Showing posts with label bacteria. Show all posts
Showing posts with label bacteria. Show all posts

Monday, 19 August 2013

First evidence that spaceflight affects community-level behavior of bacteria

Main Category: Infectious Diseases / Bacteria / Viruses
Article Date: 19 Aug 2013 - 0:00 PDT Current ratings for:
First evidence that spaceflight affects community-level behavior of bacteria
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When astronauts launch into space, a microbial entourage follows. And the sheer number of these followers would give celebrities on Twitter a run for their money. The estimate is that normal, healthy adults have ten times as many microbial cells as human cells within their bodies; countless more populate the environment around us. Although invisible to the naked eye, microorganisms - some friend, some foe - are found practically everywhere.

Microorganisms like bacteria often are found attached to surfaces living in communities known as biofilms. Bacteria within biofilms are protected by a slimy matrix that they secrete. Skip brushing your teeth tomorrow morning and you may personally experience what a biofilm feels like.

One of NASA's goals is to minimize the health risks associated with extended spaceflight, so it is critical that methods for preventing and treating spaceflight-induced illnesses be developed before astronauts embark upon long-duration space missions. It is important for NASA to learn how bacterial communities that play roles in human health and disease are affected by spaceflight.

In two NASA-funded studies - Micro-2 and Micro-2A - biofilms made by the bacteria Pseudomonas aeruginosa were cultured on Earth and aboard space shuttle Atlantis in 2010 and 2011 to determine the impact of microgravity on their behavior. P. aeruginosa is an opportunistic human pathogen that is commonly used for biofilm studies. The research team compared the biofilms grown aboard the International Space Station bound space shuttle with those grown on the ground. The study results show for the first time that spaceflight changes the behavior of bacterial communities.

Although most bacterial biofilms are harmless, some threaten human health and safety. Biofilms can exhibit increased resistance to the immune system's defenses or treatment with antibiotics. They also can damage vital equipment aboard spacecraft by corroding surfaces or clogging air and water purification systems that provide life support for astronauts. Biofilms cause similar problems on Earth.

"Biofilms were rampant on the Mir space station and continue to be a challenge on the International Space Station, but we still don't really know what role gravity plays in their growth and development," said Cynthia Collins, Ph.D., principal investigator for the study and assistant professor in the Department of Chemical and Biological Engineering at the Center for Biotechnology and Interdisciplinary Studies at the Rensselaer Polytechnic Institute in Troy, N.Y. "Before we start sending astronauts to Mars or embarking on other long-term spaceflight missions, we need to be as certain as possible that we have eliminated or significantly reduced the risk that biofilms pose to the human crew and their equipment."

In 2010 and 2011, during the STS-132 and STS-135 missions aboard space shuttle Atlantis, astronauts in space and scientists on Earth performed nearly simultaneous parallel experiments; both teams cultured samples of P. aeruginosa bacteria using conditions that encouraged biofilm formation.

Identical hardware designed for growing cells during spaceflight were used for both the flight and ground studies. According to Collins, "artificial urine was chosen as a growth medium because it is a physiologically relevant environment for the study of biofilms formed both inside and outside the human body."

Biofilms were cultured inside specialized fluid processing apparatus composed of glass tubes divided into chambers. The researchers loaded each tube with a membrane that provided a surface on which the bacteria could grow; the artificial urine was used for the bacteria's nourishment. Samples of P. aeruginosa were loaded into separate chambers within each tube.

The prepared tubes were placed in groups of eight inside another specialized device called a group activation pack (GAP) - designed to activate all of the bacterial cultures at once. The research team prepared identical sets of GAPs for the concurrent spaceflight and ground experiments.

Astronauts aboard the shuttle initiated the flight experiments by operating the GAPs and introducing the bacteria to the artificial urine medium. Scientists on Earth performed the same operations with the control group of GAPs at NASA's Kennedy Space Center in Florida. After activation, the GAPs were housed in incubators on Earth and aboard the shuttle to maintain temperatures appropriate for bacterial growth.

