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PubMed2001

Cutting edge: myeloid complement C3 enhances the humoral response to peripheral viral infection.

HSV-1 is the causative agent of cutaneous lesions, commonly referred to as cold sores. Primary exposure to the virus ordinarily occurs through the periphery, in particular through abraded skin or mucosal membranes. Under certain circumstances (e.g., in neonatals or AIDS patients), the infection becomes disseminated, often with severe consequences. Spread of HSV-1 is limited by virus-specific Ab. The development of an efficient humoral response to the virus is dependent on innate immunity component complement C3. The liver is the major source of C3, but there are also extrahepatic origins of C3 such as lymphoid macrophages. In the present study, the significance of C3 synthesis by bone marrow-derived cells was assessed by the transfer of wild-type bone marrow into irradiated C3-deficient mice. Using these chimeric mice, extrahepatic C3 was determined sufficient to initiate specific Ab and memory responses to a peripheral HSV-1 infection.

Animals↗

PubMed1989

Non-invasive tracking of peripheral ventilatory response to carbon dioxide.

We propose a new method for quantifying the ventilatory sensitivity of the peripheral chemoreceptors to changes in CO2 through analysis of the natural breath-to-breath variations in ventilation (y) and alveolar PCO2 (x). This technique is truly non-invasive in that the need for administering CO2-enriched mixtures is circumvented, and peripheral chemosensitivity is assessed while the respiratory control system operates in its normal eucapnic state, unperturbed by external interventions. The method is based on solution of the inverse problem relating the cross-correlation between alveolar PCO2 and ventilation changes, and the autocorrelation of changes in alveolar PCO2. Tests are performed using simulated data generated by a closed-loop respiratory control model. The impulse response of the controller and the convective delay between lungs and chemoreceptors are estimated from the data. Subsequently, the best exponential fit to the estimated impulse response yields values for the effective controller gain (G) and the associated time constant of the response. The estimates of G contain a small contribution from the control chemoreflex gain; however, the relation between changes in G and changes in peripheral gain remains unaltered. The effects of other details in the computation procedure, such as length of data sequence, maximum number of correlation lags and starting lag number, are also investigated.

Carbon Dioxide↗

PubMed1988

Effects of ketotifen on the responsiveness of peripheral blood lymphocyte beta-adrenergic receptors.

The effects of ketotifen therapy on the responsiveness of lymphocyte beta-adrenergic receptors was evaluated by measuring cyclic AMP elevations caused by isoproterenol in cells isolated from patients treated with ketotifen for more than 1 year. Binding of 3H-dihydroalprenolol to beta-receptors was also evaluated. The isoproterenol-induced rise in cyclic AMP relative to each individual's baseline level was greater in patients on current ketotifen therapy than in other asthmatic patients or non-asthmatic subjects. Ketotifen therapy increased the apparent equilibrium dissociation constant for specific 3H-dihydroalprenolol binding to the receptors. Receptor numbers in symptomatic asthma patients on standard drug therapy were decreased. The results indicate that long term ketotifen therapy is associated with increased responsiveness of beta-receptors to stimulation by catecholamines and that this alteration may involve changes in the receptors themselves, their membrane environment, adenylate cyclase or components of the adenylate cyclase coupling system.

Adolescent↗

PubMed1989

[Responsiveness of peripheral blood vessels to physiologically vasoactive agents in myocardial infarct].

Changes in skin vascular responsiveness (VR) to six vasoactive agents were examined in 25 patients with myocardial infarction during its acute period. In small myocardial infarction, there was a synchronous increase in all VR types on days 1-7 followed by its normalization on day 14. VR synchronization was also observed in transmural myocardial infarction, yet increased VR to vasoconstrictive agents such as noradrenaline, adrenaline, and angiotensin II remained until the end of the fourth week without showing a tendency to normalization. Abnormal VR was seen in the most severe fatal cases. The synchronous and cyclic VR changes observed in myocardial infarction were absent in patients with unstable angina that did not result in myocardial infarction.

