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At least 235 records · Page 13Linked to original sources
PubMed1985

A synthetic nonapeptide corresponding to the NH2-terminal sequence of C3d-K causes leukocytosis in rabbits.

Numerous biologically active fragments have been described that are derived from the C3 molecule. Recently, a polypeptide (Mr 41,000) generated from the alpha chain of human iC3b by limited proteolysis with plasma kallikrein was shown to exhibit several biological functions. This C3-derived cleavage product, C3d-K, suppresses mitogen- and antigen-induced proliferation of human T-lymphocytes and induces leukocytosis in rabbits. We have identified and synthesized a portion of C3d-K that is associated with the leukocytosis phenomenon. A nonapeptide corresponding to the amino-terminal nine residues of C3d-K was synthesized using conventional Merrifield solid-phase peptide chemistry; the structure of this peptide is Thr-Leu-Asp-Pro-Glu-Arg-Leu-Gly-Arg (TLDPERLGR). At a final concentration of 4 X 10(-6) M, both the nonapeptide and the des-Arg octapeptide (TLDPERLG) were capable of inducing leukocytosis in rabbits. Additionally, both peptides enhance vascular permeability when injected in guinea pig skin. These activities are similar to those previously attributed to a C3 fragment identified as C3e by Ghebrehiwet and Müller-Eberhard (Ghebrehiwet, B., and Müller-Eberhard, H.J. (1979) J. Immunol. 123, 616-621). We conclude that the nonapeptide TLDPERLGR represents the active center of the C3-derived leukocytosis factors C3e and C3d-K. This active synthetic analogue of C3d-K should prove valuable in elucidating the mechanism of action for complement-dependent leukocyte mobilization in vivo.

Amino Acid Sequence↗
PubMed1985

Bronchoalveolar lavage in patients with the adult respiratory distress syndrome.

BAL in patients with ARDS provides material containing the soluble and cellular constituents of the alveolar compartment, and hence is a useful tool for the study of the pathogenesis of ARDS. The technique is imperfect as it is prone to problems of data acquisition and interpretation. However, it is lung-specific and may be used in serial studies of patients over the course of their disease. A large amount of evidence is rapidly being accumulated which documents the presence of effectors of inflammation in the BAL fluids of patients with ARDS. Confirmation of the importance of such mediators, pathways, or cellular constituents of BAL fluid in establishing the pathogenesis of ARDS ultimately depends upon proof of the efficacy of specific clinical interventions which both arrest the activity of the effector and predictably alter the course of the disease.

Capillary Permeability↗
PubMedDate not supplied

[Initial results of the clinical use of the immunostimulant bestatin (3-amino-2-hydroxy-4-phenylbutyryl leucine) in patients with chronic polyarthritis].

We tested the efficacy of the immunomodulator Bestatin, which has been successfully applied in Japan, in a preliminary open study in ten patients with classical or definite rheumatoid arthritis. Patients whose arthritis was characterized by a low humoral activity showed a partial remission of the disease after six months' application of increasing doses of 10-60 mg in 48 hours. We found a significant increase in superoxide release from peripheral monocytes. Humoral parameters of inflammation such as erythrocyte sedimentation rate, C3a complement fraction, prostaglandin E2, and thromboxane B2 decreased. Concerning the subpopulations of lymphocytes we found a slight increase of activated T-lymphocytes and a decrease of O-cells and B-cells. The T-helper/T-suppressor ratio remained unchanged. The rheumatoid factor and the antinuclear antibodies showed no alteration under the treatment. Two weeks after withdrawal of Bestatin the improvement of the clinical and humoral parameter of the inflammation in rheumatoid arthritis vanished. No serious side effects were seen. Our results contribute to a long-term controlled study of the immunomodulator Bestatin as basic drug in the treatment of rheumatoid arthritis.

Adjuvants, Immunologic↗
PubMed1981

Human C5a des Arg increases vascular permeability.