After the microgravity samples returned to Earth, the researchers determined the thickness of the biofilms, the number of living cells and the volume of biofilm per area on the membranes. Additionally, they used a microscopy technique that allowed them to capture high-resolution images at different depths within the biofilms, revealing details of their three-dimensional structures.

What the scientists found was that the P. aeruginosa biofilms grown in space contained more cells, more mass and were thicker than the control biofilms grown on Earth. When they viewed the microscopy images of the space-grown biofilms, the researchers saw a unique, previously unobserved structure consisting of a dense mat-like "canopy" structure supported above the membrane by "columns." The Earth grown biofilms were uniformly dense, flat structures. These results provide the first evidence that spaceflight affects community-level behavior of bacteria.

Microbes experience "low shear" conditions in microgravity that resemble conditions inside the human body, but are difficult to study. According to Collins, "Beyond its importance for astronauts and future space explorers, this research also could lead to novel methods for preventing and treating human disease on Earth. Examining the effects of spaceflight on biofilm formation can provide new insights into how different factors, such as gravity, fluid dynamics and nutrient availability affect biofilm formation on Earth. Additionally, the research findings one day could help inform new, innovative approaches for curbing the spread of infections in hospitals."

NASA's Space Biology Program funded the Micro-2 and Micro-2A investigations. Related space biology research continues aboard the space station, including recently selected studies that are planned for future launch to the orbiting laboratory.

Wherever we go, microbial communities will faithfully follow, making this evidence of the effects of spaceflight on bacterial physiology relevant to human health. That bacterial biofilms exhibit different behavior in space versus on Earth is critical information as NASA strives to keep astronauts healthy and safe during future long-duration space missions

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
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Saturday, 17 August 2013

Study of melittin-based pore formation has implications for fighting cancer and bacteria

Main Category: Cancer / Oncology
Also Included In: Infectious Diseases / Bacteria / Viruses
Article Date: 17 Aug 2013 - 0:00 PDT Current ratings for:
Study of melittin-based pore formation has implications for fighting cancer and bacteria
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A new study by Rice University biophysicists offers the most comprehensive picture yet of the molecular-level action of melittin, the principal toxin in bee venom. The research could aid in the development of new drugs that use a similar mechanism as melittin's to attack cancer and bacteria.

The study appears in the Proceedings of the National Academy of Sciences.

Melittin does its damage by penetrating the outer walls of cells and opening pores that allow the contents of the cell to escape. At low concentrations, melittin forms transient pores. At higher concentrations, the pores become stable and remain open, and at still higher doses, the cell membrane dissolves altogether.

"This strategy of opening holes in the cell membrane is employed by a great number of host-defense antimicrobial peptides, many of which have been discovered over the past 30 years," said Rice's Huey Huang, the lead investigator of the study. "People are interested in using these peptides to fight cancer and other diseases, in part because organisms cannot change the makeup of their membrane, so it would be very difficult for them to develop resistance to such drugs."

But the clinical use of the compounds is complicated by the lack of consensus about how the peptides work. For example, scientists have struggled to explain how different concentrations of melittin could yield such dramatically different effects, said Huang, Rice's Sam and Helen Worden Professor of Physics and Astronomy.

In the new study, Huang and Rice graduate student Tzu-Lin Sun partnered with colleagues Ming-Tao Lee at the National Synchrotron Radiation Research Center (NSRRC) in Hsinchu, Taiwan, and with Wei-Chin Hung at the Republic of China Military Academy in Fengshan, Taiwan. The team used a combination of experiments to zero in on the molecular activity of melittin at the "minimal inhibitory concentration" (MIC), the lowest concentration that's been shown to slow the growth of target cell populations. The MIC for melittin is a dose that results in stable pore formation, rather than complete dissolution of the membrane.

