Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Immune dysfunction”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,225 records · Page 68Linked to original sources
PubMed2002

Elemental and intravenous total parenteral nutrition diet-induced gut barrier failure is intestinal site specific and can be prevented by feeding nonfermentable fiber.

OBJECTIVE: Parenteral nutrition and elemental diets both cause bacterial translocation, immune dysfunction, and increased infection in laboratory animals, whereas elemental diets, with or without fiber, ameliorate some, but not all gut barrier failure. The purpose of this study is to investigate, in an Ussing chamber system, whether elemental vs. parenteral diets induce gut barrier failure in specific anatomical sites in the intestine and whether fiber can ameliorate this phenomenon. DESIGN: Controlled study in laboratory animals. SETTING: University laboratory. SUBJECTS: Male Sprague-Dawley rats. INTERVENTIONS: Nutritional support was provided to rats for 7 days by oral total parenteral nutrition (TPN; elemental diet) 307 kcal/kg/day, intravenous TPN (parenteral diet) 307 kcal/kg/day via jugular venous catheters, or rodent chow (controls). MEASUREMENTS AND MAIN RESULTS: Permeability to bacteria in intestinal segments of ileum, jejunum, and colon was evaluated in an Ussing chamber. Results were correlated with bacterial translocation to the mesenteric lymph nodes. Intravenous TPN caused greater bacterial translocation in all small intestinal segments and the cecum when compared with chow (p <.05). Oral TPN caused gut barrier failure only in the ileal segment, but not in the remainder of the small intestine (p <.001). Addition of cellulose provided a greater protection of the ileum to permeability than did pectin (p <.01). CONCLUSIONS: TPN causes global intestinal barrier failure, but elemental diet prevents barrier failure in parts of the small intestine other than the ileum. The addition of cellulose fiber to elemental diet can ameliorate further barrier failure in the ileum.

Analysis of Variance↗
PubMedDate not supplied

Cytotoxicity to human leukocytes by topical antimicrobial agents used for burn care.

We tested two topical antimicrobial agents (TAAs), silver sulfadiazine and mafenide acetate, to determine their cytotoxic effects when human lymphocytes and neutrophils were incubated with the agents in vitro for 30 minutes. Dilute concentrations of both TAAs markedly inhibited neutrophil respiratory burst activity and mitogen-stimulated lymphocyte proliferation (p < 0.05). The components of silver sulfadiazine (silver and sulfadiazine) were separately tested, and each component inhibited both neutrophil and lymphocyte functions. Mafenide acetate markedly decreased intracellular Ca+2 flux in lymphocytes. The effects of the TAAs were partially reversed when cells were washed and resuspended in medium after they were exposed in vitro to the TAAs. Commonly used TAAs may contribute to local immune dysfunction in the patient with burns. Because evidence suggests that T lymphocytes may participate in wound healing, prolonged treatment with TAAs may also effect certain aspects of wound healing.

Burns↗
PubMed2001

Early trauma polymorphonuclear neutrophil responses to chemokines are associated with development of sepsis, pneumonia, and organ failure.

