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K Kitz

Publications and source records attributed to K Kitz.

68 records · Page 4Linked to original sources
PubMed1984

Serum antibodies against glycosphingolipids in chronic relapsing experimental allergic encephalomyelitis. Demonstration by ELISA and relation to serum in vivo demyelinating activity.

Sera from guinea pigs with spinal cord-induced chronic relapsing experimental allergic encephalomyelitis (crEAE) were tested for IgG antibodies against glycosphingolipids (GSL; galactocerebroside, ganglioside GM1, sulfatide) by an enzyme-linked immunosorbent assay and for in vivo demyelinating activity by infusion into the lumbosacral subarachnoid space of normal rats. In chronic stage-crEAE sera (40-200 days after sensitization) a high incidence (21/26) and high titers (up to 1:2560) of antibodies against one or more GSL coincided with a high incidence (22/26) of in vivo demyelinating activity. These results suggest an involvement of antibodies against various GSL in the process of demyelination.

Animals↗
PubMed1983

In vivo demyelinating activity of sera from animals with chronic experimental allergic encephalomyelitis. Antibody nature of the demyelinating factor and the role of complement.

Sera from guinea pigs and rats with chronic experimental allergic encephalomyelitis were injected into the cerebrospinal fluid (CSF) of normal recipient rats. Guinea pig sera induced demyelination in the central and (or) peripheral nervous system, whereas injection of rat sera resulted in demyelination in the peripheral nervous system only. Control sera did not induce demyelination. Demyelinating activity in guinea pig sera was confined to the IgG-fraction; in rat sera the IgG- as well as the IgM-fraction were able to induce demyelination. The demyelinating activity was abolished when the sera were absorbed with with sensitising antigen (guinea pig spinal cord tissue) or when immunoglobulins were removed from the sera. When chronic EAE sera from rats were injected into the CSF of rats, complement was not required for the induction of demyeLination. The presence of complement, however, augmented the demyelinating activity. Decomplemented chronic EAE sera from guinea pigs failed to induce demyelination after injection into the CSF of rats. Injection of control and non-demyelinating or demyelinating EAE sera into the subarachnoid space of normal recipient rats induced a weak inflammatory response with increased numbers of large mononuclear cells in the meninges. It is discussed that in vivo a complex interaction of antibodies, complement and effector cells is responsible for induction of demyelination.

Animals↗
PubMed1982

Antibodies-restricted heterogeneity in serum and cerebrospinal fluid of chronic relapsing experimental allergic encephalomyelitis.

An animal model which might help to study multiple sclerosis has long been sought. With chronic relapsing experimental allergic encephalitis (EAE), the search seems to have brought hope and evidence of comparable pathology whether concerned with clinical or neuropathological results, but no study of the cerebrospinal fluid (CSF) electrophoretic pattern has been made so far. A new sensitive method enables to study the CSF proteins: unconcentrated CSF proteins after agar gel electrophoresis are stained with silver reagents. The silver technique allows to follow the evolution of the inflammatory reaction in chronic relapsing EAE as well as in the acute form of EAE. This technique provides an additional approach to the study of EAE and an argument in favor of chronic relapsing EAE in guinea pigs as a model for multiple sclerosis.

Animals↗
PubMed1981

Fractionation of spinal cord tissue affects its activity to induce chronic relapsing experimental encephalomyelitis.

Chronic relapsing experimental allergic encephalomyelitis (EAE), an animal disease closely resembling multiple sclerosis, was induced in young guinea pigs by sensitization with guinea pig spinal cord tissue together with complete Freund's adjuvant and a high amount of mycobacterium tuberculosis. Sensitization of animals with myelin basic protein leads to an acute form of EAE, but not to a chronic demyelinating disease. The present study was designed to trace the factors of spinal cord tissue responsible for chronic disease and demyelination by using fractionated spinal cord tissue for sensitization. The following preparations were tested for encephalitogenic activity: a) total guinea pig spinal cord homogenized in chloroform/methanol (C/M), b) C/M residue (protein fraction), c) C/M extract (lipid fraction) and d) bovine brain gangliosides. C/M treated spinal cord preparations were less encephalitogenic as compared to untreated spinal cord. The protein fraction showed very little encephalitogenic activity, the histological changes were limited to perivascular inflammation without demyelination. A crude lipid fraction induced some chronic inflammation. Neither the purified lipid fraction nor gangliosides produced any EAE symptoms. The conclusion can be made that protein is necessary for the induction of chronic relapsing EAE, whereas lipid or a protein-lipid complex seems to be responsible for the demyelinating component of this disease.

Animals↗
PubMed1981

Isolated leptomeninges of the spinal cord: an ideal tool to study inflammatory reaction in EAE.

Isolated and stretched leptomeninges have several advantages for the study of basic mechanisms in inflammation of the CNS. They offer a three dimensional view of the vascular tree which has basically the functional characteristics of cerebral vessels (the tight barrier, excluding macromolecules to enter the CNS compartment). The limited, small thickness of the specimen facilitates the performance of histochemical and immunohistochemical methods.