"We want to understand how pore formation works at this critical concentration, including both at the molecular scale -- what are the shapes of the pores themselves -- and the cellular scale -- how are the pores arranged and distributed over the surface of the membrane," Huang said.

To find the answer, the team correlated the results of two different types of experiments. In the first type, which was conducted at Rice, the team used confocal microscopy to film "giant unilamellar vesicles" (GUVs), synthetic membrane-enclosed structures that are about the same size as a living cell. The outer surface of the GUV became green when bound to melittin that was labeled with a fluorescent dye. The GUV was filled with a solution that contained a red fluorescent dye.

In the experiments, Sun used a needle-like glass pipette to partially aspirate and grab dye-filled GUVs, which were then placed into a melittin-infused solution beneath the microscope. Time-lapse videos of the experiments show that dye-labeled melittin begins sticking to the surface of the GUV within seconds. Within about two minutes, so much melittin binds to the outside of the GUV that the outer surface area increases by up to 4.5 percent. At a critical threshold, the expanding surface changes configuration to accommodate the increased load of melittin. At this point, pores form across the entire surface of the GUV. On the video, the bright red dye within the GUV rapidly leaks out at this critical pore-forming stage.

"The experiment shows how the MIC brings about a new physical state that results in cell death," Huang said. "By correlating these findings with other data about the molecular characteristics of the pores themselves, we get the first complete picture of the process of stable, melittin-induced pore formation."

The molecular level data came from a series of X-ray diffraction experiments performed by Lee at NSRRC. In those experiments, samples of multilayered membranes were bombarded with X-rays. Each layer contained an ordered arrangement of pores, and the stacked layers contained a 3-D lattice of regularly arranged pores. By examining how X-rays scattered away from the sample, Lee and Hung were able to determine the precise contours of the melittin-induced pores.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
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Friday, 16 August 2013

Colorectal cancer may be triggered by mouth bacteria

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Academic Journal
Main Category: Colorectal Cancer
Also Included In: Cancer / Oncology;  GastroIntestinal / Gastroenterology;  Dentistry
Article Date: 15 Aug 2013 - 5:00 PDT Current ratings for:
Colorectal cancer may be triggered by mouth bacteria
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Two new studies published this week suggest that a type of gut bacteria found in the mouth may trigger colorectal cancer by influencing the immune response and switching on cancer genes.

The researchers believe their findings may lead to more timely and improved ways of diagnosing, preventing, and treating colorectal cancer.

Our gut contains trillions of bacteria, vastly outnumbering our own cells. These microbe communities maintain our health by training our immune system and helping us digest food. But they can also trigger disease.

There is evidence that an imbalance between the "good" and the "bad" gut bacteria may promote colon cancer.

The two new studies, published in the August 14th online issue of the journalCell Host & Microbe, focus on a genus of bacteria called Fusobacteria, and the species F. nucleatum in particular.

Colorectal cancer is the second leading cause of death from cancer among Americans. Researchers have found Fusobacteria from the mouth are also abundant in tissues from colorectal cancer patients.

Photo of open mouth
Our mouths contain millions of bacteria

But until this latest research, it was not clear whether these gut microbes actually trigger tumors, and if so, how they do it.

In the first study, the researchers found Fusobacteria in benign tumors that can become cancerous over time. This might suggest that they contribute to the early stages of tumor formation.

Then, in mice bred to have a human-like form of colorectal cancer, the team found the bacteria sped up tumor formation by summoning a type of immune cell called myeloid cells, which penetrate tumors and trigger inflammations that can lead to cancer.

Senior author Wendy Garrett, of the Harvard School of Public Health and the Dana-Farber Cancer Institute in the US, told the press:

"Fusobacteria may provide not only a new way to group or describe colon cancers but also, more importantly, a new perspective on how to target pathways to halt tumor growth and spread."