Adult↗

PubMed1998

Influence of nitric oxide synthase inhibitors on the ACTH and cytokine responses to peripheral immune signals.

Nitric oxide (NO) is an unstable gas that participates in the response of the hypothalamic-pituitary-adrenal (HPA) axis to a variety of immune signals, including turpentine-induced tissue damage and the systemic injection of the pro-inflammatory cytokine interleukin 1-beta (IL-1beta). Studies that have investigated the role of this gas in the intact rat have relied on blockade of NO formation with the NO synthase (NOS) inhibitor N(omega)nitro-L-arginine-methylester (L-NAME). They have suggested that endogenous NO blunts the ACTH response to intravenous (i.v.) IL-1beta in part by exerting an inhibitory influence on the release of hypothalamic peptides such as corticotropin-releasing factor (CRF) from nerve terminals in the median eminence. It must nevertheless be noted that, at present, evidence for this mode of action remains circumstantial. Significant controversy remains regarding the specificity of the compounds used to block NO formation, the characteristics of their effect in terms of dose and timing of administration, the possibility that their effect is restricted to IL-1beta or can be expanded to other pro-inflammatory cytokines, and the question of whether the possibility that they might also influence ACTH release by altering circulating levels of tumor necrosis factor-alpha (TNF-alpha) and IL-6. The purpose of the present study was to elucidate these points. In the first series of experiments, we determined the i.v. IL-1beta-induced ACTH response to various doses of systematically injected L-NAME (1-100 mg/kg). At 10-100, but not 1 mg/kg, L-NAME significantly (P<0.01) augmented the ACTH response to IL-1beta, with a maximum effect observed at 30 and 100 mg/kg. At the 30 mg/kg dose, L-NAME was equally effective in augmenting the ACTH response when administered between 5 and 240 min prior to the cytokine. The effect of L-NAME was fully mimicked by equivalent doses of other arginine derivatives such as N(omega)-monomethyl-L-arginine (L-NMMA) or N(omega)-nitro-L-arginine (L-NNA), indicating that controversy in the published literature concerning the influence of NO on CRF secretion does not appear to be due to the use of different arginine derivatives. The ability of other cytokines such as TNF-alpha and IL-6 to release ACTH and corticosterone was significantly (P<0.01) augmented by blockade of NO formation in a manner similar to that found with IL-1beta. To test the hypothesis that L-NAME might alter ACTH secretion at least in part by modifying the secretion of pro-inflammatory cytokines, we measured plasma concentrations of TNF-alpha and IL-6 following endotoxin injection in the presence or absence of L-NAME. Blockade of NO formation reduced TNF-alpha but increased IL-6 levels in rats administered the lipopolysaccharide (25 microg/kg i.v.). As L-NAME augments the ACTH response to TNF-alpha as well as IL-6, it is improbable that changes in TNF-alpha and IL-6 secretion during immune stimulation represents an important mechanism mediating the inhibitory influence of endogenous NO on the HPA axis activity. Collectively, these results indicate that the systemic injection of L-NAME very quickly augments the stimulatory effect of pro-inflammatory cytokines on ACTH secretion, and does so for at least 4 h. Other arginine derivatives known to block the activity of constitutive NO syntheses, such as L-NMMA and L-NNA, exert an effect that is virtually identical to that of L-NAME. The ability of L-NAME to increase the ACTH response to i.v. IL-1beta is also observed in rats injected with TNF-alpha and IL-6. Because of the opposite effects of L-NAME on the levels of these two cytokines, the influence of arginine derivatives on ACTH release is probably not due to changes in cytokines produced during immune stimulation such as endotoxemia.

Adrenocorticotropic Hormone↗

PubMed2003

Distribution and mitogen response of peripheral blood lymphocytes after exertional heat injury.

