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Results for “Immune function”

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At least 1,513 records · Page 84Linked to original sources
PubMed2005

Pulmonary contusion causes impairment of macrophage and lymphocyte immune functions and increases mortality associated with a subsequent septic challenge.

OBJECTIVE AND DESIGN: Pulmonary contusion is frequently followed by acute respiratory distress syndrome, pneumonia, and sepsis. However, immunologic alterations of circulating and resident immune cell populations contributing to the posttraumatic immunosuppression are poorly understood. We therefore characterized the influence of pulmonary contusion on peripheral blood mononuclear cells, peritoneal macrophages, splenocytes, and splenic macrophages. To address the significance of the immunosuppression associated with lung contusion, we investigated how the consecutive addition of moderate or severe sepsis affected survival after blunt chest trauma. SUBJECTS: Male C3H/HeN mice (n = 10 per group) were anesthetized and subjected to chest trauma or sham procedure. MEASUREMENTS: The cytokine release of cultured peripheral blood mononuclear cells, peritoneal macrophages, splenocytes, and splenic macrophages and plasma levels of tumor necrosis factor-alpha and interleukin-6 from those animals were quantified. Sepsis was induced via cecal ligation and puncture 24 hrs after lung contusion. MAIN RESULTS: Two hours after blunt chest trauma, plasma tumor necrosis factor-alpha and interleukin-6 were markedly increased, as was peripheral blood mononuclear cell cytokine production, lung myeloperoxidase activity, and lung chemokine concentrations. At 24 hrs and, in part, already at 2 hrs, cytokine release from peritoneal macrophages, splenic macrophages, and splenocytes was significantly suppressed. Furthermore, pulmonary contusion when followed by moderate sepsis significantly diminished survival rate when compared with chest trauma or moderate sepsis alone. CONCLUSIONS: These results indicate that pulmonary contusion causes severe immunodysfunction of splenocytes, macrophages, and monocytes in different local compartments and systemically. Moreover, this immunosuppression is associated with an increased susceptibility to infectious complications, which results in a decreased survival rate if blunt chest trauma is followed by a septic insult.

Analysis of Variance↗
PubMed2006

The effect of Panax ginseng on forced immobility time & immune function in mice.

BACKGROUND & OBJECTIVES: Panax ginseng has been used as a traditional medicine for many years mainly among Asian peoples for developing physical strength. We undertook this study to determine the immune-enhancement effect of P. ginseng using a forced swimming test (FST) and by measuring cytokine production in MOLT-4 cell culture and mouse peritoneal macrophages. METHODS: P. ginseng was orally administered to mice once a day for 7 days. The anti-immobility effect of P. ginseng on the FST and blood biochemical parameters related to fatigue, glucose (Glc); blood urea nitrogen (BUN); latic dehydrogenase (LDH); total protein (TP) and production of cytokines in human T cell line, MOLT-4 cells and mouse peritoneal macrophages were investigated. RESULTS: After two and seven days, the immobility time was decreased in the P. ginsengadministrated mice as compared to the control group; however, this reduction was not significant. In addition, the amount of TP in the blood serum was significantly increased. However, the levels of Glc, BUN, and LDH did not show a significant change. P. ginseng significantly (P<0.05) increased interferon (IFN)-gamma production and expression as compared to control at 48 h in MOLT-4 cells. P. ginseng plus recombinant IFN-gamma instead of P. ginseng alone significantly increased the production of the tumour necrosis factor (TNF)-alpha in the mouse peritoneal macrophages. INTERPRETATION & CONCLUSION: Our results suggest that P. ginseng may be useful for an immune promoter. Further studies are needed to understand the mechanism of its action.

Adjuvants, Immunologic↗
PubMed1997

Kinetics of immune functions and virus replication during HIV-1 infection.

INTRODUCTION: Kinetics of human immunodeficiency virus type 1 (HIV-1) cytotoxic T lymphocyte (CTL) responses and viral load were evaluated in HIV-1 infected homosexual men who progressed to AIDS within 3-6 years after seroconversion and in long-term survivors who remained AIDS-free for > 9 years with normal CD4+ T cell counts. METHODS: CTL against four major HIV-1 gene products (i.e. Gag, reverse transcriptase (RT), Nef and Env) were expanded in vitro under limiting dilution conditions using antigen specific stimulation. CTL activity was measured in standard split-well 51Cr-release assay. Viral load was measured both as serum HIV-1 RNA levels and frequency of circulating CD4+ T cells productively infected with HIV-1. Polyclonal T cell function in vitro was determined in whole blood lymphocyte cultures, measuring lymphoproliferative responses to CD3 monoclonal antibody. RESULTS: Long-term survival was associated with either persistently high or stable low HIV-1 specific CTL responses, accompanied by preserved in vitro polyclonal T cell reactivity and low viral load. In progressors, HIV-1 specific CTL responses were initially generated with similar kinetics as compared to long-term survivors. However, with progression to AIDS antiviral CTL activity and T cell function deteriorated simultaneously, while viral load increased. CONCLUSIONS: Our results are consistent with the hypothesis that HIV-1 specific CTL are beneficial through control of viremia to the virologic set-point and contribute to maintenance of the asymptomatic phase. However, loss of HIV-1 specific immune control as part of a more general loss of T cell function is the precipitating event in AIDS pathogenesis.

Acquired Immunodeficiency Syndrome↗
PubMed1991

Congenital syphilis in newborn rabbits: immune functions and susceptibility to challenge infection at 2 and 5 weeks of age.

