal exudate cells was studied in mice after injection with two beta (1-3) glucans, the antitumor active lentinan and the inactive pachyman, 4 days after injection of both polysaccharides, the spontaneous and phagocytosis-induced PGE and PGF release was markedly suppressed. However, only the immunopotentiator lentinan induced peritoneal exudate cells which exhibited a longer lasting diminished PG release. The data suggest that the T cell adjuvant lentinan may potentiate cellular immune responses by reducing synthesis of immune suppressive prostaglandins from peritoneal exudate cells.

Adjuvants, Immunologic↗