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PubMed2001

Crohn's disease and Mycobacterium avium subsp. paratuberculosis: current issues.

Crohn's disease is a chronic debilitating inflammatory bowel disease of unknown etiology. Proposed causes include bacterial or viral infection, diet or exposure to tobacco smoke, genetic abnormality, and immune dysfunction. The bacterium Mycobacterium avium subsp. paratuberculosis (Map) has received much research attention as a potential cause of the disease. Map causes Johne's disease in ruminants. The pathology of Johne's disease superficially resembles that of Crohn's disease in humans. Some researchers have shown evidence of Map in intestinal tissues of Crohn's disease patients. Studies are in progress to investigate the possibility that Map exists in milk from infected cows and survives pasteurization. This is a controversial subject with the potential for media attention and public outcry. We examined the current literature and concluded that insufficient evidence exists at this time to implicate any one factor, including Map in milk, as the definitive cause of Crohn's disease. The high degree of uncertainty in this issue requires regulators to recognize the need for effective risk communication as ongoing research provides additional information about the disease.

Animals↗
PubMed2005

Ice immersion as a postharvest treatment of oysters for the reduction of Vibrio vulnificus.

Vibrio vulnificus produces serious illnesses that are commonly associated with shellfish consumption, particularly raw oysters. Ingestion can result in fatal septicemia in susceptible individuals with hepatitis, cirrhosis, immune dysfunction, diabetes, or hemochromatosis (metabolic iron overload). Therefore, postharvest treatments to reduce vibrio levels in oysters have been recommended. In this study, rapid chilling by immersion of unwashed whole oysters in ice for 3 h was assessed as a postharvest treatment for reduction of V. vulnificus. Treated oysters were subsequently refrigerated at 45 degrees F (7.2 degrees C), whereas control oysters were not iced but were maintained at 45 degrees F throughout the study. Homogenized meats were monitored for total heterotrophic aerobic bacteria, V. vulnificus, and fecal coliform content before and after treatment over a 2-week period. V. vulnificus was enumerated by DNA probe hybridization of colonies from standard plate counts on nonselective medium, and recovery was compared for several media. Loss of plating efficiency was observed on standard selective and differential media compared with nonselective agars. Numbers of V. vulnificus generally declined in treated samples compared with controls; however, increases in total heterotrophic bacteria and fecal coliforms were also observed in treated samples at some time points. This study does not support the use of ice immersion as a postharvest method because of the relatively small declines in V. vulnificus numbers and the possibility of concomitant increases in fecal coliform and total bacterial contamination.

Animals↗
PubMed2006

Angioimmunoblastic T-cell lymphoma with supervening Epstein-Barr virus-associated large B-cell lymphoma.

Patients with angioimmunoblastic T-cell lymphoma can have profound immune dysfunction and immunodeficiency. Epstein-Barr virus-driven B-cell lymphoid proliferation can occur in angioimmunoblastic T-cell lymphoma, as in other immunodeficiency states. However, few cases of Epstein-Barr virus-positive B-cell lymphoma arising in patients with preexisting angioimmunoblastic T-cell lymphoma have been reported. We report a case of angioimmunoblastic T-cell lymphoma in which diffuse large B-cell lymphoma developed 56 months after the diagnosis of angioimmunoblastic T-cell lymphoma. The patient survived for 9 years after the initial diagnosis of angioimmunoblastic T-cell lymphoma, and molecular studies performed on multiple biopsy specimens during this period revealed the dynamic nature of clonal lymphoid expansion. Epstein-Barr virus latent membrane protein 1 and Epstein-Barr virus-encoded RNA were detected in the diffuse large B-cell lymphoma, suggesting that Epstein-Barr virus may have played a role in the pathogenesis of the diffuse large B-cell lymphoma.

Aged↗
PubMed1984

Persistent diffuse lymphadenopathy in homosexual men: endpoint or prodrome?

