PubMed · 2451101
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1988-04-02. Antihormones.. https://pubmed.ncbi.nlm.nih.gov/2451101/
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Recent data suggest that mast cells (MC) are involved in the regulation of leukocyte accumulation in inflammatory reactions. In this study, expression of leukocyte-chemotactic peptides (chemokines) in purified human lung MC (n = 16) and a human mast cell line, HMC-1, was analyzed. Northern blotting and reverse transcriptase-polymerase chain reaction (RT-PCR) showed baseline expression of monocyte chemoattractant protein (MCP)-1 mRNA in unstimulated MC. Exposure of MC to recombinant stem cell factor (rhSCF, 100 ng/mL) or anti-IgE (10 microgram/mL) was followed by a substantial increase in expression of MCP-1 mRNA. Neither unstimulated nor stem cell factor (SCF )-stimulated lung MC expressed transcripts for interleukin-8 (IL-8), macrophage inflammatory protein-1alpha (MIP-1alpha), MIP-1beta, or RANTES by Northern blotting. The mast cell line HMC-1, which contains a mutated and intrinsically activated SCF-receptor, was found to express high levels of MCP-1 mRNA in a constitutive manner. Exposure of HMC-1 cells to rhSCF resulted in upregulation of MCP-1 mRNA expression, and de novo expression of MIP-1beta mRNA. The SCF-induced upregulation of MCP-1 mRNA in lung MC and HMC-1 was accompanied by an increase in immunologically detectable MCP-1 in cell supernatants (sup) (lung MC [<98%], control medium, 1 hour: 159 +/- 27 v SCF, 100 ng/mL, 1 hour: 398 +/- 46 pg/mL/10(6) cells; HMC-1: control, 1 hour: 894 +/- 116 v SCF, 1 hour: 1,536 +/- 265 pg/mL/10(6)). IgE-dependent activation was also followed by MCP-1 release from MC. MC-sup and HMC-1-sup induced chemotaxis in blood monocytes (Mo) (control: 100% +/- 12% v 2-hour-MC-sup: 463% +/- 38% v HMC-1-sup: 532% +/- 12%), and a monoclonal antibody (MoAb) to MCP-1 (but not MoAb to IL-8) inhibited Mo-chemotaxis induced by MC-sup or HMC-1-sup (39% to 55% inhibition, P < .05). In summary, our study identifies MCP-1 as the predominant CC-chemokine produced and released in human lung MC. MCP-1 may be a crucial mediator in inflammatory reactions associated with MC activation and accumulation of MCP-1-responsive leukocytes.
Cholera toxin (CT) exerts many diverse regulatory effects on cells of the immune system and is considered a potent adjuvant on gut mucosal immune responses to orally presented antigens. It has been previously described that CT induces surface DR expression in human resting B-cells. As a further step toward understanding this phenomenon, the molecular mechanisms underlying the regulation of DR expression were investigated. By the use of Western analysis, it is shown that CT increases the total levels of DR protein in highly purified human tonsillar cells. [35S]Methionine incorporation studies show that the aforementioned increase is due to de novo biosynthesis of DR protein at as early as 6 hr after CT stimulation and is completed by 24 hr. [3H]Uridine uptake experiments, nuclear transcription runoff assays, and Northern analysis show that CT does not exert its effect at a transcriptional level, indicating translational regulation. Anti-IgM, which mimics B-cell antigen binding, behaves in a manner similar to CT. The B subunit of CT (B-CT) and prostaglandin E2, either alone or in combination, do not induce DR protein biosynthesis nor do they exert any effect on the transcription of DR beta 1 gene. These results show that cAMP elevation as well as binding of B-CT to GM-1 ganglioside, by themselves, do not lead to DR protein biosynthesis suggesting that other activation pathways may be involved.
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