New Mechanism Fundamental to the Spread of Invasive Yeast Infections Through Biofilm Formation Identified

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Comment: A group of researchers led by Carnegie Mellon University Biological Sciences Professor Aaron Mitchell has identified a novel regulatory gene network that plays an important role in the spread of common, and sometimes deadly, fungal infections. The findings, which establish the role of Zap1 protein in the activation of genes that regulate the synthesis of biofilm matrix. Candida albicans is a fungus, more specifically a yeast, which approximately 80 percent of people have in their gastrointestinal and genitourinary tract with no ill effects. However, at elevated levels it can cause non-life threatening conditions like thrush and yeast infections. A C. albicans infection becomes much more serious, and can be lethal, in those with compromised immune systems who have an implantable medical device, such as a pacemaker or artificial joint, or who use broad-spectrum antibiotics.

Central to such infections is the biofilm – a population of microbes, in this case C. albicans cells, joined together to form a sheet of cells. The cells in the biofilm produce extracellular components such as proteins and sugars, which form a cement-like matrix. This matrix serves to protect the cells of the biofilm, preventing drugs and other stressors from attacking the cells while acting as a glue that holds the cells together. By doing this, the matrix provides an environment in which yeast cells in the biofilm can thrive, promoting infection and drug resistance.

“Biofilms have a major impact on human health and matrix is such a pivotal component of biofilms. It is important to understand how the production of matrix is regulated,” Mitchell said.

In the study, Mitchell and colleagues found that the zinc-responsive regulatory protein Zap1 prevents the production of soluble b-1,3 glucan, a sugar that is a major component of matrix.

Nobile CJ, Nett JE, Hernday AD, Homann OR, Deneault J-S, et al. 2009 Biofilm Matrix Regulation by Candida albicans Zap1. PLoS Biol 7(6): e1000133. doi:10.1371/journal.pbio.1000133 View Full Paper

Editors Note:

Following the publication of this paper I contacted the authors to enquire if this information may have a clinical role if trying to disrupt the C Albicans Biofilm in a compromised patient. Obviously Zinc status is an important immune component but I was interested if it might make a short term strategy possible.

Dr Mitchell kindly clarified the following:.

“We do suspect that zinc reduction would reduce overall levels of biofilm matrix.  I would worry a little about extrapolating to the Candida population level though, because”:

(1) We have not shown that zinc levels control matrix, only that an inferred target of zinc regulation does.  This point is probably more picky, rather than a major concern.

(2) We do not know what the function of matrix is.  We are in a position to investigate that now but as of yet we do not have an answer.  This point is not so picky but rather is important.  (For example, matrix may be completely irrelevant for Candida to colonize the gut.) Nonetheless it would be very interesting to know how diet – especially zinc – may affect the spectrum and extent of microbial gut colonization.

Additional Comments. Zap1 sticks it to Candida Biofilms

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