Seventy homosexual men with unexplained persistent diffuse lymphadenopathy enrolled in a prospective natural history study from November 1981 to November 1982. These men had demographic, clinical, and laboratory findings similar to those of homosexual patients with the acquired immunodeficiency syndrome. Pathologic examination of lymph node biopsies from 35 patients showed florid follicular hyperplasia. Despite benign reactive pathologic findings, most patients had constitutional symptoms and recurrent non-life-threatening infections. All had evidence of immune dysfunction with B-lymphocyte activation and inversion of the T-lymphocyte helper: suppressor ratio. To date, none of our patients has developed the more malignant manifestations of the acquired immunodeficiency syndrome. The lymphadenopathy syndrome may be an alternative phenotypic response to the "acquired immunodeficiency syndrome agent."

Adult↗
PubMed1996

Understanding intestinal spore-forming protozoa: cryptosporidia, microsporidia, isospora, and cyclospora.

OBJECTIVES: To summarize recent information about the "new" gastrointestinal protozoal pathogens (cryptosporidia, microsporidia, isospora, and cyclospora) and to help practicing clinicians integrate this information into their clinical databases by emphasizing the similarities among these organisms. DATA SOURCES: Relevant English-language articles published between 1988 and 1995 were identified through a MEDLINE search done using the names of the intestinal spore-forming protozoa. Articles cited in the bibliographies of these and other articles were searched manually. STUDY SELECTION: Studies that contained information on the history, taxonomy, life cycle, epidemiology, pathogenesis, clinical manifestations, diagnosis, and treatment of the pathogens were reviewed. DATA EXTRACTION: Cryptosporidium parvum, Isospora belli, Cyclospora cayetanensis, Enterocytozoon bieneusi, and Septata intestinalis are intestinal spore-forming protozoa that cause intracellular infections, predominantly in the epithelial cells of the intestine. They are transmitted either by stool from person to person or through contaminated water or food by an infectious particle called a spore or oocyst. Asymptomatic infections occur; the most common symptom of infection is diarrhea. Infections have been associated with intestinal inflammation, disordered architecture (such as villus blunting), and abnormal function (for example, malabsorption). Mild to moderate, self-limited diarrhea is common in healthy persons, but patients with immune dysfunction can have severe intestinal injury and prolonged diarrhea. Diagnosis is made by a microscopic examination of the stool and the use of appropriate staining techniques. Effective antibiotic treatment for prolonged infection in immunocompromised patients is available for most of these infections. CONCLUSIONS: The intestinal spore-forming protozoa are four frequently identified gastrointestinal pathogens that have important similarities in epidemiology, disease pathogenesis, clinical manifestations, diagnosis, and treatment.

Animals↗
PubMed1983

Generalized lymphadenopathy in homosexual men.

The cases of 90 homosexual or bisexual men with generalized lymphadenopathy were studied by epidemiologic, clinical, pathologic, immunologic, and genetic methods. The patients ranged in age from 20 to 52 years and had histories of multiple sexually transmitted diseases and both recreational and prescription drug use. Histologically, their lymph nodes showed three patterns: explosive follicular hyperplasia; follicular involution with expansion of the paracortical area; and a mixed pattern of follicular hyperplasia and follicular involution in the same lymph node. The frequency of HLA-DR5 was significantly increased in these patients (p less than 0.005) compared with that in controls. All patients had impaired cell-mediated immunity. Opportunistic infections, lymphomas, or Kaposi's sarcoma subsequently developed in 15 patients who had had severe immune dysfunction for the previous 3 to 13 months. We suggest that generalized lymphadenopathy is part of the spectrum of a disorder manifested by acquired immunodeficiency, opportunistic infections, Kaposi's sarcoma, and malignant lymphomas.

Adult↗
PubMed1999

[Eosinophilic pustulosis in an infant accompanied by immune deficit].

