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)

Several distinct populations of sensory neurons in the ophthalmic region of the mouse trigeminal ganglion have been identified by their reactivity to antibodies raised against substance P (SP), calcitonin gene-related peptide (CGRP), cell-surface glycoconjugates SSEA3 and LD2, and the plant lectin, Bandeiraea simplicifolia lectin 1, isolectin 4 (BSIL4). Thirty-six percent of the neurons in the ophthalmic portion of the mouse trigeminal ganglion express CGRP and 17%, SP. All neurons that express SP also express CGRP. Forty percent of the neurons in the ophthalmic region of the ganglion are recognized by monoclonal antisera to SSEA3, and 66% of this population also express the neuropeptides SP or CGRP. The neuronal population recognized by BSIL4 is identical to the population with the LD2 epitope. This population of cells (BSIL4/LD2) does not express the SSEA3 glycoconjugate and is largely nonpeptidergic. All four populations of sensory neurons (SP, CGRP, SSEA3, and LD2/BSIL4) can be infected by herpes simplex virus (HSV). However, the relative proportion of SSEA3- and LD2/BSIL4-labeled cells that were infected productively with HSV was much less than expected based on the relative size of the populations of these neurons in the ophthalmic region of the ganglion.
 ...
PMID:Herpes simplex viral infection of the mouse trigeminal ganglion. Immunohistochemical analysis of cell populations. 137 Dec 69

In many cases of chronic intractable pain without any discernible causes, when both Western medical treatment and acupuncture treatment failed to eliminate the pain, this pain is often due to the unrecognized presence of viral or bacterial infection. Even effective anti-viral or bacterial agents often fail to eliminate or inhibit the infection, as these drugs may also fail to reach the most painful area where often unrecognizable circulatory disturbances co-exist. Using the Bi-Digital O-Ring Test Molecular Identification Method, we were able to localize substance P and thromboxane B2 (a good indicator of the presence and degree of circulatory disturbances) in the painful area along with virus or bacteria. Based on the Bi-Digital O-Ring Test localization method for specific substances or microbes, the author has successfully treated cases of chronic intractable pain by the combination of anti-viral or bacterial agents with either manual acupuncture, electro-acupuncture or transcutaneous electrical stimulation through a pair of surface electrodes. Among a variety of infections, the most common cause of severe intractable pain was herpes simplex virus, and the most common bacterial cause of intractable pain of moderate degree was campylobacter. In addition, chlamydia was a very common cause of mild intractable pain. When peripheral nerve fibers are hypersensitive from nerve injury due to viral infection, in addition to the drug therapy for infection, use of Vitamin B1 25 mg., 2 times a day for an average adult often accelerates recovery time. As an anti-viral agent for the herpes virus family, the author found that EPA (Omega 3 fish oil, Eicosa Pentaenoic Acid, C20:5 omega 3), at doses between 180 mg. and 350 mg (depending upon body weight) 4 times a day for 2 to 6 weeks, without prescribing the common anti-viral agent Acyclovir, often eliminated the symptoms due to viral infection including all well-known types of the herpes virus, such as herpes simplex virus, Epstein-Barr virus, and cytomegalovirus. Epstein-Barr virus and cytomegalovirus are usually not associated with intractable severe pain, but they are often associated with a recurrent burning or itching sensation and they can cause intractable frequent muscle twitching. Viruses belonging to the herpes family almost always exist between the midline of one side of the spinal cord and the midline of the front of the body where these nerves from the spinal cord end and the same virus is localized only on one side of the body at the same spinal level.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Treatment of acute or chronic severe, intractable pain and other intractable medical problems associated with unrecognized viral or bacterial infection: Part I. 197 80

Hybrid cell lines derived from neonatal rat dorsal root ganglia neurons fused with the mouse neuroblastoma N18Tg2 exhibit sensory neuron-like properties not displayed by the parental neuroblastoma. These properties include an inward (depolarizing) current with a conductance increase in response to activation of a bradykinin receptor, an inward (depolarizing) current with a conductance increase in response to the sensory excitotoxin capsaicin, the expression of sensory neuropeptides (substance P, CGRP and somatostatin), the expression of phosphatidylinositol-anchored molecules including adhesion molecules of the immunoglobulin superfamily that can be regulated in serum-free culture by nerve growth factor (N-CAM, F-3 and Thy-1), and low permissivity to herpes simplex virus infection. These lines thus provide appropriate models for the study of mechanisms involved in nociceptor activation and the regulation of expression of sensory-neuron specific markers including neuropeptides.
 ...
PMID:Novel cell lines display properties of nociceptive sensory neurons. 197 43

Following inoculation into the snout herpes simplex virus (HSV) spread to neurons in mouse trigeminal ganglion and subsequently to the brain. Capsaicin treatment of neonatal mice, which causes a loss of unmyelinated sensory neurons, some of which contain substance P, reduced the mortality rate of HSV-infected mice. Moreover, a lower percentage of mice survived the infection with reactivatable virus. There was also an extensive infection of glial cells proximal to the transitional zone in the trigeminal root between the peripheral and central nervous system. Distal to this zone there was an accumulation of substance P immunoreactivity in centrally directed fibres. This amplified degenerative effect on central branches of the substance P containing sensory nerves by glial infection may contribute to the deafferentiation pain syndrome following HSV infection.
 ...
PMID:Herpes simplex virus infection in capsaicin-treated mice. 301 97

