Carboxymethylglucan (CMG) in two different degrees of substitution of carboxymethyl groups (0.56 and 0.89) was administered to cyclophosphamide (CY) treated (200 mg/kg) C57B1/6 mice in three doses (10, 50, and 100 mg/kg) 24 h after CY. The influence of CMG administration on the cell suppression caused by CY was observed in the subsequent days. The cellularity of spleen, bone marrow and peripheral blood was quantified on days 2, 5, 8, 11, 15, and 21 after CY treatment. CY treated mice developed a significant decrease in peripheral blood cell counts, and spleen and bone marrow cellularity during the initial 5 days, followed by recovery in the next 15 days, with an overshoot reaction in spleen cellularity and erythrocyte levels. The initial cellularity depression and the following recovery was modified by both carboxymethyl derivatives of glucan. Cyclophosphamide treated mice exhibited less pronounced immunosuppression and more rapid hematopoietic recovery when administered with CMG, although this reaction was only of a modest degree. The effects were not dose dependent and the differences between the two glucans were not significant.

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[Relation and interactions between the immune and neuroendocrine systems].

For far too long, the immune system has been viewed in isolation from the rest of the body's organ system. But now it is clear that the immune system is an integral part of the organ and physiological systems of whole organism. Especially, the immune and endocrine systems share many ligands and receptors that result in constant and important bidirectional communication. A new and important function for the immune system is to serve as a sensory organ for noncognitive stimuli such as infectious agents and tumours. On the other hand the neuroendocrine system can perform important immunoregulatory activities. It also suggest that brain is not more an immunologically privileged site. Recent studies provide a new view of immunoreactivity to antigens from the nervous system and to immune and inflammatory responses in brain. These may be influenced both by the circulating cytokines derived from the immune system and/or those endogenously produced within the neuroendocrine system. There is a growing body of evidence that cytokines are an integral part of the central nervous system with an important neuromodulatory role in neural mechanisms regulating stress responses, hormonal changes and various kinds of behavior. The mutual informatory circuit inside of the immune, nervous and endocrine systems suggest that they all form the superinformation system with pivotal regulatory role in living organisms. Overall, the recognition of the immune system as our sixth sense may ultimately provide the new understanding of physiology required for successful diagnostic and therapeutic programs against disease and stress involving immune-neuroendocrine communication. (Tab. 5, Ref. 35.)

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[Prionoses--neurodegenerative diseases caused by prions, offectious proteinaceous molecules].

Prionoses are a group of human and animal neurodegenerative diseases caused by prions, infectious pathogens that differ from bacteria, fungi, parasites, viroids, and viruses. Despite intensive searches over the past three decades, no nucleic acid has been found within prions and considerable experimental data argue that prions are composed exclusively of proteins (glycoproteins). Normal prion protein (PrPC) is encoded by a gene present in all nuclear cells of humans and other mammals but is constitutively expressed mainly in neurons. PrPC is protease sensitive and nonpathogenic but it can be modified to the pathological and protease resistant form designated PrPSC which is essential for infectivity. Prion diseases are manifested as infectious, genetic, or sporadic disorders and are also named as transmissible spongiform encephalopathies (TSE). TSE culminate with a progressive and fatal degeneration of the CNS. The human prionoses include Creutzfeldt-Jakob disease (CJD), kuru, Gerstman-Sträussler-Scheinker syndrome (GSS), and fatal familial insomnia (FFI). In mammals, more than 15 different species have been described to suffer from prion disorders till now. Scrapie of sheep and goats is the oldest and the most studied of the prion diseases. Bovine spongiform encephalopathy (BSE) and transmissible mink encephalopathy are thought to result from the feeding of scrapie-infected animal products, whereas BSE has been identified in transmission to mice, domestic cats, two exotic species of ruminant, and monkey. More than 20 cases of clinically and pathologically atypical form of CJD, referred to as "new variant" CJD (vCJD) have been recognized in unusually young people in the United Kingdom. There is a strong evidence that the same prion strain is involved in both BSE and vCJD. It suggest the breaking of species barrier which results by spreading of BSE to humans, putatively by dietary exposure. Understanding the function of prion proteins and their modification to the pathological form may give new insight into the etiologic and pathogenic mechanisms also other diseases caused by aberrant proteins, including Alzheimer' disease, amyotrophic lateral sclerosis, and Parkinson's disease. (Tab. 4, Fig. 3, Ref. 76.)

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