OBJECTIVES: The modulation of polymorphonuclear neutrophil (PMN) function by injury is unpredictable, and can predispose either to hyperimmune states (adult respiratory distress syndrome [ARDS], multiple organ failure) or to immune dysfunction, infection, and sepsis. Such outcomes have been related to excess production of the CXC chemokine interleukin (IL)-8, but PMN responses to IL-8 are mediated by both the relatively stable and IL-8 specific CXC receptor 1 (CXCR1) and the labile, promiscuous CXCR2. We hypothesized that progression to septic and multiple organ failure outcomes could be related to early differences in PMN CXC receptor status. METHODS: PMNs were isolated 12 +/- 3 hours after injury from 15 major trauma patients (Injury Severity Score of 34 +/- 2, 11 men and 4 women, age 36 +/- 4 years) who survived at least 7 days. Volunteer normal PMNs (n = 6 donors) were studied for comparison. Cells were stimulated either with the CXCR2 specific agent growth-related oncogene-alpha, or with IL-8, which stimulates CXCR1 and CXRR2. Receptor response was assessed as the mobilization of cell calcium. The development of ARDS, sepsis, and pneumonia was assessed according to standardized criteria. Day 1 receptor activity in the clinical groups was then compared by analysis of variance with Tukey's or t tests as appropriate. RESULTS: In patients that were otherwise comparable, CXCR2 responses were markedly diminished in the PMNs of patients who went on to sepsis and pneumonia, but were elevated in PMNs from the patients who went on to ARDS. CXCR1 responses were modestly lower in trauma patients than volunteers, but showed no significant variations among the various clinical outcome groups. CONCLUSION: The activity of PMN CXCR2 receptors soon after injury may be reflected in the later clinical sequelae of PMN activity. High CXCR2 activity may correlate with PMN hyperfunction and outcomes such as ARDS, whereas the loss of CXCR2 function in inflammatory environments may impair PMN functions in a manner that predisposes to pneumonia or sepsis. Early responses of PMN CXC receptors to injury may influence the clinical course of trauma patients.

Adult↗
PubMed1995

Vitiligo and alopecia areata in patients with human immunodeficiency virus infection.

In patients infected with human immunodeficiency virus (HIV) the development of autoimmune diseases, while not life threatening, is an interesting phenomenon that may result from immune dysfunction or from B cell infection by HIV, Epstein-Barr virus, or other unknown viruses. Vitiligo and alopecia areata are among the autoimmune diseases that have been reported in 11 patients infected with HIV. We describe a 47-year-old man who had vitiligo and alopecia areata approximately 2 years after testing positive for HIV antibodies.

Alopecia Areata↗
PubMed1999

Moraxella catarrhalis bacteremia: a 10-year experience.

BACKGROUND: Moraxella catarrhalis commonly inhabits the upper respiratory tract and is a cause of acute otitis media and sinusitis in children. It is an infrequent cause of invasive disease. METHODS: We reviewed records of all patients with positive blood cultures for M catarrhalis admitted to our hospital during the 10-year period (1988 through 1997). RESULTS: Eleven cases were identified. Age range was 11 to 32 months. Four (44%) had risk factors for infection, including sickle cell disease (2), acquired immunodeficiency syndrome (AIDS) (1), and leukopenia (1). Upper respiratory symptoms and fever were present in all patients. Ten had acute otitis media, five had sinusitis, and three had pneumonia. All isolates were beta-lactamase producers. Treatment included intravenous cefuroxime (8), cefotaxime (2), and ceftazidime (1), followed by oral amoxicillin/clavulanate or cefuroxime axetil. CONCLUSION: Moraxella catarrhalis bacteremia should be considered in febrile young children with upper respiratory infections and/or acute otitis media especially in those with underlying immune dysfunction.

Acute Disease↗
PubMed2001

Suppression of macrophage nitric oxide production by melanoma: mediation by a melanoma-derived product.

The tumour-bearing state is known to induce immune dysfunction that contributes to increased infectious complications and tumour progression. However, the mechanisms underlying this immunosuppression remain unclear. This study investigated in a murine model the effects of melanoma growth on nitric oxide (NO) production by peritoneal macrophages in vivo and in vitro. B16 and K1735 melanoma cells were inoculated subcutaneously into C57BL/6 and C3H/HeN mice, respectively. Stimulated NO production by elicited peritoneal macrophages was examined in control and melanoma- bearing mice. An in vitro system was established to assess the effects of co-culturing melanoma cells (B16 and K1735) or melanoma-conditioned medium with normal peritoneal macrophages on subsequent NO production. NO production was significantly suppressed in macrophages from melanoma-bearing mice. Co-culture of normal macrophages with melanoma cells in a transwell system or with melanoma-conditioned media in vitro reproduced the defects observed in vivo without affecting macrophage viability, pointing to a melanoma-derived product as the basis for the observed suppression of NO production. This inhibition required RNA and protein synthesis and was dose and time dependent. Using inhibition profiles and neutralizing antibodies, it was demonstrated that this melanoma inhibitory activity was distinct from known NO inhibitors. Preliminary characterization attributed this activity to a melanoma-secreted protein moiety.