C5a were generated in human plasma by incubation with zymosan in the presence of a carboxypeptidase B inhibitor. The carboxypeptidase inhibitor was added to prevent cleavage of the carboxyl terminal arginine from C5a and enabled it to be purified on the basis of spasmogenic activity on the guinea-pig isolated ileum. When injected into rabbit skin, purified C5a induced marked plasma leakage over a 30-min period, but only if the substance was first mixed with a vasodilator substance such as prostaglandin (PG)E2. The responses to C5a + PGE2 did not appear to be related to anaphylatoxic, histamine-releasing activity because an antihistamine, mepyramine, had only a small effect on plasma leakage. Further, removal of the carboxyl terminal arginine by carboxypeptidase B abolished activity on the ileum but not in the skin. The observation that both human C5a and C5a des Arg were able to increase vascular permeability in vivo suggested a parallel with leukotactic activity in vitro. In support of this, no responses to C5a + PGE2 were obtained in rabbits depleted or circulating polymorphonuclear leukocytes. Thus, inflammatory edema resulting from extravascular complement activation may be dependent on 2 components: a leukocyte/endothelial cell interaction triggered by C5a, and the concomitant generation of a vasodilator, prostaglandin.

Anaphylatoxins↗
PubMed1984

Pathophysiologic mechanisms of allergic and pseudo-allergic reactions to foods, food additives and drugs.

Allergic or pseudo-allergic reactions elicited by per os intake of foods, food additives or drugs may be based on one or several of the following immunopathologic mechanisms: 1) specific IgE bound to mast cells and/or basophils; 2) antigen-IgE soluble complexes hitting various target cells; 3) antigen-IgG complexes generating anaphylatoxins; 4) generation of anaphylatoxins by alternate pathway complement activation; 5) release of mast cell mediators by other direct triggering mechanisms (e.g., basic peptides, peptones); 6) effects on other target cells such as neutrophils and platelets; 7) reactions mediated by specific effector lymphocytes. While allergic reactions in a classical sense involve a sensitization process leading to the formation of specific immunologic agents such as antibodies or specific T lymphocytes, pseudo-allergic reactions appear to involve the same inflammatory mediators which are formed and/or released through different mechanisms and without the necessity for specific sensitization. The complexity of the phenomena possibly involved continues to create great difficulties in the objective diagnosis of food allergy.

Anaphylatoxins↗
PubMed1984

Role of complement in the immune response.

Evidence has accumulated that shows that fragments of C3 are potent inhibitors of immune responses. A low-molecular-weight fragment of C3 and fragments possessing leukocyte-mobilizing activity have been shown to block both antigen- and mitogen-induced human T cell proliferation, and to block mixed lymphocyte culture responses and the generation of cytotoxic lymphocytes. The same fragments inhibit the development of secondary in vitro antibody responses of rat lymphocytes. C3b can be shown to inhibit the polyclonal activation of human lymphocytes by pokeweed mitogen, but it has no effect on T cell proliferation or on the generation of cytotoxic T cells. We now propose that different C3 fragments selectively act on various lymphocyte subsets and thus play a profound role in regulating both immune effector functions and the intensity of the immune response.

Animals↗
PubMed1982

Stimulation of the intracellular killing of Staphylococcus aureus by monocytes: regulation by immunoglobulin G and complement components C3/C3b and B/Bb.

The intracellular killing of Staphylococcus aureus by human monocytes requires continuous stimulation by extracellular serum factors interacting with the cells via membrane binding sites. At least 75% of the intracellular killing in the presence of fresh serum was accounted for by the combined stimulatory activities of IgG, C3/C3b, and B/Bb. C3b is a more potent stimulator than C3, and Bb stimulates the killing to the same degree as B. The stimulation of intracellular killing by C3 and C3b occurs by interaction of the stable binding site of this molecule with the C3b receptor in the monocyte membrane. The stimulation of intracellular killing by B and Bb is most probably mediated via a binding site on these proteins interacting with a receptor site in the monocyte membrane. Both complement receptors, i.e., for C3b and B, are pronase sensitive. However, only the C3b receptor can be inhibited by (Fab')2 fragments of anti-C3 receptor antibodies, indicating that the binding sites for C3/C3b and B/bb are different.

Blood Bactericidal Activity↗