Disease relevance of Pcyt1b

• METHODS: The B subunit of cholera toxin (CTB), fast blue, and a retrograde transneuronal tracer, the Bartha strain of pseudorabies virus (PRV-Ba), were injected into the upper eyelids of adult Sprague-Dawley rats after sectioning the ipsilateral branches of the facial nerve and resecting the superior cervical ganglia [1].
• The B subunit of cholera toxin (CTB) has been shown to augment mucosal responses to microbial virulence antigens, including those of Streptococcus mutans, which is the principal etiologic agent of dental caries [2].
• Following injection of CTB into the lateral DRN, retrogradely labeled ganglion cells (GCs) were observed in whole-mount retinas of both species [3].
• Two months after ischemia, the anterogradely transported neuronal tracer cholera toxin B subunit (CTB) was injected in the ischemic eyes and animals were processed 4 days later [4].
• Seven days after contusions using the Infinite Horizon impactor the area of CTB-labeled terminal fibers had a negative correlation with increasing impact force [5].

High impact information on Pcyt1b

• We found that CT or CTB alone did not affect histamine release; however, mast cell IL-6 production was significantly enhanced by CT but not by CTB [6].
• In contrast, when CTB or a monoclonal anti-GM1 antibody was also added to the medium, cycloheximide-induced neuritogenesis was amplified further on pFN and sensitivity to peptide A inhibition was abolished [7].
• The retinotectal projection was orthogradely labeled with cholera toxin subunit B (CTB) injected in the left eye and measured in serial coronal sections of the superior colliculus [8].
• The induced migration seems to be dependent on the enzymatic A-subunit of CT, since challenge with neither sorbitol nor CT B-subunit did mimic the effects of CT on CD8(+) IEL [9].
• The results were a dramatic decrease of primary sensory endings in the spinal cord of aged rats following transganglionic labeling with CTB, and also to a lesser degree with B4 [10].

Biological context of Pcyt1b

• Profile counting and frequency estimates showed that the reduction of CTB labeled profiles not was caused by impaired axonal uptake, slowed axonal transport of CTB, or by a loss of myelinated fibers in the peripheral nerve [10].
• CTB treatment (1 micrograms/ml) enhanced NGF-induced neurite outgrowth from PC12 cells, NGF-induced activation of ribosomal protein S6 kinase, and NGF-induced stimulation of trk phosphorylation [11].
• Most importantly, oral treatment with CTB-OVA conjugate could also suppress an already initiated IgE antibody response, but to achieve such a 'therapeutic effect', administration of multiple low doses of conjugate over a long time was required [12].
• These properties make CTB-gold a valuable tool for studying the connectivity and neurochemistry of pathways in the central nervous system [13].
• Cell size measurements in the rat showed that most of the CTB-positive neuron profiles were small in size after axotomy, whereas most were large in intact DRGs [14].

Anatomical context of Pcyt1b

• Highly purified, freshly isolated, rat peritoneal mast cells from Brown Norway rats were cultured in the presence of CT or its B subunit (CTB) alone or in combination with anti-IgE or bacterial LPS [6].
• We have examined the possible regulation of the NGF signaling pathway in PC12 cells by the B subunit of cholera toxin (CTB), which binds to endogenous GM1 specifically and with a high affinity [11].
• To resolve if similar regressive processes occur in the central innervation, peripheral nerves were injected with markers for unmyelinated (isolectin B4) or myelinated (cholera toxin B subunit; CTB) DRG neurons [10].
• While a significant mucosal immunoglobulin A (IgA) response was induced by KLH, there were no significant differences among the immunized groups in the levels of IgA antibodies in salivary gland, gut, vaginal, and uterine secretions, with the exception that rats immunized only orally with the KLH-CTB conjugate lacked a detectable vaginal response [15].
• Anterograde transport of the B fragment of cholera toxin (CTB) from the sciatic nerve showed a strictly ipsilateral projection to segments in L4 and L5 but both ipsi- and contralateral projections in L6 and more caudal segments [16].

Associations of Pcyt1b with chemical compounds

• The neurite extension induced with CTB was strongly suppressed by the pretreatment of tyrosine kinase inhibitors in a dose-dependent manner [17].
• OBJECTIVES: We examined whether oral prophylactic or therapeutic administration of a model allergen coupled to CTB would modulate allergen-specific IgE responses in high IgE responder Balb/c mice [12].
• Using the cholera toxin B subunit (CTB) that specifically binds to ganglioside GM1a on the plasma membrane, we investigated intracellular signaling mediated by endogenous GM1a involved in neuronal differentiation of PC12 cells [17].
• In muscimol treated animals, significantly fewer neurons expressed PV in the inhibited hemicortex, but as many CTB labelled corticospinal neurons were present as in controls, along with an equally large corticospinal projection from contralateral to the implant, significantly greater than in controls [18].
• Although the presence of a tyrosine kinase inhibitor, genistein, at a concentration of 10 microM diminished the neurite extension of PC12 cells induced with CTB, ERK activation was still observed [17].

Other interactions of Pcyt1b

• All CCT subunits identifiable with specific antibodies, namely CCTalpha, CCTbeta, CCTgamma and CCTepsilon/CCTtheta; (the latter two subunits colocalized in analyses of rat nerve samples), appeared to be labeled in "slow component b" of axonal transport along with the molecular chaperone Hsc73 and actin, a major folding substrate for CCT [19].
• Seven proteins showed significant changes in hydrocephalic H-Tx rats compared with Sprague-Dawley and normal H-Tx rats, including HMG-1, CDCrel-1A, mitochondrial ATP synthase, ERp29, NADP+-ICDH, CCT beta and gamma [20].

Analytical, diagnostic and therapeutic context of Pcyt1b

• The immune response of the female rat genital tract was evaluated with Lewis rats given primary and secondary immunizations with keyhole limpet hemocyanin (KLH) alone or coupled to the cholera toxin (CT) B subunit (CTB) by the oral or intravaginal-uterine route or a combination of routes [15].
• CTB-labeled neurons were visualized by immunocytochemistry and extensively quantified throughout the cortex [21].
• Neurons double-labeled for CTB and CART were visualized by immunofluorescence [22].
• Thus, after peripheral axotomy, CTB and CTB-HRP are markers not only for large but also for small DRG neurons and, thus, possibly also for both myelinated and unmyelinated primary afferents in the spinal dorsal horn [14].
• Vesicular glutamate transporter 2 (VGLUT2) mRNA was detected by in situ hybridization in the majority of PVH neurons retrogradely labeled from the ipsilateral RVLM with cholera toxin subunit B (CTB; 85% on average, with regional differences) [23].

References