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Biomedical subjects

C Weinstock

Publications and source records attributed to C Weinstock.

At least 19 recordsLinked to original sources
PubMed1998

Similarities and differences of the immune response to exercise and trauma: the IFN-gamma concept.

Similar to physical fitness, fitness of the immune system requires training. Animals that have been raised under sterile conditions have a poor immune system and fail to thrive. "Immune training" is normally provided by contact with live microorganisms or immunizations. Increasing evidence has suggested that moderate sports can decrease the frequency of infections while excessive, exhausting exercise can lead to the opposite, a situation that has been described by a J-curve. Following prolonged exhausting exercise, a transient partial suppression of several immune functions can be shown, and it has been suggested that this period provides a window for invasion of microbes. On the basis of data showing that endotoxin-inducible interferon-gamma (IFN-gamma) production is virtually abrogated for a short period following excessive exercise, we present the hypothesis that the rigorous regulatory blockade of one of the ways of IFN-gamma induction may be critically involved in causing the transient immunosuppression following exhaustive exercise stress.

Animals↗
PubMed1998

Zinc, iron, and magnesium status in athletes--influence on the regulation of exercise-induced stress and immune function.

Intense physical exercise has been shown to be associated with immunosuppression and increased rate of infection. The immunosuppressive effect of exhaustive exercise has been attributed to a reduced helper/suppressor T-cell ratio, low salivary levels of immunoglobulin-A, decreased lymphocyte proliferative response and natural killer cell activity, and elevation of stress hormones. Yet some athletes can withstand intense training periods without health problems while others are prone to infections. Thus it has been postulated that other factors may interfere with immunoregulation. The notion that macro- and micronutrients are involved in the regulation of immunological processes and the ability to cope with muscular and systemic exercise stress has been gaining attention. Particularly trace elements have been shown to be related to cell mediated and humoral immunity such as NK-cell activity, T- and B-cell functions, and cytokine release. Many investigations have reported decreased concentrations of trace elements in blood and tissues after training and competition. However, the magnitude of losses is highly dependent on the type and intensity of exercise, the individual regulatory state, and most important, nutrition. This paper reviews the data on zinc, iron, and magnesium status in athletes and summarizes the consequences of deficiencies in these trace elements regarding exercise tolerance and immune function. These elements were chosen since there is evidence they are related to exercise-induced stress and immune function.

Animals↗
PubMed1997

Fas- or ceramide-induced apoptosis is mediated by a Rac1-regulated activation of Jun N-terminal kinase/p38 kinases and GADD153.

In the present study, we show that Fas receptor ligation or cellular treatment with synthetic C6-ceramide results in activation or phosphorylation, respectively, of the small G-protein Rac1, Jun N-terminal kinase (JNK)/p38 kinases (p38-K), and the transcription factor GADD153. A signaling cascade from the Fas receptor via ceramide, Ras, Rac1, and JNK/p38-K to GADD153 is demonstrated employing transfection of transdominant inhibitory N17Ras, N17Rac1, c-Jun, or treatment with a specific p38-K inhibitor. The critical function of this signaling cascade is indicated by prevention of Fas- or C6-ceramide-induced apoptosis after inhibition of Ras, Rac1, or JNK/p38-K.

Antigens, Surface↗
PubMed1997

Impaired production of cytokines in a case of human leishmaniasis.

A patient presented with the unique clinical picture of diffuse cutaneous and mucosal leishmaniasis caused by Leishmania tropica. Elevated serum levels of several cytokines including interleukin (IL) 2, interferon gamma (IFN-gamma), and tumor necrosis factor alpha were found. All cytokine levels returned to normal during therapy. No IL-10 or IL-4 levels were detectable. In whole blood cultures, induction of IFN-gamma by lipopolysaccharide (LPS) was completely negative, even after therapy. Concanavalin A (Con A)-induced release of IFN-gamma, like Con A-induced release of the other cytokines, was only initially impaired but returned to normal during therapy. Induction of the other cytokines by LPS was never impaired. The low expression of human leukocyte antigen DR on monocytes increased during IFN-gamma therapy but dropped when IFN-gamma treatment was ceased. We conclude that in this patient one or more of the routes of IFN-gamma production was impaired, thus resulting in insufficient IFN-gamma production in the infected lesions (although IFN-gamma was systemically present).

Adolescent↗
PubMed1997

Effect of exhaustive exercise stress on the cytokine response.

