Progress Made in Creating 'Good' Bacteria to Fight 'Bad' Bacteria in Eye Infections

There were three major components to the study. The first established that isolates of two antibiotic-resistant ocular pathogens, Pseudomonas aeruginosa and Serratia marcescens, were all susceptible to being attacked and killed by at least one of two other bacteria , Micavibrio aeruginosavorus and Bdellovibrio baceriovorus, which act as predators against the pathogens but are believed to be "good," or non-infectious, bacteria when they exist within the human body.

In the second phase, human corneal-limbic epithelial cells that are native to the eye were exposed in vitro to M. aeruginosavorus and B. baceriovorus to test whether those "good" predator bacteria would cause either toxicity or inflammation in those cells. They did not.

In the third phase, the two "good" predator bacteria were injected into live worms from the species Galleria mellonella, which is well established as a suitable model to test the toxicity of various microbes as well as a live organism's innate immunity to those microbes.

Where injection of the pathogenic bacterium P. aeruginosa as a positive control was one hundred percent fatal to the worms, other worms injected with the two "good" predator bacteria had 11-day survival rates between 93.3 and 100 percent, a strong sign that the "good" bacteria were not toxic to the worms.

In addition a lack of change in larval pigmentation following injection suggested that the "good" bacteria also did not provoke an aggressive innate immune response in the worms.

Lead author of the study Daniel Kadouri, PhD, an assistant professor of oral biology the University of Medicine and Dentistry of New Jersey-New Jersey Dental School, said their findings leave them confident that, in isolation, pathogenic bacteria are susceptible to successful attack by predator bacteria, predator bacteria do not appear inherently harmful to ocular cells when applied topically, and a live organism can tolerate the predator bacteria well.

He said that the time to test all three phenomena simultaneously in the eye tissue of a live organism may now be at hand.

The current study builds on another recent paper published in PLoS ONE, which also described research led by Kadouri. That study used the predatory bacteria Bdellovibrio baceriovorus 109J, B. bacteriovorus HD100, and Micavibrio aeruginosavorus strain ARL-13, in targeting 14 strains of dangerous bacteria that are known to be multidrug resistant (MDR). Species targeted in that earlier research included Acinetobacter baumannii, Escherichia coli, Klebsiella pneumoniae, and Pseudomas spp., all of which are commonly encountered in health care settings.

After predator bacteria and MDR strains were co-cultured in the laboratory, the researchers found that cell viability had diminished to varying degrees in all 14 MDR strains, suggesting that while the MDR strains are strongly resistant to current antibiotics, they may have no innate defenses that would protect them against one or more of the predator bacteria.

The study has been published in the online journal PLoS ONE.

Source-ANI

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Drug-Resistant Bacteria Linked With Livestock Found Among Industrial Livestock Workers

by Kathy Jones on? July 05, 2013 at 10:44 PM Environmental Health A test of nose samples among livestock workers in North Carolina by American researchers reveals the presence of drug-resistant bacteria associated with livestock among industrial workers and not in antibiotic-free workers.
The drug-resistant bacteria examined were Staphylococcus aureus, commonly known as "Staph," which include the well-known bug MRSA (methicillin-resistant Staphylococcus aureus). New Staph strains are emerging in people who have close contact with livestock animals and for this reason have been given the name livestock-associated Staph. While everyone in the study had direct or indirect contact with livestock, only industrial workers carried antibiotic-resistant Staph with multiple genetic characteristics linked to livestock. The study by researchers at the Johns Hopkins Bloomberg School of Public Health, the University of North Carolina at Chapel Hill, the Rural Empowerment Association for Community Help, the George Washington University, and the Statens Serum Institute, published July 2 by the journal PLOS ONE, confirms earlier findings in Iowa and raises concern about antibiotics use in livestock production.

Many industrial livestock operations raise animals in large conferment buildings and use antibiotics, including non-therapeutically in animals' feed and water to promote their growth. Previous studies have detected strains of drug-resistant S. aureus from livestock, first among farm workers, and subsequently in hospital and community settings in Europe. In the United States, such strains have been detected among industrial livestock operation workers in Iowa and now North Carolina making scientists concerned that these bacteria could follow a similar trajectory into the community. North Carolina is a major livestock producer, ranking second behind Iowa in hog production in the United States.

S. aureus can cause a range of illnesses in humans, from minor to life-threatening skin, bloodstream, respiratory, urinary and surgical site infections. Like most illnesses caused by bacteria, S. aureus infections are treated with antibiotics. According to the Centers for Disease Control and Prevention, some Staph cannot be killed by antibiotics, meaning they are resistant. MRSA is a strain of Staph bacteria that is resistant to methicillin and certain first-line antibiotics called beta-lactams. Infections with drug-resistant strains, like MRSA, can be particularly difficult to treat.

The study was based on interviews and nose swabs that were collected and analyzed from individuals who worked at two different types of livestock operations in North Carolina. At industrial livestock operations, animals are grown in large confinement buildings using antibiotics. At antibiotic-free livestock operations, animals are grown without the use of antibiotics, typically outdoors on pasture. Researchers tested the S. aureus isolated from nose swabs for resistance to a range of antibiotics and for genetic markers considered to indicate that the bacteria may have come from livestock.

