Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The objective of the study was to relate plasma dehydroepiandrosterone sulfate (DHEA-S) concentrations to the progression of HIV infection in individual HIV-infected men with hemophilia and to obtain information on the cause of DH EA-S alterations. Blood samples were obtained from 16 men with hemophilia; in 9 men serial samples were available for up to 11 years after HIV-1 infection. Control samples were obtained from men of comparable ages without hemophilia or HIV infection. Measurements were made of CD4+ cell counts, plasma adrenocorticotropic hormone (ACTH), cortisol, DHEA, DHEA-S, and prolactin. Before HIV infection, men with hemophilia had significantly lower plasma levels of DHEA-S than control men. After infection, 3 of 9 subjects studied serially had little or no change in plasma DHEA-S levels or in CD4+ cell counts over 11 years. Four of the 9 i n whom AIDS developed had progressive decreases in plasma DHEA-S concentrations that, in some cases, preceded a precipitous fall in CD4+ cell counts. Major decreases in plasma DHEA-S levels before falls in CD4+ counts were observed in 2 ot her subjects who had other severe illnesses. None of the decreases in DHEA-S levels were associated with decreased concentrations of plasma cortisol, ACTH, or prolactin. We conclude that plasma DHEA-S is an indicator of general health rather than a specific indicator for progression of HIV. The decrease in plasma DHEA-S is not related to ACTH stimulation of the adrenal gland or to cortisol secretion, but it may be related to cytokines that can inhibit 17-hydroxylation of DH EA-S precursors.
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PMID:Longitudinal study of adrenal steroids in a cohort of HIV-infected patients with hemophilia. 864 55

Documented evidence supports the "cortisol connection' theory of acquired immune deficiency syndrome, linking glucocorticoid metabolism with immune function, and human immunodeficiency virus with them both. The peptide T subregion of gp 120 of human immunodeficiency virus apparently utilizes cellular melanocyte stimulating hormone receptors to competitively inhibit the blocking of interleukin-1 by melanocyte-stimulating hormone. Interleukin-1 stimulates CD8+ T-lymphocyte proliferation, as well as causing the release of corticotropin-releasing hormone, thereby stimulating the release of adrenocorticotrophic hormone and cortisol. Gp 120 also induces upregulation of adrenocorticotrophic hormone-related messenger ribonucleic acid. This apparently separate glucocorticoid metabolic route utilized by human immunodeficiency virus is the basis of the cortisol excess seen in human immunodeficiency virus infection. In vitro glucocorticoid-resistant lymphoid cells are resistant to human immunodeficiency virus infection as well. Viral resistance is also observed in patients who demonstrate glucocorticoid resistance. Glucocorticoid-responsive elements are contained in the human immunodeficiency virus (proviral and viral) genome that appear to regulate human immunodeficiency virus replication. Similarly, lymphoid-cell development and regulation depend on glucocorticoids. One may take advantage of this view of human immunodeficiency virus pathogenesis to create new methods of treatment.
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PMID:Acquired immune deficiency syndrome: the glucocorticoid solution. 881 17

Localized inflammation of a rat's hindpaw elicits an accumulation of beta-endorphin-(END) containing immune cells. We investigated the production, release, and antinociceptive effects of lymphocyte-derived END in relation to cell trafficking. In normal animals, END and proopiomelanocortin mRNA were less abundant in circulating lymphocytes than in those residing in lymph nodes (LN), suggesting that a finite cell population produces END and homes to LN. Inflammation increased proopiomelanocortin mRNA in cells from noninflamed and inflamed LN. However, END content was increased only in inflamed paw tissue and noninflamed LN-immune cells. Accordingly, corticotropin-releasing factor and IL-1beta released significantly more END from noninflamed than from inflamed LN-immune cells. This secretion was receptor specific, calcium dependent, and mimicked by potassium, consistent with vesicular release. Finally, both agents, injected into the inflamed paw, induced analgesia which was blocked by the co-administration of antiserum against END. Together, these findings suggest that END-producing lymphocytes home to inflamed tissue where they secrete END to reduce pain. Afterwards they migrate to the regional LN, depleted of the peptide. Consistent with this notion, immunofluorescence studies of cell suspensions revealed that END is contained predominantly within memory-type T cells. Thus, the immune system is important for the control of inflammatory pain. This has implications for the understanding of pain in immunosuppressed conditions like cancer or AIDS.
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PMID:Immune cell-derived beta-endorphin. Production, release, and control of inflammatory pain in rats. 920 66

