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PubMed2001

Surgical stress induces endotoxin hyporesponsiveness and an early decrease of monocyte mCD14 and HLA-DR expression during surgery.

UNLABELLED: It is generally accepted that major surgery is associated with severe alterations of the host-defense mechanisms. We investigated the effect of surgical stress on the immune system. Specifically, we studied the relationship between perioperative lipopolysaccharide (LPS) hyporesponsiveness and monocyte human leukocyte antigen-DR (HLA-DR) and CD14 expression during the perioperative period in 20 patients who underwent partial gastrectomy. This study demonstrated that surgical stress rapidly depressed monocyte mCD14 and HLA-DR expression in comparison with preanesthesia levels. Monocyte mCD14 expression recovered to preoperative levels on the first postoperative day, and monocyte HLA-DR expression recovered by the seventh postoperative day. Consistent with our previous study, LPS-induced tumor necrosis factor (TNF)-alpha production ex vivo was significantly suppressed from the beginning of the operation. On the contrary, the plasma interleukin-10 concentration started to increase after the surgical incision was made. LPS hyporesponsiveness was least at the end of the operation and returned to preoperative levels on the first postoperative day. In conclusion, the present study demonstrated that LPS responsiveness, plasma interleukin-10 concentration, and monocytes mCD14 and HLA-DR expression altered from the early period of surgery. These alterations may be related to the impairment of the immune system during the perioperative period. IMPLICATIONS: Recent studies demonstrate that surgical stress induces immune dysfunction. We found that surgical stress rapidly decreased monocyte mCD14 and human leukocyte antigen-DR expression, and endotoxin responsiveness. These findings suggest that early changes of the immune system caused by surgical stress contribute to postoperative complications such as sepsis and multiple organ failure.

Gastrectomy↗

PubMed2003

Outcomes of renal transplantation following bone marrow transplantation.

This single center retrospective study was undertaken to determine the outcome of kidney transplantation (KT) after bone marrow transplantation (BMT) and also to determine the need for immunosuppressive therapy after KT when the BMT marrow donor is the KT donor. Kidney transplantation was performed in 10 patients with BMT nephropathy (BMTN). In six patients, the KT donor was the BMT donor; these individuals were given no long-term immunosuppression. Four other patients received KT from donors who were not the marrow donor (two living donors, two cadaveric donors). After median follow up of 34 months, no patient had an episode of acute rejection. All graft losses (n = 4) resulted from patient death. Three were because of infectious processes, including two infectious deaths in patients not on immunosuppression. Median estimated actuarial patient and graft survival (Kaplan-Meier) was 105 months. We conclude that patients with BMTN who receive KT from their marrow donor do not require immunosuppression. Whether immunosuppressive therapy is given or not, outcome appears to be determined largely by BMT-related immune dysfunction.

Adolescent↗

PubMedDate not supplied

Naloxone inhibits the in vivo immunosuppressive effects of morphine and thermal injury in mice.

The effect of opioids (both exogenous and endogenous) on cell-mediated immune response in normal and thermally injured mice was evaluated with a delayed-type hypersensitivity assay. The administration of morphine sulfate to normal mice resulted in decreased delayed-type hypersensitivity response. This morphine sulfate-induced immunosuppression was prevented by concurrent treatment with the opioid antagonist, naloxone; however, naloxone alone did not alter immune response. Thermally injured mice had a suppressed delayed-type hypersensitivity response that was not further affected by morphine sulfate administration. In contrast, the immunosuppressive effects caused by burn injury, alone or in combination with the administration of morphine sulfate, were not observed in the presence of naloxone as measured by delayed-type hypersensitivity response. These results suggest that opioids depress cellular immune response and may play a role in immune dysfunction that follows thermal injury.

Animals↗

PubMed1993

Immunological findings in growth hormone-treated patients.

In vivo studies in experimental animals and in vitro studies using human lymphocytes have indicated that growth hormone (GH) is important for the development and function of the immune system. This is most clearly illustrated by the underdevelopment of the thymus in dwarf Snell mice, which is prevented by GH treatment. In contrast, in vivo studies in humans have generally shown only minor alterations of immune function in GH deficiency. GH administration to children with various growth disorders may lead to variable and subtle changes in some laboratory parameters of immune function, but no clinical symptoms associated with immune dysfunction have been reported.

Animals↗

PubMed1992

Nutrition and inflammatory events: highly unsaturated fatty acids (omega-3 vs omega-6) in surgical injury.