In the second study, another team found that Fusobacteria use a molecule that lives on the surface of the bacterial cell to stick to and then invade human colorectal cancer cells.

The molecule, called Fusobacterium adhesin A (FadA), switches on genes that spur cancer growth, triggers inflammation in the human cancer cells, and spurs tumor formation.

The team also found that tissue from healthy individuals had much lower levels of FadA than tissue from patients with benign and cancerous colorectal tumors.

Plus, they identified a compound that can stop the effects of FadA on cancer cells.

Senior author Yiping Han, of Case Western Reserve University School of Dental Medicine in the US, said:

"We showed that FadA is a marker that can be used for the early diagnosis of colorectal cancer and identified potential therapeutic targets to treat or prevent this common and debilitating disease."

In another study of mice published earlier this year, researchers identified the mechanisms that help the good gut bacteria and the immune system to coexist. A group of immune cells called innate lymphoid cells (ILCs) seem to instruct the immune T cells to trust - that is, ignore - friendly gut bacteria, thereby allowing the immune system to maintain a friendly truce with these foreign entities.

Written by Catharine Paddock PhD
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today Visit our colorectal cancer section for the latest news on this subject.

"Fusobacterium nucleatum Potentiates Intestinal Tumorigenesis and Modulates the Tumor-Immune Microenvironment"; Aleksandar D. Kostic, Eunyoung Chun, Lauren Robertson, Jonathan N. Glickman, Carey Ann Gallini, Monia Michaud, Thomas E. Clancy, Daniel C. Chung, Paul Lochhead, Georgina L. Hold, and others; Cell Host & Microbe 14(2) pp. 207 - 215 published online 14 August 2013; DOI: 10.1016/j.chom.2013.07.007; Link to Abstract.

"Fusobacterium nucleatum Promotes Colorectal Carcinogenesis by Modulating E-Cadherin/ß-Catenin Signaling via its FadA Adhesin"; Mara Roxana Rubinstein, Xiaowei Wang, Wendy Liu, Yujun Hao, Guifang Cai, Yiping W. Han; Cell Host & Microbe 14(2) pp. 195 - 206 published online 14 August 2013; DOI: 10.1016/j.chom.2013.07.012; Link to Abstract.

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posted by George B on 15 Aug 2013 at 7:15 am

"Plus, they identified a compound that can stop the effects of FadA on cancer cells."

What compound?!?

Editor's note:: Many thanks for your enquiry asking which compound stops the effect of FadA on cancer cells.

If you follow the link to the scientific report on the second study, which is included in the References tab at the bottom of our article, you will see the Abstract in Cell & Host Microbe where the researchers summarize what they did to find the compound and how they tested it:

"... FadA binds to E-cadherin, activates ß-catenin signaling, and differentially regulates the inflammatory and oncogenic responses. The FadA-binding site on E-cadherin is mapped to an 11-amino-acid region. A synthetic peptide derived from this region of E-cadherin abolishes FadA-induced CRC cell growth and oncogenic and inflammatory responses ..."

E-cadherin is a molecule that helps cells stick to each other and is important for maintaining tissue architecture. So the compound they found is a synthetic version of the part of E-cadherin that FadA binds to.

We hope this answers your query.

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'Colorectal cancer may be triggered by mouth bacteria'

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Seeking ways to effectively control bacteria in the water supply

Main Category: Water - Air Quality / Agriculture
Also Included In: Public Health;  Infectious Diseases / Bacteria / Viruses
Article Date: 15 Aug 2013 - 1:00 PDT Current ratings for:
Seeking ways to effectively control bacteria in the water supply
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Research at the University of Sheffield, published in the latest issue of Water Science and Technology: Water Supply, points the way to more sophisticated and targeted methods of ensuring our drinking water remains safe to drink, while still reducing the need for chemical treatments and identifying potential hazards more quickly.