To determine whether immune disturbances during exertional heat injury (EHI) could be distinguished from those due to exercise (E), peripheral lymphocyte subset distributions and phytohemagglutinin-stimulated CD69 mitogen responses as discriminated by flow cytometry were studied in military recruits [18.7 +/- 0.3 (SE) yr old] training in warm weather. An E group (3 men and 3 women) ran 1.75-2 miles. During similar E, 11 recruits (10 men and 1 woman) presented with suspected EHI. EHI (40.4 +/- 0.3 degrees C) vs. E (38.6 +/- 0.2 degrees C) body temperature was significantly elevated (P < 0.05). Heat illness was largely classified as EHI, not heatstroke, because central nervous system manifestations were generally mild. Blood was collected at E completion or EHI onset (0 h) and 2 and 24 h later. At 0 h (EHI vs. E), suppressor, natural killer, and total lymphocyte counts were significantly elevated, helper and B lymphocyte counts remained similar, and the helper-to-suppressor ratio was significantly depressed. By 2 h, immune cell dynamics between groups were similar. From 0 to 24 h, T lymphocyte subsets revealed significantly reduced phytohemagglutinin responses (percent CD69 and mean CD69 fluorescent intensity) in EHI vs. E. Thus immune cell dynamics with EHI were distinguishable from E. Because heat stress as reported in exercise or heatstroke is associated with similar immune cell disturbances, these findings in EHI contributed to the suggestion that heat stress of varying severity shares a common pathophysiological process influencing the immune system.

Adolescent↗

PubMed2005

Innate cell-mediated immune response and peripheral leukocyte populations in Atlantic salmon, Salmo salar L., to a live Cryptobia salmositica vaccine.

The effects of a live Cryptobia salmositica (Kinetoplastida) vaccine on the humoral and cellular immune response, and changes in the peripheral leukocyte populations of Salmo salar were investigated. The vaccine produced detectable parasitemia in the blood which peaked at 5 weeks post-vaccination (w.p.v). Antibodies were detectable at 4 w.p.v. and the antibody titer increased as parasitemia declined. Respiratory burst activity in vaccinated fish was significantly higher than in control fish; the highest activity occurred with rising parasitemia and lower activity with declining parasitemia. There was a significant increase in the proportion of granulocytes (to total leukocytes) at 4 w.p.v. At 6 w.p.v., the proportion of lymphocytes and monocytes increased significantly and remained elevated. These results demonstrate innate (respiratory burst activity and an increase in the proportion of granulocytes corresponding to rising parasitemia) and adaptive (antibody production and increases in the proportion of monocytes and lymphocytes corresponding to declining parasitemia) immune responses to the live vaccine.

Animals↗

PubMed1981

Inhibition of the proliferative response of peripheral blood lymphocytes to mycobacterial or fungal antigens by co-stimulation with antigens from various mycobacterial species.

Soluble antigen preparations from Mycobacterium leprae are reported to inhibit the response to other stimuli, of peripheral blood mononuclear cells from lepromatous leprosy cases (BL/LL) and also from tuberculoid cases (TT/BL) and normal donors. We confirm these findings and in addition, report that a similar suppressive effect is exerted by antigen from Mycobacterium vaccae, Mycobacterium nonchromogenicum and, to a lesser extent, Mycobacterium tuberculosis and Mycobactyerium kansasii. Moreover, suppression is seen using peripheral blood mononuclear cells from individuals unlikely to have encountered the organism used. The suppression is not due to toxicity of the antigen preparation, and is not indomethacin sensitive. It involves a cell found in the E-rosetting population, which loses its ability to suppress or be suppressed, after 48 hr in culture. Possible explanations include a pharmacological effect of cell wall peptidoglycolipids, or the triggering of suppressor cells specific for common mycobacterial antigens.

Antigens, Bacterial↗

PubMed2002

Dendritic cell-based proliferative assays of peripheral T cell responses to tetanus toxoid.

Antigen-specific proliferative responses of peripheral blood T cells are widely used in humans to study the T cell compartment. However, responses to autoantigens are often weak and poorly reproducible. Here we show, using a test recall antigen (tetanus toxoid), that absolute levels of proliferation, minimally detectable antigen doses, and/or ability to detect statistically significant responses can be enhanced using in vitro-generated autologous dendritic cells as antigen presenting cells.

