Researchers from UCLA's Jonsson Comprehensive Cancer Center have identified a cell-permeable peptide that inhibits a hepatitis C virus protein and blocks viral replication, which can lead to liver cancer and cirrhosis. This finding by Dr. Samuel French, an assistant professor of pathology and senior author of the study, builds on previous work by the French laboratory that identified two cellular proteins that are important factors in hepatitis C virus infection.
French and his team initially set out to identify the cellular factors involved in hepatitis C replication and, using mass spectrometry, found that heat shock proteins (HSPs) 40 and 70 were important for viral infection. HSP70 was previously known to be involved, but HSP40 was linked for the first time to hepatitis C infection, French said. They further showed that the natural compound Quercetin, which inhibits the synthesis of these proteins, significantly inhibits viral infection in tissue culture.
In this study, published Jan. 30, 2012 in the peer-reviewed journal Hepatology, French and his team demonstrated that the viral non-structural protein 5A (NS5A) directly binds to HSP70 and mapped the site of the NS5A/HSP70 complex on NS5A. While HSP70 was previously shown to bind NS5A in cells, a direct NS5A/HSP70 interaction and complex formation was established in this study. In an effort to stop this interaction, they tested peptides that might inhibit HSP70.
"This is important because we've developed a small peptide that binds to that site and blocks the interaction between the proteins that is important for viral replication," French said. "This is another, potentially highly efficacious way to block replication of hepatitis C."
An estimated 160 million people worldwide are infected with hepatitis C and the conventional treatments -- interferon and ribavirin -- can have significant side effects. A new drug targeting cellular proteins rather than viral proteins would be a valuable addition to the treatment arsenal, French said.
"We were surprised that this peptide works this well," French said. "While its mechanism is different, the activity of this peptide is comparable to other newly developed anti-virals."
The study, done in tissue culture, shows that the peptide gains entry into the cell easily and blocks the cascade of cellular events that allows the virus to replicate, French said. Blocking the HSP70 protein rather than a viral protein also reduces the chance of patients with the hepatitis C virus developing resistance to the peptide.
"There's no direct pressure on the virus, so it is less likely to mutate and develop resistance," French said. "The goal is to achieve a sustained response, essentially a cure, meaning there is no more virus replication. There are a lot of drugs coming out now that are designed to stop hepatitis C replication, but resistance is still an issue. About 10 to 20 percent of patients on the new drugs become resistant. This new peptide may help combat resistance."
Going forward, French and his team are testing variants of the newly discovered peptide to see if they can develop one with an even higher affinity and can decrease the size of the peptide to improve cellular penetration and liver targeting. The new and improved peptides will be tested in animal models.
This peptide "may be a candidate for hepatitis C therapy," the study states. "Considering the potency of the peptide in suppressing viral translation levels, treatment with this peptide may significantly improve the efficacy of conventional treatments in patients who become resistant to conventional therapies."
**Source: University of California, Los Angeles (UCLA), Health Sciences
01 February 2012
Reino Unido: Prohíben un anuncio que borra las arrugas de Rachel Weisz
El regulador de publicidad del Reino Unido ha prohibido un anuncio de una revista de cosméticos francesa L'Oreal que promociona una crema antiarrugas con una fotografía del rostro de la actriz británica Rachel Weisz.
El anuncio a doble página, publicado por primera vez en septiembre, mostró la cara de la actriz en primer plano y en blanco y negro, con una lista de 10 supuestos efectos beneficiosos de la reparación de la crema Revitalift 10.
La parlamentaria liberal demócrata Jo Swinson, que hizo campaña sobre la imagen, ha presentado una demanda contra L'Oreal, acusando a la empresa de haber retocado la imagen, engañando a los consumidores acerca de los efectos del producto.
El regulador ASA (Advertising Standards Authority), si bien reconoce que la foto parecía representar con precisión el brillo y el estado de las arrugas faciales de la actriz, consideró que "la imagen ha sido modificada a fin de cambiar sustancialmente su la piel para que parezca más suave y tersa". ASA ha concluido que el anuncio "exagera el rendimiento del producto" y podría inducir a error al consumidor.
la parlamentaria ha celebrado esta decisión, que prohíbe el uso de nuevo Oréal este anuncio. "La industria de la belleza y la publicidad debe dejar de engañar a los consumidores con imágenes engañosas", ha agregado.
El anuncio a doble página, publicado por primera vez en septiembre, mostró la cara de la actriz en primer plano y en blanco y negro, con una lista de 10 supuestos efectos beneficiosos de la reparación de la crema Revitalift 10.
La parlamentaria liberal demócrata Jo Swinson, que hizo campaña sobre la imagen, ha presentado una demanda contra L'Oreal, acusando a la empresa de haber retocado la imagen, engañando a los consumidores acerca de los efectos del producto.