"This study shows that these livestock-associated strains are present among workers at industrial livestock operations and that these strains are resistant not just to methicillin, but to multiple antibiotics - including antibiotics that are used to treat human infections," said Christopher Heaney, PhD, corresponding author of the study and assistant professor of Environmental Health Sciences and Epidemiology at the Johns Hopkins Bloomberg School of Public Health.

Workers were not experiencing Staph infections at the time of the study, but when antibiotic resistant bacteria do cause infections, they can be harder to treat. Researchers found that S. aureus that were multidrug-resistant were roughly twice as prevalent among individuals exposed to the industrial compared to the antibiotic-free livestock operation environment and S. aureus that were resistant to tetracycline - an antibiotic that has been used in industrial livestock production since the 1950's - were 19 times as prevalent among industrial compared to antibiotic-free livestock operation workers.

Source-Eurekalert

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How Immune System Peacefully Co-exists With 'Good' Bacteria?

by Bidita Debnath on? Research News Commensal bacteria is loaded in the human gut - "good" microbes that, among other functions, help the body digest food.
The gastrointestinal tract contains literally trillions of such cells, and yet the immune system seemingly turns a blind eye. However, in several chronic human diseases such as inflammatory bowel disease (IBD), HIV/AIDS, cancer, cardiovascular disease, and diabetes, the immune system attacks these normally beneficial bacteria, resulting in chronic inflammation and contributing to disease progression.

Now, researchers may finally understand an important mechanism that keeps this friendly truce intact - a finding that may lead to the development of new therapeutic strategies for such chronic diseases.

Gregory F. Sonnenberg, PhD, research associate in the Department of Medicine, Gastroenterology Division, and the Institute for Immunology at the Perelman School of Medicine, University of Pennsylvania, with postdoctoral researcher Matthew Hepworth, PhD, report in Nature that innate lymphoid cells (ILCs) directly limit the response by inflammatory T cells to commensal bacteria in the gut of mice. Loss of this ILC function effectively puts the immune system on an extended war footing against the good, commensal bacteria - a condition observed in multiple chronic inflammatory diseases.

ILCs are a class of rare immune cells that were first described a few years ago. Previous research has implicated these cells in regulating immune responses in the intestine, mostly through their ability to secrete immune-activating cytokines. But until now, researchers have had a hard time studying ILCs because it hasn't been possible to selectively eliminate them in the context of an otherwise intact immune system.

Sonnenberg, Hepworth, and their colleagues deleted a protein called RORt, required for one class of ILCs, in mice. RORt-deficient animals had exacerbated T cell responses against commensal bacteria and systemic inflammation. In contrast, deletion of previously identified ILC effector cytokines such as IL-22 and IL-17 did not elicit an immune response to commensal bacteria, suggesting the ILCs use an unidentified regulatory pathway.

When the team looked at what gene signatures the RORt-dependent ILCs expressed, they found high expression of major histocompatibility complex class II (MHCII) protein, which some cells use to display foreign proteins to the immune system and directly interact with T cells.

This, as with RORγt-deficient mice, selective deletion of MHCII in ILCs resulted in hyperactive T-cell responses directed against commensal bacteria and systemic inflammatory responses, all of which could be alleviated by depletion of commensal bacteria with broad-spectrum antibiotics. What's more, mice with the selective deletion of MHCII in ILCs also developed inflammatory bowel disease, which was driven by aberrant CD4+ T-cell responses to commensal bacteria.

This study is the first to selectively target ILCs in the presence of an intact immune system, and these findings suggest that under normal conditions, ILCs play a critical role in dampening the anti-bacterial T-cell response using MHCII. Indeed, when Sonnenberg's team looked at ILC activity directly, they found that MHCII+ ILCs could present foreign antigen to T cells and limit their expansion and pro-inflammatory properties.

Essentially, ILCs seem to instruct T cells to trust - that is, ignore -- commensal bacteria, thereby allowing the immune system to coexist with these foreign entities. Loss or dysregulation of ILCs, in turn, brought on by genetic or environmental factors such as diet or infection, for example, eliminates that protective action. This can lead to dysregulated immune activity and chronic inflammation.

"Inappropriate immune response to commensal bacteria and subsequent pathologic inflammation is a contributing factor to the pathogenesis and progression of many chronic human diseases, including inflammatory bowel disease, HIV/AIDS, viral hepatitis, cancer, cardiovascular disease, and diabetes," says Sonnenberg.

"This study provides new insight into the pathways that regulate immune responses to commensal bacteria and maintain tissue homeostasis" adds Hepworth.

Importantly, the study also identifies that MHCII+ ILCs are found in the intestinal tissues of healthy human donors. "Although it's still early days for this line of research, these findings provoke the hypothesis that MHCII+ innate lymphoid cells may be an important pathway to therapeutically target in the treatment of some chronic inflammatory diseases," suggests Sonnenberg. The Sonnenberg lab is now trying to establish if that is the case.

Source-Eurekalert

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