Animals↗
PubMed1997

Advances in the understanding and treatment of atopic dermatitis.

Atopic dermatitis is the most common chronic skin disease of young children and is frequently associated with asthma and allergies. Th2-type cytokine secreting T cells expressing the cutaneous lymphocyte-associated antigen play a central role in the induction of local IgE responses and recruitment of eosinophils in this disease. Chronic inflammation in atopic dermatitis likely involves a number of interdependent factors, including repeated or persistent exposure to allergens, which can lead to Th2-cell expansion. In addition, exotoxins secreted by Staphylococcus aureus acting as both superantigens and allergens can contribute to persistent inflammation or exacerbations of atopic dermatitis. Treatment of atopic dermatitis with topical agents such as tacrolimus ointment and phosphodiesterase-4 inhibitors offers new approaches directed at correction of the immune dysfunction associated with this disease.

Adjuvants, Immunologic↗
PubMed2002

Early circulating lymphocyte apoptosis in human septic shock is associated with poor outcome.

The role of lymphocyte apoptosis in septic shock remains a controversial issue. Using Annexin V and flow cytometry analysis on freshly isolated cells, we evaluated circulating lymphocyte apoptosis in 23 septic shock, 25 sepsis without shock, 7 nonseptic critically ill, and 25 control patients. In patients with sepsis, we compared day 1 lymphocyte apoptosis (i.e., within 3 days of the onset of infection) with that observed 5-7 days after (day 6) according to shock state, mortality, and seventy factors. At day 1, patients in septic shock exhibited higher lymphocyte apoptosis than that present in controls (16.5% +/- 3.5% vs. 3% +/- 0.5%, respectively, P = 0.0001). At day 6, patients with sepsis without shock restored undamaged CD4+ T and CD8+ T lymphocyte counts, whereas patients in septic shock increased only CD4+ T cells. Similarly, survivors restored undamaged lymphocyte count at day 6 (+70%, P < 0.001), whereas nonsurvivors did not. Day 6 undamaged lymphocyte count negatively correlated with day 1 SAPS II, day 6 LOD score, mechanical ventilation, and ICU stay duration. We observed no apoptotic effect of septic shock plasma or septic shock circulating mononuclear cells on target lymphoid cell lines. We found no alteration in any death receptors Fas, TRAIL-R1, TRAIL-R2, or in their ligands on circulating blood cells. Catecholamines and interleukin 10 levels significantly increased in patients with septic shock, but did not correlate with apoptosis levels. We conclude that lymphocyte apoptosis is rapidly increased in blood of patients in septic shock and that lymphocyte apoptosis leads to a profound and persistent lymphopenia associated with poor outcome. These results suggest that lymphocyte apoptosis is one of the main components of human septic shock immune dysfunction and could be related more to microcirculatory disturbance than to circulating factors.

Aged↗
PubMed2005

Increased levels of galactose-deficient IgG in sera of HIV-1-infected individuals.

BACKGROUND: The IgG from sera of patients with chronic inflammatory diseases of autoimmune character or some chronic microbial infections is frequently deficient in galactose on N-linked glycans. However, this phenomenon has not been investigated at length in human viral infections. OBJECTIVES: To evaluate the glycosylation of serum IgG in HIV-1-positive patients. METHODS: Psathyrella velutina lectin was used in enzyme-linked immunosorbent and Western blot assays to determine glycosylation. In addition, gas-liquid chromatography and mass spectrometry were utilized to confirm the galactose deficiency observed in the lectin-binding assays. RESULTS: HIV-1-infected individuals had significantly higher levels of galactose-deficient IgG than healthy controls. In fact, the galactose deficiency of the N-linked glycans observed in other diseases was even more profound in HIV-1 infection. This deficiency was primarily restricted to IgG when total serum glycoproteins were evaluated and IgG1 was the subclass most affected in all patients. Also, a significant increase in lectin binding was observed on IgG2 and IgG4 from HIV-1-positive females compared with HIV-1-negative females. CONCLUSIONS: Identification of deficient galactosylation of serum IgG from HIV-1-infected patients extended the spectrum of diseases in which this phenomenon has been observed. In addition, the results suggest yet another aspect of immune dysfunction as a result of HIV-1 infection.