Given the poor prognosis and high cost of care for patients with acute inflammatory responses (often leading to organ failure and/or allograft rejection), immunomodulation of this hyperresponse represents an important priority for research in nutritional medicine. The primary goal of nutritional support in inflammatory disease is to provide adequate energy, particularly through use of novel lipids (to alter eicosanoid pathway toward a more regulated inflammatory state), and protein to meet endogenous requirements for tissue repair IL-1 production, and restored cellular function, thus preventing secondary infection (52). Manipulation of macrophage eicosanoid production by use of omega-3 PUFA may reduce the cellular immune response (by competing with arachidonic acid, which produces inflammatory eicosanoids of the 2- and 4-series), whereas inclusion of MCT found in coconut oil may lower the arachidonic acid content of membrane phospholipids. As more data are obtained on the use of such tailored therapies in critically ill patients, a new generation of parenteral and enteral diets will be developed to reduce inflammation and immune dysfunction.

Diet↗

PubMedDate not supplied

[Intestinal absorption of D-xylose in children infected with the human immunodeficiency virus].

AIM: To evaluate the intestinal absorption in HIV-infected children children 14 months to 14 years and to investigate its relationship to diarrhea, nutritional status, immune dysfunction, classical enteric parasites and Cryptosporidium. METHODS: Intestinal absorption was investigated by measuring serum D-xylose. Fecal samples were investigated for classical pathogens and Cryptosporidium. The sample size was calculated considering a 30% prevalence of altered D-xylose absorption in HIV-infected children with a 5% accuracy. Statistical procedures used were: descriptive measurements, multiple correspondence analysis and logistic regression. RESULTS: D-xylose absorption was altered in only 8 out of 104 (7.7%) and Cryptosporidium was positive in 33 out of 104 (31.73%) HIV-infected children. The multiple correspondence analysis suggested an association between an altered D-xylose test and Cryptosporidium. D-xylose malabsorption was not associated with diarrhea, nutritional status, immune disfunction and classic enteric parasites. CONCLUSIONS: Intestinal malabsorption evaluated through the D-xylose test was an uncommon finding in HIV-infected children. Intestinal dysfunction when present seems to be related to Cryptosporidium, but not to diarrhea, nutritional status, immune disfunction and classic enteric parasites.

Adolescent↗

PubMed1987

Altered lymphocyte subsets during cardiopulmonary bypass.

Peripheral blood lymphocyte subsets were quantified by immunofluorescence in nine patients undergoing open heart surgery for coronary artery, valvular, and congenital heart disease. Compared with normal preoperative values, all patients developed an absolute lymphopenia, a reduction in T4 (helper) lymphocytes, and a statistically significant reversal of the T4/T8 ratio two hours after cardiopulmonary bypass (CPB). These changes could be caused by mechanical or immunogenic injury. A return to normal of the T4 subset and T4/T8 proportion occurred 24 hours after surgery. Whereas transient inactivation of immunoreactive lymphocyte clones may prevent unwanted immunization to blood products received during surgery, such temporary immune dysfunction could make certain patients liable to infectious sequelae. Viral-induced postperfusion syndromes, transmission of human T lymphotropic virus (HTLV) III by blood products, and reports of acquired immune deficiency syndrome after CPB foster a concern regarding postoperative infections under these circumstances.

Adult↗

PubMed1990

Immune responses in humans while receiving adoptive immunotherapy with recombinant interleukin-2 and lymphokine-activated killer cells: acute anergy to mitogens and recall antigens.

In this study we evaluated the in vitro immunologic responses of 11 patients receiving immunotherapy with either interleukin-2 (IL-2, 3 X 10(6) units/m2) or IL-2 plus lymphokine-activated killer cells (LAK) over a 30-day period. Blastogenic responses to mitogens or recall antigens were found to significantly decrease during therapy. Pokeweed mitogen immunoglobulin (Ig) production decreased significantly in 7 patients or showed no change. In vivo skin tests for cell-mediated immunity were also performed and the average number of positive responses before IL-2/LAK therapy decreased to no positive responses (day 29 of therapy). Experiments were performed to determine whether decreased responses were a result of active suppression or a dilution effect by immature/mature cells that cannot respond to mitogen or antigen. Pre-therapy cells were mixed with fresh autologous (anergic) cells from day 29 of therapy in varying ratios. Blastogenesis and Ig production was measured. Our findings demonstrate that the decreased immune response observed during and after therapy is a result not of active immunosuppression but rather of a dilution effect by cells with immune dysfunction. We conclude that: (1) in vitro blastogenesis or Ig production tests using mitogens or antigens for patients undergoing IL-2 immunotherapy have no predictive value, and (2) the immune cells that are present are refractory.