The circadian rhythms of plasma growth hormone (GH), insulin-like growth factor type I (IGF-I), cortisol, adrenocorticotropic hormone (ACTH), thyroid-stimulating hormone (TSH), and prolactin (PRL) were evaluated in 13 HIV-seropositive patients (8 males and 5 females; mean age [+/-SD], 30 +/- 5 years), classified as CDC C2. Sixteen clinically healthy subjects (9 males and 7 females; mean age [+/-SD], 32 +/- 8 years) were chosen as control group. Samples were taken every 4 hr from 04:00 to 20:00 and every 2 hr from 20:00 to 04:00. Plasma GH was evaluated by IRMA procedure, plasma IGF-I by RIA (after separation of soluble IGF-I from IGF-I-binding proteins, using acid-ethanol extraction), plasma cortisol by a solid-phase RIA, plasma ACTH by double-antibody RIA, and serum TSH and serum PRL by a solid-phase two-site fluoroimmunometric assay. Rhythmometric data were analyzed by single and population mean cosinor analysis; the comparison of the parameters of the rhythm between patients and controls was carried out by the mesor test and the amplitude-acrophase Hotelling test. Alterations of the circadian pattern of GH, IGF-I, cortisol, ACTH, TSH, and PRL were demonstrated in HIV-seropositive patients. In fact, the circadian profiles of these hormones were clearly flattened and no statistically significant 24-hr rhythm was detectable (with the exception of cortisol). These results are consistent with the hypothesis that alterations of the circadian temporal structure may already be present in HIV-seropositive patients without wasting and infectious complications.
AIDS Res Hum Retroviruses 1997 Sep 20
PMID:Circadian secretory pattern of growth hormone, insulin-like growth factor type I, cortisol, adrenocorticotropic hormone, thyroid-stimulating hormone, and prolactin during HIV infection. 931 Feb 92

We present two patients with manifest acquired immunodeficiency syndrome (AIDS) suffering from a generalized cytomegalovirus (CMV) infection. Over the course of several weeks they had developed a state of increasing lethargy and fatigue and one patient had noticed a darkening of his skin. These and other symptoms (vomiting, diarrhoea, hypotension) were suggestive of adrenal insufficiency. Laboratory findings included an increase of serum potassium levels, a decrease of serum sodium concentrations and elevated levels of the adrenocorticotropic hormone (ACTH). These findings, as well as the prompt therapeutic response to hydrocortisone established the diagnosis of adrenal insufficiency. Although definitive proof is lacking, generalised CMV infection is the most likely cause of our patients' symptoms. For the early initiation of appropriate substitution therapy, persons infected with the human immunodeficiency virus (HIV) with signs of CMV infection should be carefully and repeatedly monitored for clinical and laboratory signs of adrenal insufficiency.
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PMID:Primary adrenal insufficiency in two patients with the acquired immunodeficiency syndrome associated with disseminated cytomegaloviral infection. 940 82