BACKGROUND: Eosinophilic is a skin eruption which occurs in the first years of life, progressing by pruriginous flare-ups with amicrobial papulopustulae on a hairless scalp. Eosinophil infiltration of the skin is variable (follicular or perifollicular dermal infiltration). In adults, eosinophilic pustulosis is often associated with immune deficiency, but this association has not been reported in children. We report two cases. CASE REPORTS: Two boys had a pruriginous papulopustular eruption involving the scalp and the trunk which had progressed with periods of exacerbation since birth. Search for bacteriological or mycological involvement was negative. Histology showed folliculitis with major polynuclear eosinophil infiltration. Both children had a past history of repeated skin and extracutaneous infections strongly suggesting an immune deficit. Buckly syndrome was suspected in the second case. DISCUSSION: Juvenile eosinophilic pustulosis belongs to the spectrum of childhood eosinophilic dermatoses. The presence of eosinophil infiltration in the skin demonstrates localized or systemic immune dysfunction. A hematology and immunology work-up is needed in case of associated skin or deep infections.

Adult↗
PubMed1999

Caspase-mediated degradation of T-cell receptor zeta-chain.

We recently reported an association between loss in T-cell receptor (TcR) zeta-chain expression and tumor-induced apoptosis of T lymphocytes. In this study, the possibility that zeta-chain serves as a direct substrate for activated caspases was investigated. Here, we report that two DXXD motifs, which are putative recognition sequences for caspase-3-related proteases and are present in the amino acid sequence of the zeta-chain, are cleaved in apoptotic Jurkat T lymphocytes. Cleavage of zeta-chain in Jurkat cells ligated by agonistic anti-Fas antibody was inhibited in the presence of peptide inhibitors of caspases, including the pan-caspase inhibitor N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone and N-benzyloxycarbonyl-Asp-Glu-Val-Asp-fluoromethyl ketone, an inhibitor of caspase-3-like activity. Fas-induced cleavage of zeta-chain was also inhibited in Jurkat cells overexpressing the intracellular inhibitors of caspase activity, Bcl-2 or cytokine response-modifier A. In vitro translated zeta-chain was cleaved in a similar fashion by recombinant caspase-3 or caspase-7 in a dose-dependent manner. In the presence of N-benzyloxycarbonyl-AspGlu-Val-Asp-fluoromethyl ketone, no cleavage of in vitro translated zeta-chain was observed. These results suggest that the loss of TcR zeta-chain, previously associated with tumor-induced immune dysfunction and more recently associated with tumor-induced apoptosis of T lymphocytes, is mediated by a direct degradation of the zeta-chain by activated caspases. This is the first report of involvement of caspases in degradation of the zeta protein.

Amino Acid Sequence↗
PubMed1999

The association of opportunistic infections with the occurrence of trimethoprim/sulfamethoxazole hypersensitivity in patients infected with human immunodeficiency virus.

Hypersensitivity from trimethoprim/sulfamethoxazole (TMP/SMX) has been linked to a reactive nitroso intermediate from sulfamethoxazole metabolism, which may be altered in patients with human immunodeficiency virus (HIV) infection. The authors determined the clinical factors that are associated with TMP/SMX hypersensitivity in patients with HIV. In a case control study, 54 controls currently tolerating TMP/SMX prophylaxis were randomly matched by date of hypersensitivity reaction in case patients to 28 patients with a history of a rash consistent with erythema multiforme from TMP/SMX. Demographic data, coadministered medications, laboratory data, and histories of opportunistic infections were extracted on all patients. A highly significant association was observed between the number of opportunistic infections and the occurrence of TMP/SMX hypersensitivity (p < 0.001), despite comparability of CD4 counts between case patients and controls (p > 0.1). A tendency for protection from TMP/SMX hypersensitivity in blacks was also observed (p = 0.066). These observations suggest that the mechanisms by which HIV produces cellular immune dysfunction and alters drug detoxification may be linked.

AIDS-Related Opportunistic Infections↗
PubMed1999

[Cytokines in patients with chronic renal failure during non-invasive therapy].

