מתוך medicontext.co.il
By Karla Gale
WESTPORT, CT (Reuters Health) – Dendritic cells react to phylogenetically diverse pathogens by broadly modulating gene expression, a team of investigators from Cambridge, Massachusetts, report.
"Dendritic cells can discriminate between pathogens and act as a messenger for the rest of the immune system," Dr. Nir Hacohen, of the Whitehead Institute for Biomedical Research, told Reuters Health.
Dr. Hacohen's team exposed human monocyte-derived dendritic cells to influenza A, Escherichia coli, and Candida albicans. Using microarray analysis, the investigators identified genes whose expression levels changed in response to the pathogens.
Of the approximately 6800 genes represented on the genome chip, 1330 genes changed expression levels when exposed to the pathogens. "Such a large-scale change in gene expression demonstrated that dendritic cells are able to undergo a marked transformation in their cellular phenotype."
Influenza was able to modulate the expression of an exclusive subset of 58 genes, while E. coli modulated an exclusive subset of 118 genes. In addition, all three types of pathogens regulated a common set of 166 genes, the investigators report.
Whether or not dendritic cells can mount specific responses to individual species of pathogens remains to be seen, Dr. Hacohen said. "The few experiments we have done suggest that dendritic cells can discriminate modestly between pathogens in the same class, but there's a lot more work to do on that."
He noted that the discriminatory response is "almost certainly a receptor-mediated response." He and his coinvestigators will be testing several receptor candidates. Eventually, he said, they hope to use their findings to develop "pathogen-specific treatment and detection."
In a related commentary titled "Chip Shots–Will Functional Genomics Get Functional?", Dr. Robert L. Modlin, of the University of California at Los Angeles, and Dr. Barry R. Bloom, of the Harvard School of Public Health in Boston, question the practical value of these findings.
"It is one thing for the expression of 1000 genes to be altered by infection and neatly classified into families, but quite another to know which of these genes are crucial for host defense, and which promote microbial invasion, survival, and pathogenesis, " they write.
The two editorialists suggest that answering such questions will require "reverting to the quaint hypothesis-driven, low-throughput approach once known as experimental biology."
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