Fifteen athletes were investigated 24 h before, 1 h after, and 20 h after an exhaustive exercise stress test (mean duration 68 min). Testing for cytokines was done in serum, urine, and the supernatants of whole blood cell cultures, which were stimulated with lipopolysaccharide (LPS), concanavalin A (Con A), or phythaemagglutinin (PHA). Elevated levels of interleukin 6 (IL-6) and soluble IL-2 receptor (sIL-2R) were found 1 h after the run in both serum and urine samples. TNF-alpha in serum was also increased, whereas IL-2 in urine was decreased after the exercise. All other testings in serum and urine (including IFN-gamma) gave borderline or negative results. In cell cultures, the LPS-induced release of the inflammatory cytokines TNF-alpha, IL-1, and IL-6 was suppressed 1 h after exercise. Also, the Con-A-induced and LPS-induced release of IFN-gamma, and the PHA-induced release of IL-2 were suppressed 1 h after exercise. In contrast, Con-A-induced release of IL-2 was mildly increased after the run. We conclude that exercise of the intensity and duration described here causes an activation of the immune system, which is immediately counter-regulated. Twenty hours after the exercise, most of the observed changes were back to pre-exercise levels, indicating only a short duration for this suppressive counter-regulation.

Adult↗
PubMed1997

Essential fatty acids, immune function, and exercise.

The immunologic response to exercise comprises numerous alterations within the immune system, but how these processes are regulated is still largely unknown. Exercise-related immunological changes include signs of inflammation, such as release of inflammatory mediators, activation of various white blood cell lines and complement, and induction of acute phase proteins. Nevertheless, signs of immunosuppression, such as decreased T and B cell function or impaired cytotoxic or phagocytic activity, can also be observed. Some data suggest that essential fatty acids help regulate inflammatory processes, modulating both cytokine release and the acute phase response. Positive effects of changing dietary essential fatty acids have been demonstrated in chronic inflammatory diseases. In contrast, little is known about the contribution of fatty acids to the exercise-induced immunologic reaction. Essential fatty acids may determine alterations within the immune system following exercise. Therefore, future studies are necessary to evaluate the influence of the fatty acid composition on the inflammatory or immunosuppressive component following heavy exertion.

Acute-Phase Reaction↗
PubMed1994

The cytokine response to strenuous exercise.

Several groups have now investigated the cytokine response to strenuous exercise. In this article we try to summarize known data on this topic. Significant, albeit mild increases in plasma levels of the monokines IL-1, TNF-alpha, IL-6, and of soluble IL-2 receptor have been reported following strenuous exercise. Increased excretion of cytokines after exercise can also be shown in the urine of athletes. Modulation of cytokine release by strenuous exercise can also be demonstrated using in vitro cell cultures. Several authors have shown an increase in endotoxin-stimulated monokine release following exercise. In contrast, using whole blood cultures we found strongly depressed production of interferon gamma (in response to mitogen or endotoxin) following strenuous exercise. The potential significance of cytokine modulation for exercise-related immunological problems is discussed.

Cells, Cultured↗
PubMed1993

Prevention of endotoxin-induced monokine release by human low- and high-density lipoproteins and by apolipoprotein A-I.

Interaction of endotoxin (lipopolysaccharide [LPS]) with human lipoproteins is known to prevent the LPS-induced activation of human monocytes and release of cytokines (monokines). LPS was exposed to lipoprotein classes separated by ultracentrifugation and to apolipoprotein A-I. Then monocytes were added, and the LPS activation of monocytes was determined by measuring the induced monokines. Failure of LPS to induce monokine release was called LPS inactivation caused by lipoproteins or apolipoproteins. The LPS inactivation is shown to be a function of low-density lipoproteins. High-density lipoproteins inactivate LPS to a much lesser extent. The very-low-density lipoproteins cannot inactivate LPS. Lipid components seemed not absolutely required for LPS inactivation, because purified human apolipoprotein A-I without its physiological lipid complement also inhibits LPS-induced monokine release.

Adult↗
PubMed1992

The role of lipoproteins in the inactivation of endotoxin by serum.

The lipopolysaccharide (LPS)-induced release of cytokines from human monocytes can be prevented by previous interaction of serum with LPS. This inactivation is a function of lipoproteins. Here we show that LPS can be inactivated by low-density lipoproteins (LDL) as well as by high-density lipoproteins (HDL). The effects of heparin and EDTA on LPS inactivation by serum are also described.