The research team, from the University of Sheffield's Faculty of Engineering, studied four bacteria found in the city's drinking water to see which combinations were more likely to produce a 'biofilm'. Biofilms are layers of bacteria which form on the inner surfaces of water pipes.

"Biofilms can form on all water pipes and as these are usually non-harmful bacteria, they don't present a problem," explains lead researcher, Professor Catherine Biggs. "However, biofilms can also be a safe place for harmful bacteria such as Escherichia coli or Legionella to hide. If the bacterial growth is too heavy, it can break off into the water flow, which at best can make water discoloured or taste unpleasant and at worst can release more dangerous bacteria. Our research looks at what conditions enable biofilms to grow, so we can find ways to control the bacteria in our water supply more effectively."

Funded by the Engineering and Physical Sciences Research Council, the research isolated four bacteria from water taken from a domestic tap: two were widely found in drinking water everywhere, one was less common and one was unique to Sheffield. The researchers mixed the bacteria in different combinations and found that, in isolation, none of them produced a biofilm. However, when any of the bacteria were combined with one of the common forms, called Methylobacterium, they formed a biofilm within 72 hours.

"Our findings show that this bacterium is acting as a bridge, enabling other bacteria to attach to surfaces and produce a biofilm and it's likely that it's not the only one that plays this role," says Professor Biggs. "This means it should be possible to control or even prevent the creation of biofilms in the water supply by targeting these particular bacteria, potentially reducing the need for high dosage chemical treatments."

Domestic water supplies in the UK are regularly tested for levels of bacteria and, if these are too high, water is treated with greater concentrations of chlorine or pipe networks are flushed through to clear the problem. However, the standard tests look for indicator organisms rather than the individual types which are present. Testing methods being developed by the Sheffield team - as used in this research - involve DNA analysis to identify the specific types of bacteria present.

"The way we currently maintain clean water supplies is a little like using antibiotics without knowing what infection we're treating," says Professor Biggs. "Although it's effective, it requires extensive use of chemicals or can put water supplies out of use to consumers for a period of time. Current testing methods also take time to produce results, while the bacteria are cultured from the samples taken.

"The DNA testing we're developing will provide a fast and more sophisticated alternative, allowing water companies to fine tune their responses to the exact bacteria they find in the water system."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our water - air quality / agriculture section for the latest news on this subject.

Bacteriological water quality compliance and root cause analysis: an industry case study

Kate Ellis, Bernadette Ryan, Michael R. Templeton and Catherine A. Biggs; Water Science & Technology: Water Supply Vol 13 No 4 pp 1034-1045 © IWA Publishing 2013 doi:10.2166/ws.2013.092

University of Sheffield

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Thursday, 15 August 2013

Potential for new antibiotics following finding that protein delays cell division in bacteria

Main Category: Infectious Diseases / Bacteria / Viruses
Also Included In: Genetics
Article Date: 14 Aug 2013 - 0:00 PDT Current ratings for:
Potential for new antibiotics following finding that protein delays cell division in bacteria
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In 1958 a group of scientists working in Denmark made the striking observation that bacterial cells are about twice as large when they are cultured on a rich nutrient source than when they are cultured on a meager one. When they are shifted from a nutrient-poor environment to a nutrient-rich one, they bulk up until they have achieved a size more appropriate to their new growth conditions.

It has taken 60 years to figure out how the bacteria are able to sample their surroundings and alter their cell cycles so that they grow to a size suited to the environment.

In 2007 Petra Levin, PhD, a biologist at Washington University in St. Louis, reported in Cell that a soil bacterium named Bacillis subtilis has a protein that senses how much food is available and, when food is plentiful, temporarily blocks the assembly of a constriction ring that pinches a cell in two to create two daughter cells.

Now Norbert Hill, a graduate student in her group, reports in a recent online edition of PLoS Genetics that Escherichia coli uses a similar protein to help ensure cell size is coordinated with nutrient conditions.