Humans↗

PubMed1999

Neuroendocrine host factors and inflammatory disease susceptibility.

The etiology of autoimmune diseases is multifactorial, resulting from a combination of genetically predetermined host characteristics and environmental exposures. As the term autoimmune implies, immune dysfunction and dysregulated self-tolerance are key elements in the pathophysiology of all these diseases. The neuroendocrine and sympathetic nervous systems are increasingly recognized as modulators of the immune response at the levels of both early inflammation and specific immunity. As such, alterations in their response represent a potential mechanism by which pathologic autoimmunity may develop. Animal models of autoimmune diseases show pre-existing changes in neuroendocrine responses to a variety of stimuli, and both animal and human studies have shown altered stress responses in the setting of active immune activation. The potential role of the neuroendocrine system in linking environmental exposures and autoimmune diseases is 2-fold. First, it may represent a direct target for toxic compounds. Second, its inadequate function may result in the inappropriate response of the immune system to an environmental agent with immunogenic properties. This article reviews the relationship between autoimmune diseases and the neuroendocrine system and discusses the difficulties and pitfalls of investigating a physiologic response that is sensitive to such a multiplicity of environmental exposures.

Animals↗

PubMed2006

Injury-induced suppression of effector T cell immunity requires CD1d-positive APCs and CD1d-restricted NKT cells.

Overwhelming infection remains the leading cause of death from serious burn injury despite recent advances in the care of burn patients and a better understanding of immune and inflammatory consequences of injury. In this study, we report a critical requirement for CD1d-restricted NKT cells and CD1d expression by APCs in the immune dysfunction that occurs early after burn injury. Using a well-established murine scald injury model with BALB/c and BALB/c CD1d knockout mice, we investigated whether peripheral T cell immunity was affected by the presence or absence of CD1d-restricted NKT cells in the early stages after injury. Using Ag-specific delayed-type hypersensitivity, T cell proliferation, and cytokine production as indices of immune responsiveness, we observed that both CD1d expression by APCs and CD1d-restricted NKT cells are required for immune suppression after injury. Via adoptive transfer of splenocytes from injured mice to uninjured recipients, we found injury-induced suppression of immunity to be Ag specific, long lasting, and critically dependent on cell surface expression of CD1d by APCs. Together, our results suggest that the defects in T cell responsiveness that occur subsequent to severe burn injury are not merely the result of global or passive suppression, but instead represent an active form of CD1d/NKT cell-dependent immunologic tolerance.

Adoptive Transfer↗

PubMed1994

Alcohol, immunomodulation, and disease.

Recent research findings point to a spectrum of alcohol-induced immune dysfunctions in animal models and humans. Use of alcohol in vivo causes abnormalities in the function and/or structure of a broad array of cells involved in humoral and cellular immunity, including lymphocytes, Kupffer cells and other macrophages, as well as the endothelium of blood vessels and lymphatics. Regulatory cytokines and neuroendocrine factors can mediate some of these immunomodulatory effects which may be further re-phased, exaggerated or unbalanced by other drugs of misuse. A variety of animal models is available to study acute and chronic alcoholism, non-alcohol drug misuse, AIDS as well as other opportunistic infections, and neoplasias, which hold promise of clarifying the role of alcohol as an immunomodulator.

Acquired Immunodeficiency Syndrome↗

PubMed1983

Is schizophrenia an immunologic receptor disorder?

A model is proposed for an autoimmune etiology for schizophrenia. We propose that schizophrenia is a syndrome (not a disease). We suggest that autoantibodies (and/or cell-mediated immunity) directed against autologous neurotransmitter receptors are responsible for the ebb and flow of psychotic symptomatology. The hypothesis is predicated on autoimmune models in other known receptor diseases as well as on the newly emerging recognition that general immune dysfunction exists in certain schizophreniform psychoses.

Antibody Formation↗

PubMed1982

Evaluation of the immune response to type III pneumococcal polysaccharide as a means to evaluate T-independent immune function in the rat.