Many patients with acquired immune deficiency syndrome (AIDS) have symptoms consistent with adrenal insufficiency, but only a small subset of these patients meet criteria for adrenal insufficiency during a short corticotropin (ACTH) stimulation test. We hypothesized that patients with AIDS and symptoms of adrenal insufficiency who produce normal amounts of cortisol in response to administration of 0.25 mg cosyntropin may nevertheless produce lower amounts of cortisol in a course of 24 hours than comparably sick AIDS patients without symptoms of adrenal insufficiency or comparably sick patients without AIDS. We studied four groups of male patients: AIDS patients with symptoms suggestive of adrenal insufficiency but with a normal response to cosyntropin (group I), AIDS patients without symptoms suggestive of adrenal insufficiency (group II), human immunodeficiency virus (HIV)-negative patients with serious acute or chronic illness (group III), and healthy subjects (group IV). The following variables were examined: age, CD4 cell count, Acute Physiologic and Chronic Health Evaluation (APACHE) score, serum cortisol and plasma ACTH at baseline; serum cortisol at 30 and 60 minutes after intravenous administration of 0.25 mg cosyntropin; and 24-hour urinary free cortisol. The four groups had a similar mean age and baseline plasma ACTH and serum cortisol levels. However, a change in cortisol from baseline to 30 and 60 minutes after administration of cosyntropin was significantly smaller in both groups of AIDS patients than in the sick patients without AIDS and normal subjects. There were also differences noted between the two groups of AIDS patients: both baseline and stimulated levels of cortisol tended to correlate directly with ACTH levels in patients without symptoms of adrenal insufficiency, while this relationship appeared to be inverse in patients with symptoms suggestive of adrenal insufficiency (r = -.57 to -.7, P < .05 to .14). The 24-hour urinary free cortisol levels were similar among all groups, but correlated strongly with baseline and stimulated serum cortisol levels only in patients with AIDS and symptoms of adrenal insufficiency (r = .8 to .9, P < .002 to .015). We conclude that (1) AIDS patients with and without symptoms of adrenal insufficiency may have either normal adrenal function or somewhat suboptimal adrenal reserve as demonstrated by a blunted cortisol response during the short ACTH stimulation test in comparison to HIV-negative comparably sick patients or healthy subjects; and (2) 24-hour urinary free cortisol is not a useful test for detection of subtle abnormalities of adrenal function in patients with AIDS.
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PMID:Twenty-four-hour urinary free cortisol in patients with acquired immunodeficiency syndrome. 962 68

Disruption of the linkage among the immune, nervous, and endocrine systems may contribute to the pathology and symptoms of acquired immunodeficiency syndrome (AIDS). We investigated the role of human immunodeficiency virus (HIV) in altering these linkages via induction of corticotropin (ACTH) by lymphocytes. Cultured T lymphocytes (H9 cell line) were infected with HIV-1, after which ACTH production was measured and characterized at various time intervals by immunofluorescence and Western blotting. We report a coordinate expression of ACTH and p24 HIV core protein in H9 cells. Also, the kinetics of HIV-induced ACTH production by H9 T lymphoma cells are demonstrated using three different strains of HIV as well as UV-inactivated HIV. ACTH production corresponded with the appearance of p24 antigen and was maximal 35 days after infection. UV-inactivated HIV and the viral envelope protein, gp120, were also able to induce ACTH production in these cells, indicating that viral replication was not required for the ACTH induction. The HIV-induced ACTH was synthesized de novo and had the size and biological activity of pituitary ACTH. Inhibition of ACTH in HIV-infected lymphocyte cultures by anti-ACTH antiserum enhanced viral p24 expression. The significance of lymphocyte ACTH in AIDS is not clear, but these results suggest that it may restrict HIV replication and possibly infection.
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PMID:Human immunodeficiency virus induction of corticotropin in lymphoid cells. 985 80