Delaying division even just a little bit leads to an increase in daughter cell size. Once stabilized at the new size, cells take advantage of abundant nutrient sources to increase and multiply, doubling their population at regular intervals until the food is exhausted.

Because both the B. subtilis and E. coli proteins interact with essential components of the division machinery, understanding how they function will help in the discovery of antibiotics that block cell division permanently. A group in Cambridge, England, is already working to crystallize the E. coli protein docked on one of the essential components of the constriction ring.

If they are successful they may be able to see exactly how the protein interferes with the ring's assembly. An antibiotic could then be designed that would use the same mechanism to prevent division entirely, killing the bacteria.

Why do bacteria get bigger on a good food source?

Bacteria increase and multiply by a process called binary fission. Each cell grows and then the divides in the middle to produce two daughter cells. What could be simpler?

But the closer you look, the less simple it becomes. For binary fission to work the cell must make a copy of its circular chromosome, unlink and separate the two chromosomes to create a gap between them, assemble a constriction ring in the middle of the cell and coordinate the growth of new cell membrane as the ring cinches tight and pinches the mother cell in two. To complicate matters, bacteria don't necessarily do these steps one by one but can instead work on several steps simultaneously.

Most of the time the goal is to produce daughters the same size as the mother cell. But when food is plentiful, bacteria start making more copies of their DNA (as many as 12) in anticipation of divisions to come, and they can't easily cram all the extra DNA into standard-sized cells. So they grow bigger to accommodate the extra genetic material and remain large as long as the food lasts.

The inventory of partly copied chromosomes fuels rapid population growth, because a cell doesn't start from scratch when it needs another copy of its chromosome. Under optimum conditions, E. coli, for example, divides once every 17 minutes. If they are allowed to grow unhindered this means that in 24 hours 1 bacterium becomes about 5 x 1021 bacteria (that is 5 with 21 zeros after it.)

How do bacteria know the pickings are rich?

In B. subtilis and E. coli the signal is a modified sugar called UDP-glucose. Presumably, the richer the growth medium, the higher the level of this sugar inside the cell.

In both bacteria UDP-glucose binds to a protein and the sugar-protein complex then interferes with the assembly of the constriction ring. In the case of B. subtilis the protein is called UgtP and in the case of E. coli it is OpgH.

"It's interesting," Hill said, "that both organisms, which are more different from one another than we are from bakers' yeast, are using the same system to coordinate changing size in response to nutrient availability."

UgtP and OpgH are bifunctional proteins that are "moonlighting" as elements of the cell-division control systems. In both cases their day jobs are to help build the cell envelope. "We think they are communicating not only how much glucose there is in the cell, but also how fast the cell is growing," Levin said. "The sensor says not only is food abundant, but we're also growing really fast, so we should be bigger."

Both proteins delay division by interfering with FtsZ, the first protein to move to the division site, where it assembles into a scaffold and recruits other proteins to form a constriction ring.

"Very little is known about the assembly of the ring," Hill said. "There are a dozen essential division proteins and we don't know what half of them do. Nor do we understand how the ring develops enough force to constrict."

"We do know FtsZ exists in two states," Hill added. "One is a small monomer and the other is many monomers linked together to form a multi-unit polymer. We think the polymers bind laterally to form a scaffold and then, with the help of other proteins, make a meshwork that goes around the cell.

UgtP and OpgH both interfere with the ability of FtsZ to form the longer polymers necessary for assembly of the constriction ring.

When nutrient levels are low, UgtP and OpgH are sequestered away from the division machinery. FtsZ is then free to assemble into the scaffold supporting the constriction ring so the cell can divide. Because division proceeds unimpeded, cells are smaller when they divide.

What about other bacteria?

This control system helps to explain the 60-year-old observation that bacterial cells get bigger when they are shifted to a nutrient-rich medium.

