Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P20366 (substance P)
 21,176 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We examined 101 sera from 32 adult sporadic amyotrophic lateral sclerosis (ALS) patients, including nine with positive enzyme-linked immunosorbent assay (ELISA) serum antibodies against human spuma retrovirus (HSRV) [human foamy virus (HFV)] envelope (env) and/or capsid (gag) proteins, for peptide seroreactivity. Synthetic peptides 10 to 14 amino acids in length were selected from HSRV (3), maedi-visna virus (1), human nerve growth factor-beta (1), and human amyloid-beta sequences (1). Eighteen of 101 ALS sera compared with six of 144 control sera reacted to any of the sequences (p < 0.01) (i.e., 8/32 ALS patients and 2/93 control patients bound to a synthetic peptide, p < 0.01). Peptide VLA- [NGF beta(1-14)] was reproducibly recognized by one of the 93 neurologic controls, and one of the 32 ALS patients reproducibly reacted to synthetic peptides [EET-, HSRVenv/NGF beta(55-61)] and [GSN-, beta-amyloid(25-35)] simultaneously. This amyloid-A(25-35) peptide corresponds to the neurotoxic and neurotrophic tachykinin homology sequence described by Yanker. Only ALS patients (no controls) reacted with the visna/CNTF peptide SMC- and HSRVbcl-1/amyloid(740-751) peptide EGP-. Testing a total of 245 sera from 125 patients, three reproducible reactivities (two ALS, one OND) were observed both with and without glutaraldehyde linkage. Of the four peptides recognized either by more than one serum from the same patient with ALS or by sera from ALS patients only (EET-, GSN-, SMC-, EGP-), two share a circumscript homology with maedi-visna virus envelope glycoprotein (Table 1).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Retroviral synthetic peptide serum antibodies in human sporadic amyotrophic lateral sclerosis. 800 25

Substance P (SP), a potent modulator of neuroimmunoregulation, is expressed in human immune cells. We observed elevated plasma SP levels in HIV-infected men compared with uninfected subjects. In the present study, we investigated the possible cellular source of the increased SP level caused by HIV infection. Using real-time reverse transcriptase-polymerase chain reaction, we demonstrated that monocyte-derived macrophages (MDM) and lymphocytes from both placental cord blood and adult peripheral blood expressed SP mRNA, which was significantly increased by HIV infection. HIV-induced SP expression was positively related to virus replication in the infected MDM. Purified recombinant HIV envelope glycoprotein 120 (gp120) derived from both the macrophage-tropic strain (MN) and the T lymphocyte-tropic strain (IIIB), when added to MDM cultures, enhanced SP mRNA expression. The gp120-induced SP expression was abrogated by pretreating the cells with soluble CD4. Furthermore, the activation of HIV in the latently infected promonocytic cell line (U1) and T-cell line (ACH-2) up-regulated SP mRNA expression. These data support the hypothesis that interaction of HIV and SP may have significant in vivo relevance to the immunopathogenesis of HIV infection and AIDS.
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PMID:HIV enhances substance P expression in human immune cells. 1191 72

HIV-1 infection has significant effect on the immune system as well as on the nervous system. Breakdown of the blood-brain barrier (BBB) is frequently observed in patients with HIV-associated dementia (HAD) despite lack of productive infection of human brain microvascular endothelial cells (HBMEC). Cellular products and viral proteins secreted by HIV-1 infected cells, such as the HIV-1 Gp120 envelope glycoprotein, play important roles in BBB impairment and HIV-associated dementia development. HBMEC are a major component of the BBB. Using cocultures of HBMEC and human astrocytes as a model system for human BBB as well as in vivo model, we show for the first time that cannabinoid agonists inhibited HIV-1 Gp120-induced calcium influx mediated by substance P and significantly decreased the permeability of HBMEC as well as prevented tight junction protein down-regulation of ZO-1, claudin-5, and JAM-1 in HBMEC. Furthermore, cannabinoid agonists inhibited the transmigration of human monocytes across the BBB and blocked the BBB permeability in vivo. These results demonstrate that cannabinoid agonists are able to restore the integrity of HBMEC and the BBB following insults by HIV-1 Gp120. These studies may lead to better strategies for treatment modalities targeted to the BBB following HIV-1 infection of the brain based on cannabinoid pharmacotherapies.
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PMID:Cannabinoids inhibit HIV-1 Gp120-mediated insults in brain microvascular endothelial cells. 1894 Dec 31