El regulador ASA (Advertising Standards Authority), si bien reconoce que la foto parecía representar con precisión el brillo y el estado de las arrugas faciales de la actriz, consideró que "la imagen ha sido modificada a fin de cambiar sustancialmente su la piel para que parezca más suave y tersa". ASA ha concluido que el anuncio "exagera el rendimiento del producto" y podría inducir a error al consumidor.
la parlamentaria ha celebrado esta decisión, que prohíbe el uso de nuevo Oréal este anuncio. "La industria de la belleza y la publicidad debe dejar de engañar a los consumidores con imágenes engañosas", ha agregado.
*AFP
Massachusetts General study defines a new genetic subtype of lung cancer
A report from investigators at the Massachusetts General Hospital (MGH) Cancer Center has defined the role of a recently identified gene abnormality in a deadly form of lung cancer. Tumors driven by rearrangements in the ROS1 gene represent 1 to 2 percent of non-small-cell lung cancers (NSCLC), the leading cause of cancer death in the U.S. The researchers show that ROS1-driven tumors can be treated with crizotinib, which also inhibits the growth of tumors driven by an oncogene called ALK, and describe the remarkable response of one patient to crizotinib treatment. "ROS1 encodes a protein that is important for cell growth and survival, and deregulation of ROS1 through chromosomal rearrangement drives the growth of tumors," says Alice Shaw, MD, PhD, of the MGH Cancer Center -- co-lead author of the paper which has been published online in the Journal of Clinical Oncology. "This finding is important because we have drugs that inhibit ROS1 and could lead to the sort of dramatic clinical response we describe in this paper."
The current findings add ROS1 to the list of genes known to drive NSCLC growth when altered -- a list that includes KRAS, mutations of which account for about 25 percent of cases; EGFR, accounting for 10 to 15 percent; and ALK, rearranged in about 4 percent. Altogether, known cancer-causing genetic changes have been found in a little more than half of NSCLC tumors. Originally identified in brain tumors, ROS1 rearrangement previously had been identified in one NSCLC patient and one NSCLC cell line. The current study was designed to determine the frequency of ROS1 rearrangement in NSCLC and to define the characteristics of patients with ROS1-rearranged tumors.
The investigators screened tumor samples from more than 1,000 NSCLC patients treated at the MGH, Vanderbilt University, the University of California at Irvine, and Fudan University in Shanghai, China. ROS1 rearrangement was identified in 18 tumor samples, for a prevalence of 1.7 percent; ALK rearrangements were identified in 31 samples, with no samples showing alterations in both genes. Patients with ROS1-positive tumors tended to be younger, never to have smoked and to have a type of lung cancer called adenocarcinoma -- characteristics very similar to those of ALK-positive patients.
An earlier MGH study of an experimental ALK inhibitor had found the drug suppressed the growth of a ROS1-positive cell line in addition to ALK-positive cell lines, suggesting that ROS1-positive tumors might be sensitive to the ALK-inhibitor crizotinib. This observation led corresponding author John Iafrate, MD, PhD, and his team to develop a diagnostic test that could identify ROS1-positive tumors. Around the time that test became clinically available, a lung cancer patient whose tumor had not responded to drugs targeting EGFR mutations was referred to the MGH Cancer Center for genetic testing. His tumor was negative for ALK but later proved to harbor a ROS1 rearrangement, and he was enrolled in an extension of the crizotinib clinical trial first reported in the October 28, 2010, New England Journal of Medicine.
"When he enrolled in the trial last April, this patient was extremely sick -- with significant weight loss and very low oxygen levels -- and was barely able to walk," says Shaw. "Within a few days of starting crizotinib, he felt better; and by the time we scanned his chest at seven weeks, the tumors had essentially disappeared from his lungs." Nine months after starting crizotinib therapy, this patient continues to do well. Additional ROS1-positive patients have been enrolled in this trial at MGH, at UC Irvine and at the University of Colorado.
Shaw is an assistant professor of Medicine and Iafrate is an associate professor of Pathology at Harvard Medical School. Co-lead authors are Kristin Bergethon, MGH Pathology, and Sai-Hong Ignatius Ou, MD, PhD, University of California at Irvine. The study was supported by grants from the National Institutes of Health and from Pfizer, which received FDA approval for crizotinib in August 2011.
**Source: Massachusetts General Hospital
The current findings add ROS1 to the list of genes known to drive NSCLC growth when altered -- a list that includes KRAS, mutations of which account for about 25 percent of cases; EGFR, accounting for 10 to 15 percent; and ALK, rearranged in about 4 percent. Altogether, known cancer-causing genetic changes have been found in a little more than half of NSCLC tumors. Originally identified in brain tumors, ROS1 rearrangement previously had been identified in one NSCLC patient and one NSCLC cell line. The current study was designed to determine the frequency of ROS1 rearrangement in NSCLC and to define the characteristics of patients with ROS1-rearranged tumors.