Since the rat is frequently the experimental animal of choice for toxicology testing, studies were undertaken to adapt assays routinely used to evaluate immune function in mice so that immune function could likewise be evaluated in collaborative projects employing toxicant-treated rats. Contrary to previous reports in the literature, Type III pneumococcal polysaccharide (S3) was immunogenic in rats. Specific antibody responses to S3 were demonstrated in two strains of rats following immunization by either the subcutaneous (sc) or intraperitoneal (ip) route with purified S3, with S3 contained in polyvalent pneumococcal polysaccharide vaccine (pneumovax), or with heat-killed Type III Streptococcus pneumoniae. Dose-response studies demonstrated that the optimal immunizing dose in Sprague-Dawley or Fischer rats was 25 micrograms S3. Reimmunization with S3 on d 21 did not produce an anamnestic response, and the kinetic data were consistent with S3 being a thymus-independent (T-independent) antigen in the rat. In contrast to our previous studies in the mouse, concurrent sc or ip injections of pertussis vaccine did not modify the response to S3 in rats. Sprague-Dawley rats acquired the capacity to respond immunologically to S3 between 24 and 31 d of age. In mature animals, sex had no effect on the ability to respond to S3. The utility of this model as a means of characterize toxicant-induced immune dysfunction was demonstrated using the prototype immunotoxicant cyclo-phosphamide.

Aging↗

PubMed2001

Role of interleukin-10 in monocyte hyporesponsiveness associated with septic shock.

OBJECTIVES: The purpose of this study was to examine the pattern of tumor necrosis factor (TNF)-alpha and interleukin (IL)-10 release in endotoxin-stimulated septic monocytes and to determine the role of IL-10 and transforming growth factor (TGF)-beta in monocyte hyporesponsiveness during septic shock. DESIGN: Monocytes isolated from ten healthy controls and ten patients with septic shock were incubated with endotoxin and cytokine release was assessed. Next, normal monocytes were incubated with either normal or septic serum and stimulated with endotoxin. Finally, normal monocytes were incubated with septic serum either with anti-IL-10 antibodies or anti-TGF-beta antibodies and then stimulated with endotoxin. MEASUREMENTS: TNF-alpha, IL-10, and TGF-beta levels were measured in the serum and in culture supernatants by enzyme-linked immunosorbent assay. SETTING: Research laboratory. MAIN RESULTS: IL-10 and TNF-alpha levels were significantly increased in septic serum, whereas TGF-beta levels were not different from controls. Normal monocytes increased TNF-alpha and IL-10 release in response to endotoxin. In contrast, septic monocyte TNF-alpha release was attenuated in response to endotoxin (1.8 +/- 0.5 vs. 1.0 +/- 0.4 ng/mL, stimulated vs. baseline), whereas IL-10 release increased significantly from baseline (173 +/- 91 vs. 8 +/- 4 pg/mL, stimulated vs. baseline). Incubation of normal monocytes with septic serum attenuated TNF-alpha release in response to endotoxin (32% +/- 8% of normal serum; p < .01), whereas IL-10 release was increased (285% +/- 84% of normal serum; p < .05). When normal monocytes were incubated with septic serum combined with anti-IL-10 antibodies, TNF-alpha release increased significantly to 75% +/- 17% of normal serum (p < .05 vs. septic serum alone). Incubation of normal monocytes with anti-TGF-beta antibodies did not significantly affect either TNF-alpha or IL-10 release in response to endotoxin. CONCLUSION: Monocytes from patients with septic shock exhibit persistent IL-10 release at a time when TNF-alpha release is downregulated. The continued release of IL-10 may contribute to impairment of monocyte proinflammatory cytokine release and the development of immune dysfunction in septic shock.

Down-Regulation↗

PubMed1981

Darier's disease: a partially immunodeficient state.

Darier's disease (Keratosis follicularis) a dominantly inherited keratinizing disorder of the skin, is associated with the development of severe, progressive viral and bacterial skin infections. We investigated the possibility that an inadequacy of the immune system might be responsible for this tendency. Seven of our 8 patients with Darier's disease showed complete anergy to common skin test antigens and their peripheral blood lymphocytes failed to produce the lymphokine, leukocyte inhibitory factor (LIF) in vitro when stimulated with the same antigens. One Darier's patient and 6 controls showed positivity to at least one skin test antigen and produced lymphokine in vitro to the appropriate antigen. All patients had normal leukocyte and differential counts and normal numbers of circulating T and B cells. All 8 patients with Darier's disease demonstrated no proliferative response to optimal doses of the T cell mitogen Con A while showing normal responses to the T cell stimulant PHA and the T cell dependent B cell stimulant PWM. This previously unreported finding suggests a subtle abnormality of T cells in Darier's and might be a marker for these patients. Serum from 2 patients with Darier's disease did not suppress the in vitro immunologic activity of lymphocytes from normals. Finally, 13-Cis-retinoic acid in dosages adequate to clear their skin disease did not alter the in vivo or in vitro immunologic functions in 3 Darier's patients, suggesting that the immune dysfunction is not a secondary phenomenon.

Adult↗

PubMed1988

Effect of vitamin B complex on the immunodeficiency produced by surgery of gastric cancer patients.