Experiments were performed to further elaborate on our congenital syphilis rabbit model. Attempts were made to determine whether in utero exposure to Treponema pallidum would stimulate immune reactivity and whether this activity would, in turn, affect lesion development upon challenge infection. Newborn rabbits aged 2 or 5 weeks were obtained from control does or from does infected intravenously with T. pallidum during pregnancy. Congenitally infected newborns exhibited increased immunologic functions. Concanavalin A-induced T-lymphocyte proliferation was elevated at both 2 and 5 weeks. In addition, macrophage Ia expression and RPR antibody titers were increased at 5 weeks. In separate experiments, newborn rabbits from control does or from does infected during pregnancy were challenged intradermally with viable organisms at either 2 or 5 weeks of age. Subsequent lesion severity was markedly increased in those newborns previously exposed to treponemes in utero. These observations further strengthen our model for congenital transmission of T. pallidum during pregnancy. We propose that at least some of the tissue pathology in syphilitic infection is associated with activated host defenses.

Age Factors↗
PubMed1989

Surgery, sepsis, and nonspecific immune function in neonates.

An audit of 143 neonatal surgical operations identified low birth weight infants as being at particular risk of developing post-operative sepsis following major surgical trauma. Activity of the nonspecific immune system was examined pre- and post-operatively in order to elucidate the susceptibility to post-operative sepsis of these infants. A chemiluminescence micro-method was developed specifically for this purpose. Neonatal plasma was shown to have significantly impaired opsonising activity, and activity was further reduced in low birth weight infants. Levels of immunoglobulin and complement factors were also reduced, particularly in the low birth weight infant. Following major surgical trauma polymorph activity was significantly lower in low birth weight infants than in mature neonates.

Anti-Bacterial Agents↗
PubMed1980

[Effect of smoking on immune function (author's transl)].

Several tobacco antigens have been isolated inducing both precipitating and reaginic antibodies in humans and experimental animals. Chronic smoking leads to histological changes in the respiratory tract. --Alterations of humoral immunity have been demonstrated in the respiratory tract of smokers. Smoking may impair the systemic humoral immunity both in vitro and in vivo. Cell-mediated immunity are altered locally and systematically in smokers. --The clinical incidence of tobacco allergy is not sure, but there are evidences that allergic individuals are more sensitive to the nonspecific noxious effects of active or passive smoking than healthy individuals.

Adult↗
PubMed1992

The effects of dietary restriction on immune function and development of autoimmune disease in BXSB mice.

Chronic energy intake restriction (CEIR) prolonged the median life span and inhibited autoimmunity and development of autoimmune disease in BXSB mice, as has been established for mice of several other autoimmune-prone, short-lived strains. Whether imposed just after weaning or delayed until manifestations of disease had appeared, CEIR inhibited or reversed development of autoimmunity and immune complex-based renal disease in male BXSB mice. CEIR also prevented the formation of anti-DNA antibodies and prevented the increase in circulating immune complex levels that is typically observed in male mice of this strain. Moreover, CEIR inhibited development of splenomegaly and prevented the normal age-associated decline of a number of immunological functions, including interleukin 2 production, cell-mediated cytotoxic responses, and mixed lymphocyte reactivity. The observed improvement in cell-mediated immune responses was attributed largely to the capacity of CEIR to inhibit development of the splenomegaly that occurs concomitant with expansion of a non-T, non-B lymphoid cell population. These findings emphasize that CEIR, even when imposed relatively late in life in BXSB mice, can influence expression of autoimmunities and autoimmune diseases of different genetic origins and presumed pathogenetic bases.

Age Factors↗
PubMed1990

Adverse effects of aspirin, acetaminophen, and ibuprofen on immune function, viral shedding, and clinical status in rhinovirus-infected volunteers.

A double-blind, placebo-controlled trial was conducted to study the effects of over-the-counter analgesic/antipyretic medications on virus shedding, immune response, and clinical status in the common cold. Sixty healthy volunteers were challenged intranasally with rhinovirus type 2 and randomized to one of four treatment arms: aspirin, acetaminophen, ibuprofen, or placebo. Fifty-six volunteers were successfully infected and shed virus on at least 4 days after challenge. Virus shedding, antibody levels, clinical symptoms and signs, and blood leukocyte levels were carefully monitored. Use of aspirin and acetaminophen was associated with suppression of serum neutralizing antibody response (P less than .05 vs. placebo) and increased nasal symptoms and signs (P less than .05 vs. placebo). A concomitant rise in circulating monocytes suggested that the suppression of antibody response may be mediated through drug effects on monocytes and/or mononuclear phagocytes. There were no significant differences in viral shedding among the four groups, but a trend toward longer duration of virus shedding was observed in the aspirin and acetaminophen groups.

Acetaminophen↗
PubMed1999

Immune function and psychological factors in patients with coronary heart disease (I).

As part of studies on the effects, especially the preventive effects, of exercise and psychological factors on cardiovascular diseases, the association between psychological tendencies and immune response was evaluated in patients with coronary heart disease who were receiving exercise therapy. The Pearson's product-moment correlation coefficients between natural killer (NK) cell activity and various psychological scales were obtained. For the Moudsley Personality Inventory, NK cell activity had a significant positive correlation with the extraversion scale and a significant negative correlation with the neuroticism scale. NK cell activity also had a significant positive correlation with the playful humor scale and a significantly negative correlation with the Self-rating Depression Scale. The positive correlation of NK cell activity with the extraversion scale and the humor scale and its negative correlation with the neuroticism scale suggest an association between a positive-feeling tendency and high NK cell activity. The negative correlations of NK activity with the depression scale and neuroticism scale indicate that decreased or excessive expression of feelings inhibits NK cell activity. Thus, high NK activity appears to be associated with optimal expression of feelings.

Aged↗