Adult↗
PubMed2006

Pathogenesis of AIDS lymphoma: role of oncogenic viruses and B cell activation-associated molecular lesions.

PURPOSE OF REVIEW: We discuss recently published studies that elucidate the pathogenesis of AIDS-associated lymphoma. RECENT FINDINGS: Several recent reports have provided valuable new information on the role of gamma-herpesviruses in the pathogenesis of AIDS-associated lymphoma. In addition to this, significant new information has become available on how B cell activation-associated DNA-modifying events, involving activation-induced cytidine deaminase and DNA polymerase-eta, contribute to the molecular lesions that result in AIDS-associated lymphoma. In particular, new evidence that oncogenic viruses can directly induce activation-induced cytidine deaminase expression and oncogene mutation in human B cells is of central relevance to better understanding the pathogenesis of AIDS-associated lymphoma. SUMMARY: New information provides insights into the contributions of immune dysfunction and oncogenic virus infection to pathogenesis of AIDS-associated lymphoma, and may lead to new potential targets for therapeutic intervention in these cancers.

Cell Transformation, Neoplastic↗
PubMed2003

Eosinophilic granuloma of the orbit: understanding the paradox of aggressive destruction responsive to minimal intervention.

PURPOSE: To describe the findings and outcomes in eosinophilic granuloma (unifocal Langerhans-cell histiocytosis [LCH]) of the orbit and to explain the paradox of aggressive bone destruction responsive to minimal intervention. METHODS: Retrospective, consecutive, interventional case series of patients treated from 1985 to 2001. Minimum inclusion criteria were demonstration of CD1a positivity or Birbeck granules, treatment by a single surgeon, systemic evaluation by a pediatric oncologist, and follow-up of 12 months. A pathogenetic construct was assembled from general LCH concepts and the specific orbital findings. RESULTS: Seven patients met study criteria. All were male, 2 to 16 years of age. All had eyelid or forehead swelling and osteolytic defects, with symptoms of 2 to 6 weeks' duration. All underwent incisional biopsy, with frozen-section examination suggestive of LCH in 6 of 7 cases. The 2 earliest patients received low-dose irradiation after simple biopsy. The 5 most recent patients had subtotal curettage at the time of biopsy; 4 of 5 received simultaneous intralesional corticosteroid injection. In all cases, systemic evaluation showed no other focus of LCH, reossification was timely, and no local recurrence or additional focus was noted in follow-up of 1 to 17 years. CONCLUSIONS: Transient immune dysfunction may provoke the cytokine-mediated proliferation of pathologic Langerhans cells within the hematopoietic marrow of the anterolateral frontal bone. These cells cause osteolysis through elaboration of interleukin-1 and prostaglandin E2. Corticosteroids can inhibit the mediators. We recommend incisional biopsy, frozen-section provisional diagnosis, subtotal curettage, intralesional corticosteroid instillation, postoperative systemic evaluation, and long-term surveillance.

Adolescent↗
PubMed2006

Impact of nutrition on ageing and disease.

PURPOSE OF REVIEW: The globe is suffering a tsunami of chronic diseases, affecting especially the elderly and those with a dysfunctioning immune system. The fundamental principles of optimal health and optimal ageing are abstaining from smoking, modest alcohol consumption, regular physical exercise and a diet rich in fish and plants and low in condensed calories, sugar and dairy products. RECENT FINDINGS: Dietary supply and production of advanced glycation end products leads to the accumulation of these products in the tissues and is strongly associated with ageing of the vascular endothelium, nervous system, eyes and other vital organs. Telomeres, which are not involved in DNA repair, remain unrepaired and loose with time. A decline in innate and acquired immunity is seen with increasing age and maintenance of low basal immune activity (degree of inflammation) seems important for health and longevity: 'people who are predisposed to weak inflammatory activity may live longer'. SUMMARY: Supplementation with vitamins has little effect on ageing/prevention of chronic diseases, but antiinflammatory molecules like polyphenols are more effective, especially when combined with reduced intake of calorie-condensed foods. The effect of probiotics on ageing needs further exploration. The effects of caloric restriction, proven effective in other species to control aging and prolong lifespan, have not been fully explored in humans.