Patients with chronic renal failure (CRF) present an immunodeficient state manifested by an abnormally high incidence of malignant tumors, enhanced susceptibility to certain infections diseases, poor responses to influenza and hepatitis B vaccines. This state coexists paradoxically with activation of most immunocompetent cells, mostly monocytes and lymphocytes. A complexed net of reciprocally acting reasons of immunological processes in patients with CRF remains still unclear. Immunological response is bounded with release and functioning of cytokines. Plasma levels of many cytokines in patients with CRF are higher than in healthy control. The main role in this process plays the state of activation of monocytes provoked by the circulating endotoxins, which has been confirmed in those patients. Moreover, chronic renal failure itself and reactive oxygen species can cause a disregulation of production and elimination of these cytokines. The decreased clearance of cytokines due to renal failure can cause an accumulation of those proteins in blood. The origin, physiological role and disordered production of cytokines needs still further investigations in order to get a better understanding of a nature of dysfunction immune system in CRF patients.

Cytokines↗
PubMed1999

The significance of immune disorder in tropical spastic paraparesis.

The reports of the occurrence of HTLV-1 infection and/or HTLV-1 associated myelopathy (HAM/tropical spastic paraparesis (TSP) in patients with certain organ-specific and nonorgan-specific autoimmune diseases prompted us to assess the relationship between TSP and humoral autoimmunity. Blood samples from 76 TSP patients, 60 asymptomatic HTLV-1 carriers and 100 HTLV-1 seronegative blood donors were examined for the presence of organ-specific and nonorgan-specific autoantibodies, reactive serological tests for syphilis, immunoglobulin and complement concentrations as well as immunecomplexes. High prevalences of autoantibodies (39/76, 51%), reactive serological tests for syphilis (23/76; 30%), hypergammaglobulinaemia (69/76, 90%) and complement fixing immune complexes (44/76, 58%) were found in the TSP patients. These indicators of immunological disorder were found in statistically significantly lower prevalences in asymptomatic HTLV-1 carriers (12/60, 20%; p < 0.001; 6/60, 10%; p < 0.05; 32/60, 53%; p < 0.001 and 8/60, 13%; p < 0.001, respectively) and HTLV-1 seronegative blood donors (8/100, 8%; p < 0.001; 3/100, 3%; p < 0.001; 15/100, 15%; p < 0.001 and 5/100, 5%; p < 0.001, respectively). The profiles of autoimmune phenomena observed in the patient and control groups revealed that they were associated with TSP rather than mere HTLV-1 infection and consequently pathogenetic significance. The array of immunological features present in TSP was suggestive of autoimmune disease resulting from immune dysfunction. Studies which explore the possible existence of HTLV-1 induced autoantibodies with specificity for antigens of the spinal cord in TSP might be useful in elucidating its pathogenesis.

Adolescent↗
PubMed1999

What is the role of interleukin 10 in polymicrobial sepsis: anti-inflammatory agent or immunosuppressant?