Antigen Presentation↗

PubMed1994

In vitro glutathione supplementation enhances interleukin-2 production and mitogenic response of peripheral blood mononuclear cells from young and old subjects.

The effect of in vitro glutathione (GSH) supplementation on mitogenic response, interleukin-1, interleukin-2 and prostaglandin E2 production, and cellular GSH level in peripheral blood mononuclear cells (PBMC) from healthy young and old human subjects was studied. In vitro addition of GSH increased cellular GSH level (P < 0.001). Glutathione supplementation at concentrations between 2 to 10 mmol/L enhanced lymphocyte proliferation but at low concentrations (0.5 and 1 mmol/L) decreased mitogenic response. Glutathione-induced enhancement of lymphocyte proliferation due to phytohemagglutinin or concanavalin A was greater in the PBMC from old subjects than in those from young subjects. At optimal concentration (5 mmol), GSH increased interleukin-2 production (P < 0.05) and decreased prostaglandin E2 and leukotriene B4 production (P < 0.01) in both age groups. Furthermore, decreased PBMC mitogenic response by in vitro addition of prostaglandin E2 was reversed by GSH supplementation. Glutathione did not have an effect on interleukin-1 production by PBMC from young subjects; however, GSH supplementation tended (P = 0.08) to increase interleukin-1 production by PBMC from old subjects. We conclude that GSH supplementation enhances T cell-mediated mitogenic response in young and old subjects. This effect is due at least in part to decreased eicosanoid production.

Adult↗

PubMedDate not supplied

The lung parenchymal strip as a model of peripheral airway responsiveness.

Twenty-four patients scheduled for surgery for carcinoma of the lung were challenged with inhaled methacholine. A greater than 20% fall in the forced expiratory volume in 1 s (FEV1) was recorded in nine of these patients. The PD20 (dose of methacholine producing a 20% fall in FEV1) values ranged from 0.6 to 5.6 mumol methacholine. Following surgery, lung tissue was prepared as lung parenchymal strips for in vitro studies. There was no correlation between in vivo airway responsiveness to methacholine (PD20) and in vitro sensitivity as measured by the EC50 (the concentration of agonist producing half the maximal tension [Tmax]) for carbachol (r = -0.17; n = 16) or histamine (r = 0.23; n = 24). The variation in in vivo and in vitro responsiveness was not due to the presence of inflammatory cells in the peripheral lung tissue. Of the 38 lung parenchymal strips studied with histamine, 17 demonstrated a variable relaxation response at low concentrations followed by contraction at higher concentrations. The presence or absence of this relaxation response could not be explained in terms of variable proportions of airway or vascular smooth muscle.

Airway Resistance↗

PubMedDate not supplied

Cycling in the idiotypical proliferative response of peripheral blood lymphocytes in normal and Salmonella typhi-immunized rabbits.

A partially inbred rabbit was immunized with repeated intravenous administrations of Salmonella typhi during a two year period, and three antiidiotypic sera were prepared against anti-S. typhi antibodies. An idiotype which was detectable by a heterologous precipitation reaction with one of the antiidiotypic sera and which was associated with anti-S. typhi antibodies was found using a radiobinding inhibition test in the normal serum from all rabbits examined in the colony, but not in any of unrelated rabbits. Peripheral blood lymphocytes from the idiotypic proband rabbit showed a cycling in the proliferative response with all the three antiidiotypic sera. The response with two of the three antisera subsided following repeated immunizations, with concomitant decline in the idiotype level in the serum, whereas the response with other serum was observed even after the lapse of 6 months after the repeated immunizations, the idiotype persisting in the serum. Peripheral blood lymphocytes from normal rabbits of the colony also showed a fluctuation in the proliferative response with the antiserum against the cross-reactive idiotype and expressed at intervals a suppressive activity on the proliferative response when mix-cultured with the responding lymphocytes in the presence of the antiidiotypic serum.