We studied the effect of vitamin B complex (vitamin B1, B6 and B12 complex) on the immune responsiveness in gastric cancer patients who underwent surgery. The depression of blastogenic responses to both PHA and PWM was observed 2 weeks after surgery in half of the patients treated with Vitamedin but the degree was significantly less than that in the control patients without vitamin B treatment whose lymphocyte responses were depressed. Moreover, the blastogenic responses were induced by vitamin B administration 2 or 4 weeks after surgery in 5 of the 8 stage III-IV patients whose lymphocytes had not responded prior to surgery. Four weeks after surgery, the patients without vitamin B treatment showed only a tendency of recovery of their lymphocyte responses, whereas the recovery of blastogenic responses in the patients treated with vitamin B was significant. Essentially similar results were obtained with skin reactions to PHA and PPD. These results suggest that the administration of vitamin B1, B6 and B12 complex is useful for the protection against and the recovery of immune dysfunction produced by surgery in cancer patients.

Humans↗

PubMed1996

Immunosuppression may lead to progression of hepatitis C virus-associated liver disease in hemophiliacs coinfected with HIV.

OBJECTIVE: The aim of this study was to examine the interaction between HIV and hepatitis C virus (HCV) in hemophiliacs coinfected with the viruses and to investigate the possible relationship between immunosuppression and liver failure. METHODS: To identify risk factors for impending liver failure in hemophiliacs coinfected with HIV and HCV, we analyzed clinical and laboratory parameters, including CD4 count, aminotransferases (ALT, AST), cholinesterase, alkaline phosphatase, bilirubin, and gamma-glutamyltransferase, during 3 yr of follow-up (1990-1993) in four groups of patients: hemophiliacs with progressive immunodeficiency who were coinfected with HCV and HIV (group A, n = 49); hemophiliacs with stable immune function who were seropositive for HIV and HCV (group B, n = 95); hemophiliacs who were infected with HCV but not HIV (group C, n = 72); and homosexuals with progressive immunodeficiency who were infected with HIV but not HCV (group D, n = 24). RESULTS: Univariate analysis of data for group A showed a significant rise in gamma-glutamyltransferase and alkaline phosphatase (p < 0.01) that was not seen in groups B, C, and D. In a multivariate Cox regression analysis, age (odds ratio, 1.054 per yr; 95% confidence interval, 1.014-1.096 per yr), decline in CD4 count (odds ratio, 1.063 per cell/microl; 95% confidence interval, 1.037-1.091 per cell/microl), and alkaline phosphatase level (odds ratio, 1.012 per U/L; 95% confidence interval, 1.002-1.021 per U/L) emerged as independent determinants of death. CONCLUSIONS: Our data suggest that progressive immune dysfunction in hemophiliacs coinfected with HIV and HCV may influence progression of liver failure. In these patients cholestasis is an additional prognostic marker for survival that may reflect both exhausted immunity and impaired liver function.

Acquired Immunodeficiency Syndrome↗

PubMed1998

Future directions in exercise and immunology: regulation and integration.

Although it is difficult to predict future directions in a rapidly expanding field such as exercise immunology, recently published research along with that presented at this Symposium allow us to ask some key questions which may point to new directions: 1) Are athletes immunocompromised? Athletes are not clinically immunodeficient, yet endurance athletes are at increased risk of illness. Long-term prospective studies are needed to understand the relationship between infection, training variables and immune parameters. 2) Is downregulation of nonspecific immunity beneficial or harmful? In athletes, neutrophils appear to be downregulated, and this may alter resistance to illness. Alternatively, neutrophils are mediators of tissue damage during inflammation. Downregulation of neutrophil function may be protective by limiting chronic inflammation. In athletes, mild immunosuppression may reflect a compromise between the body's attempts to limit inflammation while maintaining immune function. 3) What mediates communication between events in skeletal muscle and the immune system? Leukocyte mobility is affected by metabolic and mechanical factors during exercise. Exercise increases cytokine levels in damaged skeletal muscle and expression of adhesion molecules. Future work is likely to focus on the role of cytokines and adhesion molecules in mediating exercise-induced changes in leukocyte mobility. 4) Can exercise training provide a "countermeasure" against immunosuppressive events? Moderate exercise training may have a role in stimulating the immune system during certain diseases (e.g., HIV-infection), immune dysfunction (e.g., chronic fatigue syndrome) or reduced responsiveness (e.g. aging, spaceflight). It is also likely that future study will apply molecular biology techniques to further identify mechanisms by which exercise influences immune function.

Animals↗