Aged↗
PubMed2006

Non-alcoholic steatohepatitis and metabolic syndrome.

PURPOSE OF REVIEW: Non-alcoholic steatohepatitis is part of a disease spectrum, non-alcoholic fatty liver disease, ranging from simple steatosis to cirrhosis, which is the most frequent cause of abnormal liver tests. There is clinical and epidemiological evidence that non-alcoholic fatty liver disease is the hepatic manifestation of the metabolic syndrome, having in common insulin resistance. RECENT FINDINGS: The interest in the metabolic syndrome concept has been questioned. Insulin resistance, oxidative stress, mitochondrial dysfunction, immune deregulation and adipokines seem to be crucial in the pathogenesis of non-alcoholic fatty liver disease. The main treatment continues to rely on lifestyle changes, including weight loss strategies. Bariatric surgery in morbidly obese patients and insulin-sensitizing agents seem to be beneficial. SUMMARY: There is strong evidence of the association of non-alcoholic steatohepatitis with the features of the metabolic syndrome, with its increased cardiovascular risk. Population interventions in order to change lifestyles and diet patterns that constitute risk factors for both situations are urgently needed. There is, however, evidence that in the presence of other risk factors, insulin resistance may be less important. These secondary forms of non-alcoholic steatohepatitis must be recognized, as they are potentially treatable by withdrawing the steatogenic factor.

Fatty Liver↗
PubMed2003

Epstein-Barr virus infection is not associated with fibroadenomas of the breast in immunosuppressed patients after organ transplantation.

Epstein-Barr virus has been linked to an increasing number of nonhematolymphoid conditions. Epstein-Barr virus was recently described in association with fibroadenomas of the breast occurring in immunosuppressed patients. To further investigate the potential association of Epstein-Barr virus with fibroadenoma in the context of immune dysfunction, 11 cases of fibroadenoma of the breast in immunosuppressed organ transplant recipients were examined. Cases were evaluated for the presence of Epstein-Barr virus by polymerase chain reaction, in situ hybridization, and immunohistochemical methods. The presence of Epstein-Barr virus genomic DNA was studied by polymerase chain reaction amplification using primers flanking the BamHI-W fragment of the Epstein-Barr virus genome, as well as the Epstein-Barr virus nuclear antigen-4 and latent membrane protein-1 genes. Cases were also evaluated for the presence of defective heterogeneous Epstein-Barr virus DNA. In addition, morphologic analysis by in situ hybridization for Epstein-Barr virus-encoded RNA-1 and immunohistochemistry for latent membrane protein-1 were performed. Epstein-Barr virus DNA was detected in 4 of 11 (36%) cases with BamHI-W polymerase chain reaction. Polymerase chain reaction studies for Epstein-Barr virus nuclear antigen-4 and latent membrane protein-1 genes were positive in two and four cases, respectively. No defective Epstein-Barr virus genomes were identified in any of the cases. Quantitative polymerase chain reaction demonstrated low levels of Epstein-Barr virus in the fibroadenomas studied. Despite the detection of Epstein-Barr virus genomes in a subset of the cases examined, the constituent epithelial and stromal components of all fibroadenomas demonstrated no evidence of Epstein-Barr virus-encoded RNA-1 by in situ hybridization or latent membrane protein-1 expression by immunohistochemistry. Rare Epstein-Barr virus-encoded RNA-1-positive lymphocytes were observed in some cases, which may account for the positive polymerase chain reaction results. The findings of the present study argue against a significant relationship between Epstein-Barr virus and fibroadenomas of the breast in the setting of transplant-associated immunosuppression.