Bacterial Toxins↗
PubMed1992

Low density lipoproteins inhibit endotoxin activation of monocytes.

Human serum and low density lipoproteins (LDLs) were shown to inactivate endotoxin (lipopolysaccharide [LPS]) by testing the effect of LPS interactions with serum or LDL on the activation of human monocytes. Sera and LDL preparations from four patients with familial hypercholesterolemia were used to demonstrate the inhibition of LPS from inducing interleukin-1 release. Before LDL removal by immunoapheresis, the patients' sera were able to inactive approximately fivefold more LPS than after LDL removal. The LPS-inactivating capacity lost during apheresis could essentially be retrieved in the LDL-rich eluate from the immunoadsorption columns. Because patients were treated frequently with immunoapheresis, their LDL levels before LDL removal were not markedly elevated. These patients' sera before LDL removal were shown to inactivate amounts of LPS comparable to those inactivated by the sera from three healthy volunteers. LDL prepared by ultracentrifugation showed similar LPS inactivation as LDL prepared by immunoapheresis. We conclude that the inhibition of LPS-induced monocyte activation by human serum is dependent to a large extent on the LDL fraction. LDLs were demonstrated to inhibit LPS from inducing interleukin-1 release by human monocytes.

Adult↗
PubMed1992

The role of lipoproteins in inactivation of endotoxin by serum.

Lipopolysaccharide (LPS)-induced release of cytokines from human monocytes can be prevented by previous interference of serum with LPS. This inactivation is a function of lipoproteins. Here we show that low-density lipoproteins as well as high-density lipoproteins can inactivate LPS. The effects of heparin and EDTA on LPS inactivation by serum are also described.

Cytokines↗
PubMed1985

Development of cell surface linkage complexes in cultured fibroblasts.

The possible role of a 140K membrane-associated protein complex (140K) in fibronectin-cytoskeleton associations has been examined. The 140K was identified by the monoclonal antibody JG22E. Monoclonal and polyclonal antibodies to the 140K showed identical patterns of binding to the cell membranes of fixed and permeabilized chicken embryonic fibroblasts; localization was diffuse, but with marked concentration in cell-to-extracellular matrix contact sites. Correlative localization with interference reflection microscopy and double-label or triple-label immunofluorescence showed that 140K co-distributed with extracellular fibronectin fibrils and intracellular alpha-actinin in microfilament bundles at extracellular matrix contact sites but tended not to co-localize with tropomyosin present in bundles at sites farther from adhesion sites. In addition, binding of antibodies to 140K, alpha-actinin, and fibronectin was excluded from vinculin-rich focal adhesion sites at the cellular periphery. A progressive development of cell surface alpha-actinin-140K-fibronectin associations was observed in early spreading cells. The anti-140K monoclonal antibody JG22E inhibited the attachment and spreading of both normal and Rous sarcoma virus-transformed chicken embryonic fibroblasts to a fibronectin substratum. However, the anti-140K monoclonal antibody became a positive mediator of cell attachment and spreading if it was adsorbed or cross-linked to the substratum. Our results provide the first description of a membrane-associated protein complex that co-localizes with fibronectin and microfilament bundles, and they suggest that the 140K complex may be part of a cell surface linkage between fibronectin and the cytoskeleton.

Animals↗
PubMed1984

Psychophysiological aspects of cancer.

"Cancer" refers to carcinoma, sarcoma, lymphoma, and leukemia. Hans Selye, with his stress-adaptation theory, opened the door for the holistic conceptualization of disease. Gotthard Booth laid a solid basis for the demonstration of an often important psychobiological (holistic) aspect of cancer, and also an overall theory of spontaneous regression. Booth was also a leader in demonstrating that severe masked depression generally long precedes cancer. Sir MacFarlane Burnet demonstrated in 1970 in Immunological Surveillance the enormous power and complexity of the cellular immune system, which apparently carries out surveillance against, detects, invades, and destroys many cancer cells daily in the normal human body. Cancer is thus far from a one-way process. The connection of the defensive process to the cerebral cortex is largely a discovery attributable to Selye, and to several Russian scientists. The course and outcome of cancer are notoriously unpredictable when age, sex, and lesion and spread are known. Two surgeons, Everson and Cole, in 1966 thoroughly documented 176 cases (previously published) of histologically proven untreated cancer which underwent proven so-called spontaneous regression. Several investigators, without known contradiction, have found that depression quite regularly long precedes cancer. "Spontaneous" regressions are basic.

Cerebral Cortex↗