Putative Role of {beta}-1,3 Glucans in Candida albicans Biofilm Resistance

[Guest guest]

My alt doc was suggesting I take beta-glucan, so I started looking it

up. However, now I'm confused. I thought taking it was supposed to

help fight infections, but it looks like it can contribute to drug

resistance. Beta-glucans come from fungus (also oats etc), so I'm not

surprised to see them associated with candida. I just started reading

on this subject so basically know nothing. Can anybody clue me in on

what beta-glucan actually is then? Good? Bad? Stimulates the immune

system because it is actually bad? Beta-1,3 Glucanas is good but the

stuff you buy in commercial preparations is bad? (Sigh, I know it's

not possible to reduce complex subjects to good and bad, but I can

hope, can't I?)

- Kate

1: Antimicrob Agents Chemother. 2007 Feb;51(2):510-20. Epub 2006 Nov 27.

Putative Role of {beta}-1,3 Glucans in Candida albicans Biofilm

Resistance.

* Nett J,

* Lincoln L,

* Marchillo K,

* Massey R,

* Holoyda K,

* Hoff B,

* Vanhandel M,

* Andes D.

600 Highland Ave., Room H4.572, Madison, WI 53792.

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Biofilms are microbial communities, embedded in a polymeric

matrix, growing attached to a surface. Nearly all device-associated

infections involve growth in the biofilm life style. Biofilm

communities have characteristic architecture and distinct phenotypic

properties. The most clinically important phenotype involves

extraordinary resistance to antimicrobial therapy, making biofilm

infections very difficulty to cure without device removal. The

current studies examine drug resistance in Candida albicans biofilms.

Similar to previous reports, we observed marked fluconazole and

amphotericin B resistance in a C. albicans biofilm both in vitro and

in vivo. We identified biofilm-associated cell wall architectural

changes and increased beta-1,3 glucan content in C. albicans cell

walls from a biofilm compared to planktonic organisms. Elevated

beta-1,3 glucan levels were also found in the surrounding biofilm

milieu and as part of the matrix both from in vitro and in vivo

biofilm models. We thus investigated the possible contribution of

beta-glucans to antimicrobial resistance in Candida albicans

biofilms. Initial studies examined the ability of cell wall and cell

supernatant from biofilm and planktonic C. albicans to bind

fluconazole. The cell walls from both environmental conditions bound

fluconazole; however, four- to fivefold more compound was bound to

the biofilm cell walls. Culture supernatant from the biofilm, but not

planktonic cells, bound a measurable amount of this antifungal agent.

We next investigated the effect of enzymatic modification of beta-1,3

glucans on biofilm cell viability and the susceptibility of biofilm

cells to fluconazole and amphotericin B. We observed a dose-dependent

killing of in vitro biofilm cells in the presence of three different

beta-glucanase preparations. These same concentrations had no impact

on planktonic cell viability. beta-1,3 Glucanase markedly enhanced

the activity of both fluconazole and amphotericin B. These

observations were corroborated with an in vivo biofilm model.

Exogenous biofilm matrix and commercial beta-1,3 glucan reduced the

activity of fluconazole against planktonic C. albicans in vitro. In

sum, the current investigation identified glucan changes associated

with C. albicans biofilm cells, demonstrated preferential binding of

these biofilm cell components to antifungals, and showed a positive

impact of the modification of biofilm beta-1,3 glucans on drug

susceptibility. These results provide indirect evidence suggesting a

role for glucans in biofilm resistance and present a strong rationale

for further molecular dissection of this resistance mechanism to

identify new drug targets to treat biofilm infections.

PMID: 17130296 [PubMed - in process]