Animals↗

PubMed2004

Cortisol and dehydroepiandrosterone affect the response of peripheral blood mononuclear cells to mycobacterial antigens during tuberculosis.

The effect of cortisol and/or dehydroepiandrosterone (DHEA) on the immune response to antigens obtained from Mycobacterium tuberculosis was studied in vitro by using peripheral blood mononuclear cells obtained from patients at various stages of lung tuberculosis (TB) and from healthy control people (HCo). The results obtained show for the first time that addition of cortisol within concentrations of physiological range can inhibit the mycobacterial antigen-driven proliferation of cells from HCo and TB patients and the production of interferon-gamma (IFN-gamma), indicating that endogenous levels of cortisol may contribute to the decreased lymphoid cell response to mycobacterium antigens observed in TB patients. DHEA did not affect lymphoid cell proliferation, IFN-gamma production and the cortisol-mediated inhibitory effects. Interestingly, we found that DHEA, but not cortisol, suppressed the in vitro transforming growth factor-beta production by lymphoid cells from TB patients with an advanced disease, which is indicative of a selective direct effect of this hormone.

Adjuvants, Immunologic↗

PubMed1981

Marek's disease as a model for the Landry--Guillain--Barré syndrome: latent viral infection in nonneuronal cells accompanied by specific immune responses to peripheral nerve and myelin.

In the chicken, Marek's disease virus (MDV) induces a demyelinating peripheral neuropathy that, early in the course of the disease, is histopathologically indistinguishable from that seen in the Landry--Guillain--Barré syndrome in man. A continuing role for a productive infection in the pathogenesis of this disease is unlikely, since neither MDV nor MDV antigens can be characteristically detected in nerves or spinal ganglia examined at necropsy. The authors investigated the possible role of a latent viral infection by explanting and maintaining in vitro the sciatic nerves and spinal ganglia from diseased birds. In these tissues, viral specific products were induced and detected by immunofluorescence and ultrastructural methods early after explanation in well-isolated Schwann cells, satellite cells, and lymphocytes. Later, virus was detected in fibroblasts, macrophages, and neoplastic lymphoblastoid cells. Neurons and myelinating Schwann cells, in contrast, did not replicate the agent. Specific cell-mediated and humoral immune responses to chicken peripheral nerve and peripheral nerve myelin were demonstrated early in the course of the disease. When considered relative to potential pathogenetic mechanisms, these results suggest that Marek's disease neuropathy is initiated by the establishment of a latent viral infection in neuronal supporting cells. A specific immune response to viral-induced antigens on these cells could, in turn, result in subsequent demyelination.

Animals↗

PubMed1986

Immunological studies on Crohn's disease. VI. Increased chemiluminescent response of peripheral blood monocytes.

Oxidative metabolic activity can be measured by a luminol-dependent chemiluminescence (CL) assay. To investigate the phagocytic activity of blood cells, CL responses were assessed in 26 patients with Crohn's disease (CD) and 26 healthy controls, using heparinized peripheral blood. Significantly (p less than 0.005) increased CL responses of whole blood cells were found in 26 patients with CD. However, CL activity was not directly related to disease activity nor to other clinical parameters. The CL responses did not correlate with the number of white blood cells, neutrophils nor monocytes. In consideration of the increased CL, there is the possibility that functional abnormalities in some components of blood cells leads to elevations in CL responses of whole blood cells. To obtain support for this proposal, blood cells were separated into neutrophils and monocytes, and CL of neutrophils or monocytes were studied, using the same number of each type of cells as that of the controls. The oxidative metabolism of monocytes from CD patients was significantly (p less than 0.005) higher than that of controls, while the phagocytic activity of neutrophils was similar to that in the controls. These data suggest that elevations in CL activity of whole blood cells were not due to alterations of the neutrophils but rather to abnormalities in the monocytes. Further attention directed to the significance of monocyte function in the pathogenesis of CD is warranted.