Herpes simplex virus is most probably maintained in the ganglion neurons of the peripheral nervous system of humans in a latent form that can reactivate to produce recurrent disease. As an approximation of this cell-virus interaction, we have constructed a herpes simplex virus latency in vitro model system using human fetus sensory neurons as the host cell. Human fetus neurons were characterized as neuronal in origin by the detection of the neuropeptide substance P and the neuron-specific plasma membrane A2B5 antigen. Virus latency was established by blocking complete expression of the virus genome by treatment of infected human neurons with a combination of human leukocyte interferon and (E)-5-(2-bromovinyl)-2'-deoxyuridine for 7 days. After removal of inhibitors, virus latency was maintained for at least 9 days. This in vitro model will provide a system to analyze, in a primary human neuron, the state of the herpes simplex virus genome during establishment and maintenance of experimental latency.
 ...
PMID:Herpes simplex virus latency in isolated human neurons. 609 Nov 42

Experimental herpes simplex keratitis in the mouse produced a rapid fall in both corneal sensitivity and levels of corneal substance P (SP). This finding supports the association of SP with sensory neurones and shows that such levels can be used as an indication of damage to neurones resulting, for example, from infection with HSV. However, the delay in recovery of SP compared to the more rapid and complete recovery of sensitivity suggests that SP in the cornea is not directly involved in mediation of the blink reflex.
 ...
PMID:Corneal sensitivity and substance P in experimental herpes simplex keratitis in mice. 618 14

Inoculation of the scarified cornea with herpes simplex virus (type 1) leads to herpetic infection of trigeminal ganglion cells. A recent study of the susceptibility of ganglion cells revealed that there may be at least four populations of trigeminal ganglion cells that are infectable by herpes. Two classes were identified by their neuropeptide content: Substance P or calcitonin gene-related peptide. One class was identified by its affinity for a monoclonal antibody, SSEA-3. The fourth class was recognized by its common affinity for both the monoclonal antibody LD2 and for the lectin Bandeiraea simplicifolia isolectin. However, there has been no direct evidence of which types are infected directly as a result of retrograde transport from the corneal site and which may be infected by cell-to-cell spread. The aim of this study was to determine which classes of neurons, which are known to become infected with HSV after ocular inoculation, supply corneal innervation. We have identified four classes of trigeminal ganglion neurons that supply axons to the central cornea of the mouse, on the basis of their ability to transport Fluoro-Gold retrograde from axons in the central corneal epithelium and stroma. About 40% of the neurons that innervate the cornea contain Substance P or calcitonin gene-related peptide; about 60% of the neurons that innervate the cornea react with the monoclonal antibody SSEA-3. About 36% of all neurons in the whole ophthalmic division react with the LD2 or Bandeiraea simplicifolia isolectin, and Fluoro-Gold labels only 2% of them.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Immunohistochemical identification of trigeminal ganglion neurons that innervate the mouse cornea: relevance to intercellular spread of herpes simplex virus. 767 19

Several viruses are known to utilize cellular integrin molecules to gain entry into cells. Because of the ability of herpes simplex virus type 1 (HSV-1) to disrupt cellular adhesion, as seen particularly in ocular infections, we examined the ability of several peptides, containing known integrin recognition sequences, to interfere with plaque formation of HSV-1 in epithelial cells. We also examined the possible involvement of tachykinins in virus entry. We did not detect any decrease in plaque formation by HSV-1 in the presence of Arg-Gly-Asp, Asp-Gly-Glu-Ala, or EILDV peptides or in the presence of monoclonal antibodies to the human beta1 or beta4 integrin subunit. Substance P or inhibitors of the NK1 or NK2 tachykinin receptors also had no inhibitory effects on HSV-1 plaque formation.
 ...
PMID:Lack of detectable interaction between HSV-1 and integrins or tachykinins. 982 Aug 48

Neuropeptides are able to modulate cytokine production by macrophages in response to various stimulators. In this study, the effects of neuropeptides substance P (SP) and calcitonin gene-related peptide (CGRP) on production of pro-inflammatory cytokines TNF and IL-1 beta by macrophages were considered. Mouse peritoneal macrophages were infected with herpes simplex virus type-1 (HSV-1), or remained unstimulated, and cytokine assays were performed after 12 h. IL-1 beta and TNF secretion by unstimulated macrophages have been significantly increased in the presence of SP and CGRP. Each neuropeptide, alone or in coordination with the other, caused significant increase in IL-1 beta and TNF production by HSV-infected mouse peritoneal macrophages. It was concluded that the macrophage-mediated inflammatory response to HSV-1 is enhanced in the presence of these neuropeptides.
 ...
PMID:Neuropeptides (SP and CGRP) augment pro-inflammatory cytokine production in HSV-infected macrophages. 1463 37

We examined the utility of herpes simplex virus (HSV) vector-mediated gene transfer of vascular endothelial growth factor (VEGF) in a mouse model of diabetic neuropathy. A replication-incompetent HSV vector with VEGF under the control of the HSV ICP0 promoter (vector T0VEGF) was constructed. T0VEGF expressed and released VEGF from primary dorsal root ganglion (DRG) neurons in vitro, and following subcutaneous inoculation in the foot, expressed VEGF in DRG and nerve in vivo. At 2 weeks after induction of diabetes, subcutaneous inoculation of T0VEGF prevented the reduction in sensory nerve amplitude characteristic of diabetic neuropathy measured 4 weeks later, preserved autonomic function measured by pilocarpine-induced sweating, and prevented the loss of nerve fibers in the skin and reduction of neuropeptide calcitonin gene-related peptide and substance P in DRG neurons of the diabetic mice. HSV-mediated transfer of VEGF to DRG may prove useful in treatment of diabetic neuropathy.
 ...
PMID:HSV-mediated gene transfer of vascular endothelial growth factor to dorsal root ganglia prevents diabetic neuropathy. 1592 Apr 61


1 2 Next >>