Animals↗
PubMed1981

In vivo effect of sera from animals with chronic relapsing experimental allergic encephalomyelitis on central and peripheral myelin.

Sera from guinea pigs with acute or chronic relapsing experimental allergic encephalomyelitis (EAE) were injected into lumbosacral subarachnoid space of normal recipient rats. Seventeen of 37 sera induced demyelination in the CNS, and 27 of 37 sera caused demyelinated peripheral nerve fibers in the roots. The highest incidence of demyelinating activity of EAE sera was noted in those from donor animals sampled during the early chronic stage of the disease [40--100 days post sensitization (dps)]. Only few sera from animals sampled during the acute and subacute stage (10--40 dps) were able to induce demyelination. Sera from animals sampled between 100 and 200 dps showed a lower incidence of demyelinating activity as compared to those from the early chronic phase of the disease. There was no clear-cut correlation between the serum-demyelinating activity and the severity of the demyelinating disease in the donor animals. The patterns of demyelination in the central as well as peripheral nervous system of recipient animals were characterized by vesicular disruption of myelin or myelin stripping. Myelin degradation was performed mainly be macrophages. In the CNS some astrocytes also contained debris. Astrocytes increased in size, and mitosis of astrocytes was observed. Oligodendrocytes appeared to be unaffected. No demyelination was found when the sera from animals sensitized with CFA alone or with guinea pig liver tissue were injected into the subarachnoid space of normal recipient rats. Two possible mechanisms of demyelination are discussed: Antibody-mediated complement-dependent and antibody-dependent cell-mediated demyelination.

Animals↗
PubMed1981

Histogenesis of demyelinating lesions in the spinal cord of guinea pigs with chronic relapsing experimental allergic encephalomyelitis.

Spinal cord lesions in Hartley guinea pigs with chronic relapsing experimental allergic encephalomyelitis (EAE) were studied by light, transmission and scanning electron microscopy at different stages of the formation of demyelinated plaques. In addition the inflammatory response in the meninges was studied in isolated pia mater preparations separated from the spinal cord surface. In initial chronic lesions in the spinal cord, inflammation was restricted to penetrating parenchymal veins of the spinal cord and meninges. With the formation of large demyelinated plaques in the spinal cord, massive fibrosis of the meninges with infiltration by inflammatory cells was noted in an area covering the surface of the lesion. In plaques which reach the spinal cord surface, inflammatory cells could be seen passing between the pia and the spinal cord substance. In chronic remyelinated lesions, adhesions between meningeal fibroblasts and the astroglial limiting membrane were seen. In addition a topographical correlation between the distribution of spinal cord veins and venules and demyelinated plaques was found. These observations indicate that spinal cord lesions in chronic relapsing EAE are initiated by perivenous inflammation in the parenchyma and the meninges. Plaque formation, especially in spinal cord surface lesions, is additionally enhanced by the entrapment of inflammatory cells in the fibrosed meninges. The exchange of macrophages through the glia-limiting membrane may be responsible for the more rapid debris removal in the spinal cord in comparison with brain lesions in chronic relapsing EAE.

Animals↗
PubMed1979

Effect of different preparation procedures on the ultrastructure of gonococci.

Culture samples of Neisseria gonorrhoeae and Escherichia coli were studied by transmission and electron microscopy to evaluate the effect of different preparation procedures on the pilation of these organisms. Unfixed as well as fixed bacteria showed only few, long, filamentous appendages when investigated in ultrathin sections, negatively stained specimens, or critical-point dried preparations. Snap-frozen specimens of E. coli showed many short and thin pili after being shadowed with carbon and platinum whereas those of N. gonorrhoeae showed only some type-C-like pili. Thus, the number and morphological appearance of pili appear to be greatly influenced by the preparation techniques used for study by electronmicroscopy. Conclusions as to the type and the infectivity of a bacterial strain can, therefore, not be based on purely morphological criteria.

Bacteriological Techniques↗
PubMedDate not supplied

The development of periventricular lesions in chronic relapsing experimental allergic encephalomyelitis in guinea-pigs: a light and scanning electron microscopic study.

Periventricular lesions in the centrum semiovale are the most frequent changes in the brain in chronic relapsing experimental encephalomyelitis in guinea-pigs. They are generally distributed symmetrically at the lateral angle of the ventricular wall. The number of lesions and their size increases in anterior-posterior direction. Typically periventricular lesions in the later chronic stages are similar to those in multiple sclerosis. Earlier lesions generally originate in the depth of the white matter and secondarily, by extension, reach the ventricular surface. Lesions developing at later stages after sensitization may also originate from the ventricular wall and extent into the centrum semiovale. In these latter, severe structural changes in the ventricular ependyma may generally be found. Increased intracranial pressure in these animals may be one of the possible mechanisms leading to the peculiar topographical distribution of the periventriuclar lesions.

Animals↗