Purified preparations of the esterase derived from the first component of complement (C'1 esterase) increased vascular permeability in guinea pig skin, an effect inhibited by triprolidine, an antihistaminic agent, but not by soy bean trypsin inhibitor. The permeability-increasing and esterolytic properties of C'1 esterase were inhibited in parallel by the serum inhibitor of C'1 esterase, diisopropylphosphofluoridate and extremes of temperature and pH. Moreover, the permeability-increasing and esterolytic properties evolved in parallel when C'1 esterase was generated from its subcomponents. How C'1 esterase induces changes in vascular permeability remains unexplained, although the possibility that its action is mediated through a histamine-like agent is attractive.

https://rupress.org/jem/article-pdf/118/5/681/1081240/681.pdf

Complement as a mediator of inflammation. enhancement of vascular permeability by purified human c'1 esterase.

Skin transplanted as a homograft from one animal to a genetically dissimilar animal of the same species is rejected after nine to twelve days, probably because of actively acquired immune reactions (Medawar 1944, 1945; Billingham, Brent and Medawar 1954; Billingham, Brent, Medawar and Sparrow 1954). The acquired resistance is termed either transplantation immunity (Billingham, Brent and Medawar l956a) or, when occurring after homologous transplants, homograft sensitivity (Lawrence 1959). Homograft sensitivity may be revealed in a number of different ways. The most usual test is to apply at a later date to that sensitised host, a second skin graft, either from the same donor or from another member of the same inbred strain. Induced sensitivity is manifested by the earlier rejection at five to six days of the second-set graft, compared with nine to twelve days for the first-set graft (Medawar 1944; Billingham, Brent and Medawar 1954). Other tissues may be used to sensitise a host, provided the tissue contains nucleated cells. Medawar ( 1946a) found that injections of homologous leucocytes, but not homologous red blood corpuscles, would evoke transplantation immunity in rabbits. Subsequently it was shown with inbred strains of mice that, whereas the injection of isolated nuclei prepared from spleen, thymus and kidney cells would each evoke sensitivity to donor tissue, the injection of concentrated suspensions of cytoplasm obtained from liver and kidney cells would not do so (Billingham et a!. l956a). These workers concluded that the substances responsible for inducing transplantation immunity reside principally in the nuclei of cells. Makinodan, Gengozian and Albright (1958) reached a similar conclusion using red marrow cells, and they produced evidence that the antigens evoking the immunity were principally in the nucleated red and white blood cells of the marrow. This conclusion has, however, been challenged by Santos, Cole and Garver (1959). The transplantation of fresh homologous cartilage does not apparently evoke sensitivity to donor tissue. Craigmyle (1958) found that the implantation into rabbits of two hundred milligrams of diced homologous cartilage from the same donor on two occasions did not usually elicit transplantation immunity. Peacock, Weeks and Petty (1960) were also unable to produce transplantation immunity in mice after the insertion of relatively enormous cartilage homografts. The explanation may be that the matrix of cartilage prevents the transplantation antigens of chondrocytes from reaching the tissue fluids of the host in sufficient amounts to evoke transplantation immunity. There is only one published report of the capacity of bone to elicit transplantation immunity, by Chalmers (1959), who transplanted homografts of fresh iliac bone from hooded rats intramuscularly into Wistar rats; three weeks later a skin graft obtained from each donor was applied to the corresponding recipient. The second-set skin homografts underwent an early rejection at five to six days compared with a mean survival time of 109 days for the first-set homografts of skin. Chalmers concluded that homografts of iliac bone will evoke transplantation immunity and that the tissue antigens of iliac bone which evoke immune responses in their hosts have antigens in common with skin. Furthermore, freeze-drying altered the tissue antigens in iliac homografts, because subsequent skin grafts from the same donor did not undergo early rejection but survived slightly longer than the first-set skin homografts; this Chalmers called an “enhancement effect.”

Studies in the transplantation of bone. V. The capacity of fresh and treated homografts of bone to evoke transplantation immunity. 1963.

SUMMARY A lethal mixture of the three factors (I, II, III) of anthrax toxin had none of the following enzyme activities: adenosine triphosphatase, alkaline or acid phosphatase, catalase, collagenase, ribonuclease, desoxyribonuclease, gelatinase, hyaluronidase, lecithinase, lipase, proteinase. The mode of action of anthrax toxin is unknown. Although factor II is the only factor which is immunogenic when injected alone, the addition of factor I results in an increased immunizing activity; however, the activity of this mixture can be decreased by adding factor III. The possible effect of these results on preparations used to immunize against anthrax is discussed.

/pdf/the-three-factors-of-anthrax-toxin-their-immunogenicity-and-4vmd7692of.pdf

The Three Factors of Anthrax Toxin: their Immunogenicity and Lack of Demonstrable Enzymic Activity

The induction of permeability-increasing activity in human plasma by activated hageman factor.

The wide variety of reactions covered by the term “acute inflammation,” and the great number of reports of inflammation-like effects initiated by preparations from blood and tissues excuse any attempt to cover the field in this paper. Also, mediators of inflammation have been exhaustively discussed in recent reviews.IJ Of many of the mediators proposed, little more can be said than that they had some effect or other on blood vessels, and had the chemical precipitability and the nondialysability of large molecules. Some have been extracted, by rather strenuous means, from tis sue^.^-^ Their significance is usually dubious for severa1 reasons, of which two may be mentioned. When they are found in a11 tissues examined, it often appears that they were derived from the contained blood; and when they occur only in certain organs, like kidneys or testes,8 they have only a remote claim to consideration as mediators of inflammation in general. This paper, therefore wili be confined largely to the more extensively investigated blood substances. The inflammatory effects to be accounted for may be ranged in an order that corresponds roughly to the strength of the injury required to induce them. One siich order would be: changes in caliber and reactivity of the biood vessels; alteration in the properties and topography of the endothelial cells; increased permeability to plasma proteins; the diapedesis of leukocytes; increased fragility of the vessel walis; and, with severe injury short of immediate destruction of the tissue, stasis of the biood within the vessels-a change which appears to be closely associated with subsequent necrosis of the inflammed tissues. Little is known of the mediation of a phenomenon like stasis, and what is known of large moiecular mediators of the emigration of leukocytes is dealt with by Hurley. At this stage we may note that there appears to be no necessary connection between the changes that let proteins and those that let leukocytes go through a given part of the vessel wall. This leaves increased permeability to plasma proteins-an event obviously of major importance in the inflammatory reaction. We should make a correspondingly major contribution to our understanding of inflammation if we could solve its mechanism. Macromolecular mediators are usually envisaged as being part of a chain of activation whose end is a micromolecule, immediately responsible for the inflammatory event in question-the “immediator,” as it were. That a substance increases permeability tells us little on this point, since the test is made in the tissues of an animal that contain ali the ingredients for the eiaboration of the final mediator; and it may, at the outset, be hard to decide just where the substance lies in the chain of causation between injury and effect. In some types of injury, we appear to have pinpointed a micromolecule, such as histamine, as the final mediator; and in other types, we shall probably find other micromolecules. There is, however, no good reason why a large molecular substance should not be an immediator; for example, a depolymerizing enzyme acting on the basement membrane so as to alter its porosity. and thus increase vascular permeability.

Large molecular substances as mediators of the inflammatory reaction.

Enzyme-Like Globulins from Serum reproducing the Vascular Phenomena of Inflammation. V. Activable Permeability Factor in Human Serum.

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Enzyme-Like Globulins from Serum reproducing the Vascular Phenomena of Inflammation. V. Activable Permeability Factor in Human Serum.