We show that infection of primary monocyte-derived macrophages (MDMs) and blood lymphocytes (PBLs) by human immunodeficiency virus type 1 (HIV-1) R5 strains, but not that of PBLs by X4 strain HIV-1LAI, is inhibited by beta-chemokines RANTES and MIP-1alpha. A biotinylated disulfide-bridged peptide mimicking the complete loop of clade B consensus V3 domain of gp120 (V3Cs), but not a biotinylated V3LAI peptide or a control beta-endorphin peptide of approximately the same molecular weight (MW), was found to bind specifically to MDM membrane proteins, in particular two proteins of 42 and 62 kDa migrating as sharp bands after electroblotting onto Immobilon, and this was specifically inhibited by anti-V3 antibodies. When biotinylated V3Cs was incubated with intact MDMs, which were then washed and lysed, and the resulting material was incubated with streptavidin-agarose beads and electroblotted onto Immobilon, fresh V3Cs also bound to proteins of the same molecular weight recovered in the V3Cs-interacting material. This binding was inhibited by anti-V3 antibodies, and no binding occurred with the control peptides. V3Cs also bound to soluble recombinant CD4, and CD4 monoclonal antibody Q4120 specifically recognized the V3Cs-interacting 62-kDa protein, which should thus correspond to CD4. Recombinant radiolabeled RANTES, MIP-1alpha, and MIP-1beta, but not IL-8, also bound to a 42-kDa protein on the membrane of MDMs as well as to the V3Cs-interacting 42-kDa protein, and excess unlabeled V3Cs inhibited such binding. This protein was also recognized by antibodies to CCR5, the RANTES/MIP-1alpha/MIP-1beta receptor. These data show that V3Cs binds to MDM membrane proteins that comprise CD4 and CCR5, and that multimolecular complexes involving at least gp120 V3, CD4, and CCR5 are formed on the surface of MDMs as part of V3-mediated postbinding events occurring during HIV-1 infection.
AIDS Res Hum Retroviruses 1998 Dec 20
PMID:Interaction of human immunodeficiency virus type 1 envelope glycoprotein V3 loop with CCR5 and CD4 at the membrane of human primary macrophages. 987 Mar 13

It is now largely established that the immune and neuroendocrine systems cross-talk by using similar ligands and receptors. In this context, the thymus-hypothalamus/pituitary axis can be regarded as a paradigm of connectivity in both normal and pathological conditions. For example, cytokines and thymic hormones modulate hypothalamic-pituitary functions: (a) interleukin (IL)-1 seems to upregulate the production of corticotropin-releasing factor and by adrenocorticotropin by hypothalamic neurons and pituitary cells, respectively; (b) thymulin enhances LH secretion. Conversely, a great deal of data strongly indicate that the hypothalamic-pituitary axis plays a role in the control of thymus physiology. Growth hormone (GH) for example, enhances thymulin secretion by thymic epithelial cells (TEC), both in vivo and in vitro, also increasing extracellular matrix-mediated TEC/thymocyte interactions. Additionally, gap junction-mediated cell coupling among TEC is upregulated by ACTH. In a second vein, it was shown that GH injections in aging mice increased total thymocyte numbers and the percentage of CD3-bearing cells, as well concanavalin-A mitogenic response and IL-6 production. In addition to mutual effects, thymus-pituitary similarities for cytokine and hormone production have been demonstrated. Cytokines such as IL-1, IL-2, IL-6, interferon-gamma, transforming growth factor-beta and others can be produced by hypothalamic and/or pituitary cells. Conversely, hormones including GH, PRL, LH, oxytocin, vasopressin and somatostatin can be produced intrathymically. Moreover, receptors for various cytokines and hormones are expressed in both the thymus and the hypothalamus/pituitary axis. Lastly, it is noteworthy that a thymus-pituitary connectivity can also be seen under pathological situations. In this regard, an altered HPA axis has been reported in AIDS, human falciparum malaria and murine rabies, that also show a severe thymic atrophy.
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PMID:Immunoneuroendocrine connectivity: the paradigm of the thymus-hypothalamus/pituitary axis. 987 43

Adrenal insufficiency is known to be a complication of HIV infection, although estimates of its prevalence and severity vary. Adrenal insufficiency is the most serious endocrine complication that occurs in persons with HIV infection. Patients with acquired immune deficiency syndrome (AIDS) are considered to be at high risk for primary or secondary adrenal insufficiency. We describe 3 patients with AIDS who had clinical features suggestive of adrenal insufficiency, but their corticotropin (ACTH) stimulation tests were normal. Repeat testing confirmed the diagnosis in one patient, and further testing with the overnight metyrapone test revealed evidence of secondary adrenal insufficiency in the other patients. Persistent clinical improvement was evident on subsequent glucocorticoid therapy. A normal response to the ACTH stimulation test can be dangerously misleading. Patients with AIDS and suspected adrenal insufficiency who have normal screening by the ACTH stimulation test should undergo further testing for secondary adrenal disease.
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PMID:Adrenal insufficiency in HIV infection: a review and recommendations. 1121 16


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