BACKGROUND: Controversy exists concerning the role of interleukin 10 (IL-10) in sepsis. When IL-10 is used in models of endotoxemia, it appears to protect (by anti-inflammatory effects), whereas in models of polymicrobial sepsis it seems to be deleterious (by immunosuppression?). However, little direct evidence for such an immunosuppressive role is available for polymicrobial sepsis. Thus the aim of this study was to determine whether IL-10 contributes to lymphocyte immunosuppression in a model of cecal ligation and puncture (CLP) and whether neutralization of IL-10 has any salutary effects on survival after sepsis. METHODS: To assess the former, polymicrobial sepsis was induced in male C57BL/6J wild-type (+/+) and C57BL/6J-IL-10 knockout(-/-) mice by CLP. Splenocytes were harvested 24 hours later and stimulated with concanavalin A to assess their proliferative capacity and their ability to release the Th1 lymphokines interleukin 2 and interferon gamma (by enzyme-linked immunosorbent assay, nanograms/millilter). To further verify the immunosuppressive role of IL-10, splenocytes were obtained from male C3H/HeN mice 24 hours after CLP and then stimulated in the presence or absence of anti-IL-10 monoclonal antibody (Mab, 4 micrograms/mL). To assess the in vivo effects of IL-10 neutralization on survival after CLP, C3H/HeN mice (16 per group) were given 250 micrograms of anti-IL-10 Mab (intraperitoneally) either immediately after CLP (before the initiation of the hyperdynamic phase) or 12 hours after CLP (the beginning of the hypodynamic state). Control mice were given nonspecific rat immunoglobulin G. RESULTS: These data indicate that IL-10 deficiency (-/-) prevents the depression of the proliferative capacity and Th1 lymphokine production after sepsis. Analysis of the interleukin 2-interferon gamma production patterns and proliferative capacity in lymphocytes treated with anti-IL-10 Mab confirmed the role of IL-10 in suppressing lymphocyte responsiveness in CLP. Interestingly, however, only delayed administration (12 hours after CLP) of anti-IL-10 markedly increased survival of mice (Fisher's exact test, P < .05). CONCLUSION: The results not only illustrate IL-10's role in septic immune dysfunction but document that anti-IL-10 administration beyond the initial proinflammatory hyperdynamic state of polymicrobial sepsis improves survival of animals subjected to sepsis.

Animals↗
PubMedDate not supplied

[Effect of Onchocerca volvulus infestation on plasma vitamin A concentration in school children in a rural region of Cameroon].

Vitamin A deficiency is known to be associated with immune dysfunction and common childhood infections. However, little is known about the relationship between vitamin A deficiency and onchocerciasis in children. The aim of this study was to determine the prevalence of vitamin A deficiency and to investigate the relationship between vitamin A status and onchocerciasis. A total of 231 children, aged 6 to 15 years, were randomly selected between March 1995 and April 1996 at Yambassa and Balamba (central province of Cameroon). They were examined: we determined their vitamin A status and whether they had onchocerciasis. We diagnosed onchocerciasis by skin biopsy and the detection of antibodies against Onchocerca volvulus in the blood. We found that 101 of the 231 children examined (43.73%) had palpable nodules and/or microfilariae and the remaining 130 (56.27%) had been exposed to the parasite but had no clinical signs of infestation. Some children tested negative for skin microfilariae but positive by ELISA. Thus, 197 (85.28%) children were found to be infested with O. volvulus (group A) and the remaining 34 (14.72%) were found to have been exposed to the parasite but to have no clinical signs of onchocerciasis (group B). Plasma vitamin A concentrations were marginal, with concentrations below 0.7 mumol/l (20 mug/dl) recorded for 82.25% of the subjects. Children with onchocerciasis were more likely to have low vitamin A status. The mean plasma vitamin A concentration of infested children (0.52 +/- 0.14 mumol/l) was significantly lower (p < 0.05) than that of the children exposed but not infested. The parasite, O. volvulus, uses the vitamin A present in host tissues during its development, leading to a decrease in plasma retinol concentration.

Adolescent↗
PubMed1999

Retroviruses and autoimmune diseases.

The possible involvement of retroviruses in the development of autoimmune diseases has long been discussed. Exogenous retroviral infections and aberrant endogenous retroviral expressions can possibly induce immune dysfunction directly or indirectly. In addition to observations of autoimmune disease-like features in animal models, indirect evidences implicating retroviruses in human autoimmune diseases have been shown in a number of reports. However, direct evidence for the etiologic role of retroviruses in human autoimmune diseases has not yet been obtained.

Animals↗
PubMed1999

Spontaneous apoptosis in lymphocytes from patients with Wiskott-Aldrich syndrome: correlation of accelerated cell death and attenuated bcl-2 expression.