Adolescent↗
PubMed2004

Immunophenotypes, apoptosis, and expression of Fas and Bcl-2 from peripheral blood lymphocytes in patients with secondary early syphilis.

OBJECTIVES: Whether syphilis influences lymphocyte apoptosis has not been reported so far. GOAL: The goals of this study were to determine whether syphilis influences lymphocyte apoptosis and to investigate the molecular mechanism of apoptosis. STUDY DESIGN: Peripheral blood lymphocyte (PBL) immunophenotypes, apoptosis, and expression of Fas (CD95) and Bcl-2 were detected by flow cytometry in 33 patients with secondary early syphilis and 30 healthy subjects. RESULTS: Compared with the control subjects, the percentage of CD4 T cells and the ratio of CD4:CD8 were significantly decreased, and that of CD8 T cells and the apoptotic rates of PBLs and CD4 T cells were obviously increased in syphilitic patients. Fas overexpression and Bcl-2 downexpression in the syphilitic group were observed in PBLs and CD4 cells but not in CD8 and CD19 cells. CONCLUSIONS: The increased apoptosis of PBLs and CD4 T cells by Fas-mediated death pathway and downexpression of Bcl-2 protein could account for immune dysfunction in secondary early syphilis, which is responsible for the incomplete clearance of Treponema pallidum from the lesions and the chronic infection.

Adolescent↗
PubMed2006

Necrotizing fasciitis caused by Aeromonas hydrophilia in an immunocompetent child.

Necrotizing fasciitis is a rapidly progressive and potentially fatal infection. It is characterized by extensive subcutaneous and muscle necrosis. Aeromonus hydrophilia is a gram-negative faculatively anaerobic bacillus that is part of the normal flora of nonfecal sewage and is found in most water systems, soil, and fresh brackish water. Necrotizing fasciitis caused by A. hydrophilia have occurred in children who had underlying systemic diseases or immune dysfunction. We report a 14-year-old boy without underlying systemic diseases or immunodeficiency who developed necrotizing fasciitis secondary to A. hydrophilia and he was successfully treated with extensive surgical debridement and systemic antibiotics.

Adolescent↗
PubMed2003

Pemphigus vulgaris: an acquired blistering disease.

Pemphigus vulgaris is one of a group of autoimmune disorders that are caused by autoantibodies against the desmoglein adhesion molecules of squamous epithelial cells. It is a rare form of immune dysfunction that can prove vexing to the patient and physician, but it has distinct clinical and histologic findings. We report a case of a patient with the autoimmune blistering disease pemphigus vulgaris localized to the oral cavity and discuss the important clinical, immunopathologic, and therapeutic factors of this disease. This case report highlights the unusual nature of pemphigus vulgaris, the modalities used in its diagnosis, and effectiveness of therapy. Pemphigus vulgaris is an uncommon disease blistering disorder due to desmoglein autoantibodies, whose presentation can be alarming and puzzling to the clinician. Awareness of the disease's presentation and mechanism will allow for an efficient diagnostic evaluation and timely treatment.

Adult↗
PubMed2006

Local and distant burn injury alter immuno-inflammatory gene expression in skeletal muscle.

BACKGROUND: Severe burn trauma mediates immune dysfunction, infection, and multiple organ dysfunction syndrome. We are investigating the immuno-inflammatory response by characterizing gene expression changes in skeletal muscle after local and distant burn injury. METHODS: Male CD1 mice in three experimental groups, control (unburned), hind limb (local burn), and 30% total body surface area (distant burn), were killed between 6 hours and 10 days postburn; and changes in gastrocnemius muscle global gene expression were assessed using microarrays. RESULTS: The 35 immuno-inflammatory genes are differentially expressed in both models, with an additional 20 and 30 genes specific to distant and local burn, respectively. These genes encode chemokines, oxidative-stress, complement, and defense/immune functions. CONCLUSION: Burn mediates a common systemic response, independent of the site or extent of injury, and also specific responses to local versus distant trauma. A transcriptome profile of genes that initiate and sustain systemic inflammation has been identified.

Animals↗