Crohn Disease↗

PubMed1993

[Analysis of immunosuppressive activity of lecithin-bound iodine (LBI) on antigen-induced IL2 responsiveness in peripheral blood lymphocytes from patients with allergic diseases].

The effect of lecithin-bound iodine (LBI) on antigen-induced IL2 responsiveness, useful in in vitro test for the detection of etiological antigen and disease activity in allergic diseases, was investigated. In peripheral blood mononuclear cells (PBMC) from asthmatic children, LBI suppressed Dermatophagoides farinae (Df)-induced IL2 responsiveness in a dose dependent manner, in a range of 0.01 to 100 micrograms/ml. Similarly, LBI also suppressed ovalbumin (OVA)-induced IL2 responsiveness in PBMC from patients with atopic dermatitis, sensitized with OVA, in concentration of 0.1 to 100 micrograms/ml. Moreover, purified protein derivative (PPD)-induced IL2 responsiveness was equally inhibited by LBI, at doses of between 0.1 and 100 micrograms/ml. However, LBI could not overcome the responses induced by concanavalin A (Con A) until it reached unphysiological concentrations of as high as 100 micrograms/ml. The fact that antigen-induced IL2 responsiveness was suppressed by LBI at concentrations comparable to blood levels of LBI in individuals medicated suggests that LBI is a weak immunosuppressant. IL2-responding T cells were more sensitive to LBI than antigen-presenting cells in Df-induced IL2 responsiveness, although LBI suppressed both cell populations. Taken together, LBI could work as a weak immunosuppressant to inhibit lymphocyte responses to allergen and to improve clinical status in allergic diseases, including bronchial asthma caused by Df and atopic dermatitis provoked by OVA.

Antigens↗

PubMed1989

Endogenous release of interferon-gamma and diminished response of peripheral blood mononuclear cells to antigenic stimulation.

The capacity of T lymphocytes to proliferate in response to stimulation and the amount of representative lymphokines produced in vitro often correlate with the immunocompetence of patients. However, direct and indirect measurement of endogenous interferon-gamma (IFN-gamma) brings some evidence that decreased in vitro production of IFN-gamma by T lymphocytes is associated with increased concentrations in vivo. The data indicate that both a functional inhibition of IFN-gamma and its continuous presence at high levels may result in hyporesponsiveness or unresponsiveness of immune cells. A possible role of IFN-gamma in the induction of tolerance is discussed.

Animals↗

PubMed1999

Impaired mitogenic response of peripheral blood T cells in ulcerative colitis is not due to apoptosis.

An abnormal immune response may play a pathogenic role in ulcerative colitis (UC). Animal models suggest that T-cell regulation may be of central importance in the inflammatory process. Our aims were the characterization of the phenotype and functional status of circulating T-cells in ulcerative colitis patients and to determine if activation-induced cell death in CD4 and CD8 lymphocytes in patients differs from healthy controls. Forty-eight patients (24 women and 24 men) fulfilling the histopathological, clinical, and immunological criteria for UC were studied. T-cell phenotype and function were studied in blood lymphocytes from patients with ulcerative colitis and healthy donors by flow cytometric analysis, as well as [3H]thymidine incorporation. There were no significant differences in the percentage of T-cell subpopulations (CD3, CD4, CD8) and NK cells in the different groups. The percentage of cells in growth phase S+G2M at two and three days of phytohemagglutinin (PHA) stimulation was significantly decreased in UC patients, but the percentage of CD4+ and CD8+ cells in UC patients that showed apoptosis was not significantly different than that in the control group. Proliferative responses to IL-4 also suggested that a reduced responsiveness to this cytokine may be involved in UC. In conclusion, the impaired proliferative response to PHA of T lymphocytes from UC patients is not associated with an in vitro increase in the apoptotic response in CD4+ or CD8+ cells. A reduced IL-4 response may be involved in this peculiar mitogenic response. These changes may be pathogenic or a favorable adaptive mechanism.

Adult↗