Wiskott-Aldrich syndrome (WAS) is an X-linked recessive disorder characterized by thrombocytopenia, eczema, and a progressive deterioration of immune function. WAS is caused by mutations in an intracellular protein, WASP, that is involved in signal transduction and regulation of actin cytoskeleton rearrangement. Because immune dysfunction in WAS may be due to an accelerated destruction of lymphocytes, we examined the susceptibility to apoptosis of resting primary lymphocytes isolated from WAS patients in the absence of exogenous apoptogenic stimulation. We found that unstimulated WAS lymphocytes underwent spontaneous apoptosis at a greater frequency than unstimulated normal lymphocytes. Coincident with increased apoptotic susceptibility, WAS lymphocytes had markedly attenuated Bcl-2 expression, whereas Bax expression did not differ. A negative correlation between the frequency of spontaneous apoptosis and the level of Bcl-2 expression was demonstrated. These data indicate that accelerated lymphocyte destruction by spontaneous induction of apoptosis may be one pathogenic mechanism by which the progressive immunodeficiency in WAS patients develops.

Adolescent↗
PubMed1999

Progress in our understanding of the biology of psoriasis.

This review describes the progress made in our understanding of the basic biology of psoriasis and how newer, safer clinical approaches to control the disease may result from these developments. It reveals how epidermal hyperproliferation can be permanently induced using transgenic mouse models, how the discovery of methods to generate humanized mouse monoclonal antibodies may be used to control the synthesis of autocrine and paracrine growth factors, how programmed cell death (apoptosis) is regulated in the epidermis, and how the abnormal synthesis of superantigens, cytokines, and chemokines can result in immune dysfunction and generate increased angiogenesis, inflammation, and epidermal hyperproliferation.

Animals↗
PubMed1999

HIV disease-related neutropenia: an independent risk factor for severe infections.

An increasing number of clinical studies have been reported in which neutropenia has been identified as an important independent risk factor in the development of infectious complications in patients with HIV and AIDS. Information on the clinical significance of infecting pathogens and the causes of neutropenia within different patient groups will be discussed, and may have clinical implications in subsequent disease management in these groups. Although the use of highly active antiretroviral therapy has shown some promise in the treatment of HIV-associated hematologic disturbances and immune dysfunction, the rate of virological failure with this treatment over time suggests that these disturbances could reappear in the near future, as well as their associated infectious complications.

Acquired Immunodeficiency Syndrome↗
PubMed2000

HIV-1 gp120- and gp160-induced apoptosis in cultured endothelial cells is mediated by caspases.

The immune dysfunction and cell destruction that occur in the human immunodeficiency virus (HIV)-infected host appear to result from the direct cytopathic effects of viral infection and the effects of viral proteins on uninfected bystander cells. Recently, the alpha-chemokine receptor CXCR4 has been reported to mediate apoptosis in neuronal cells and in CD4(+) and CD8(+) T cells after its binding to HIV-1 envelope proteins. In the current study, it was observed that human umbilical vein endothelial cells (HUVEC) undergo apoptosis after their treatment with the HIV-1 envelope proteins gp120/160. Anti-CXCR4 monoclonal antibody decreased HIV-1 gp120/160-induced apoptosis, suggesting that the CXCR4 chemokine receptor mediates the apoptotic effects of these HIV envelope glycoproteins. Further studies revealed that caspases play an important role in this process because the pretreatment of cells with a general caspase enzyme inhibitor decreased the extent of HUVEC apoptosis induced by gp120/160. In addition, it was found that caspase-3 was activated on HIV-1 gp120/160 treatment of these cells. It was also observed that gp120/160 treatment slightly increased the expression of the pro-apoptotic molecule Bax. These results suggest that HIV-1 envelope glycoproteins can disrupt endothelial integrity through the interaction with CXCR4, thereby facilitating virus transit out of the bloodstream and contributing to the vascular injury syndromes seen in acquired immunodeficiency syndrome. (Blood. 2000;96:1438-1442)

Apoptosis↗