Comparing the mechanisms that govern cell division in E. coli and B. subtilis reveals conserved aspects of cell size control, including the use of UDP-glucose, a molecule common to all domains of life, as a proxy for nutrient availability, and the use of moonlighting proteins to couple growth-rate-dependent phenomena to the central metabolism.

But much more is known about these model organisms, which many labs study, than the average bacterium. Nobody is sure how many species of bacteria there are - somewhere between 10 million and a billion at a guess - and they don't all divide the way B. subtilis and E. coli do.

The whimsically named giant bacterium Epulopiscium fiselsoni ("Fishelson's guest at a fish's banquet") that lives in the guts of sturgeonfish, has the gene for FtsZ but doesn't divide by binary fission. And then there are bacteria like the pathogen Chlamydia traachomatis that don't have a gene for anything like FtsZ. "We don't know how these bacteria divide, much less maintain an appropriate cell size," Levin said.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our infectious diseases / bacteria / viruses section for the latest news on this subject. Please use one of the following formats to cite this article in your essay, paper or report:

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Washington University in St. Louis. "Potential for new antibiotics following finding that protein delays cell division in bacteria." Medical News Today. MediLexicon, Intl., 14 Aug. 2013. Web.
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'Potential for new antibiotics following finding that protein delays cell division in bacteria'

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Monday, 5 August 2013

Removing a protein enhances defense against bacteria staphylococcus aureus in CGD mice

Main Category: Infectious Diseases / Bacteria / Viruses
Also Included In: Immune System / Vaccines;  Blood / Hematology
Article Date: 05 Aug 2013 - 0:00 PDT Current ratings for:
Removing a protein enhances defense against bacteria staphylococcus aureus in CGD mice
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Deletion of a protein in white blood cells improves their ability to fight the bacteria staphylococcus aureus and possibly other infections in mice with chronic granulomatous disease (CGD), according to a National Institutes of Health study. CGD, a genetic disorder also found in people, is marked by recurrent, life-threatening infections. The study's findings appear online in The Journal of Clinical Investigation.

A team of researchers from NIH's National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) compared three groups: CGD-afflicted mice with the protein Olfm4; CGD-afflicted mice in which the protein had been deleted, and healthy mice in which the protein had been deleted. Olfm4, also known as olfactomedin 4, is sometimes helpful in limiting tissue damage but can also hinder white blood cells' ability to kill bacteria.

The researchers found that the white blood cells in mice without the protein could better withstand staphylococcus aureus infection, a major threat to patients with CGD.

"Although treatment for CGD has greatly improved over the past several years, the disease remains challenging," said Dr. Wenli Liu, staff scientist and lead author. "Our research suggests a novel strategy that might pave the way toward developing new treatments to fight against common and often deadly infections."

The results also suggest another potential method to treat methicillin-resistant staphylococcus aureus (MRSA) and other drug-resistant bacteria in patients without CGD, used alongside other therapies. MRSA is a strain of bacteria that has become resistant to antibiotics most often used to treat staph infections. Most commonly contracted in hospitals, MRSA represents a significant public health threat.

"Over the years, MRSA and other bacteria have evolved to be resistant to many antibiotics," said Griffin P. Rodgers, M.D., NIDDK director and study lead. "This study suggests an alternative approach to combat infection by strengthening white blood cell capabilities from within the cells, in addition to resorting to traditional antibiotic treatment."

The research group is now investigating how changing Olfm4 levels in human cells enhances immunity to and from a variety of drug-resistant bacteria. The findings may put researchers closer to developing drug treatment for people, possibly through development of an antibody or small molecule that could inhibit Olfm4 activity.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our infectious diseases / bacteria / viruses section for the latest news on this subject.

The study was supported by the Intramural Research Program at NIDDK. Administrative and technical support were provided by the National Heart, Lung, and Blood Institute and the National Institute of Allergy and Infectious Diseases, both part of NIH.

NIH/National Institute of Diabetes and Digestive and Kidney Diseases

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