The investigators screened tumor samples from more than 1,000 NSCLC patients treated at the MGH, Vanderbilt University, the University of California at Irvine, and Fudan University in Shanghai, China. ROS1 rearrangement was identified in 18 tumor samples, for a prevalence of 1.7 percent; ALK rearrangements were identified in 31 samples, with no samples showing alterations in both genes. Patients with ROS1-positive tumors tended to be younger, never to have smoked and to have a type of lung cancer called adenocarcinoma -- characteristics very similar to those of ALK-positive patients.
An earlier MGH study of an experimental ALK inhibitor had found the drug suppressed the growth of a ROS1-positive cell line in addition to ALK-positive cell lines, suggesting that ROS1-positive tumors might be sensitive to the ALK-inhibitor crizotinib. This observation led corresponding author John Iafrate, MD, PhD, and his team to develop a diagnostic test that could identify ROS1-positive tumors. Around the time that test became clinically available, a lung cancer patient whose tumor had not responded to drugs targeting EGFR mutations was referred to the MGH Cancer Center for genetic testing. His tumor was negative for ALK but later proved to harbor a ROS1 rearrangement, and he was enrolled in an extension of the crizotinib clinical trial first reported in the October 28, 2010, New England Journal of Medicine.
"When he enrolled in the trial last April, this patient was extremely sick -- with significant weight loss and very low oxygen levels -- and was barely able to walk," says Shaw. "Within a few days of starting crizotinib, he felt better; and by the time we scanned his chest at seven weeks, the tumors had essentially disappeared from his lungs." Nine months after starting crizotinib therapy, this patient continues to do well. Additional ROS1-positive patients have been enrolled in this trial at MGH, at UC Irvine and at the University of Colorado.
Shaw is an assistant professor of Medicine and Iafrate is an associate professor of Pathology at Harvard Medical School. Co-lead authors are Kristin Bergethon, MGH Pathology, and Sai-Hong Ignatius Ou, MD, PhD, University of California at Irvine. The study was supported by grants from the National Institutes of Health and from Pfizer, which received FDA approval for crizotinib in August 2011.
**Source: Massachusetts General Hospital
Según un estudio el 36% de los varones japoneses se muestra «indiferente o reacio» a mantener relaciones sexuales
Aunque se encuentren en una edad de gran ebullición hormonal, los japoneses de entre 16 y 19 años se muestran poco interesados por el sexo. Eso es al menos lo que se desprende de un estudio publicado por la Asociación de la Planificación Familiar de Japón. Un 36% de los varones entre 16 y 19 años encuestados se muestran indiferentes o reacios a mantener relaciones sexuales. Estos datos significan un incremento de un 19% con respecto a los regsitrados en 2008. Pero la indiferencia se extiende también entre la población femenina. Aunque no aparecen en la encuesta, se deduce que las chicas esto del sexo las deja todavía más frías.
El estudio también ha abordado la vida sexual de las parejas casadas. Aproximadamente el 40% de los casados no habían tenido relaciones sexuales en el último mes, un aumento del 4% de la misma encuesta realizada dos años antes y casi un 10% más que en 2004.
Este tipo de conductas constituyen un verdadero problema en Japón, país que tiene una de las tasas de natalidad más bajas del mundo y una de la poblaciones más envejecidas.
El estudio también ha abordado la vida sexual de las parejas casadas. Aproximadamente el 40% de los casados no habían tenido relaciones sexuales en el último mes, un aumento del 4% de la misma encuesta realizada dos años antes y casi un 10% más que en 2004.
Este tipo de conductas constituyen un verdadero problema en Japón, país que tiene una de las tasas de natalidad más bajas del mundo y una de la poblaciones más envejecidas.
Surprise finding redraws 'map' of blood cell production
A study of the cells that respond to crises in the blood system has yielded a few surprises, redrawing the 'map' of how blood cells are made in the body. The finding, by researchers from the Walter and Eliza Hall Institute, could have wide-ranging implications for understanding blood diseases such as myeloproliferative disorders (that cause excess production of blood cells) as well as used to develop new ways of controlling how blood and clotting cells are produced.
The research team, led by Drs Ashley Ng and Maria Kauppi from the institute's Cancer and Haematology division, investigated subsets of blood 'progenitor' cells and the signals that cause them to expand and develop into mature blood cells. Their results were recently published in the journal Proceedings of the National Academy of Sciences.
Dr Ng describes blood progenitor cells as the 'heavy lifters' of the blood system. "They are the targets for blood cell hormones, called cytokines, which Professor Don Metcalf and colleagues have shown to be critical for regulating blood cell production," Dr Ng said. "In times of stress, such as bleeding, during infection or after chemotherapy, it is really the progenitor cells that respond by replacing lost or damaged blood cells."
Dr Kauppi said the research team was particularly interested in myeloid progenitor cells, which produce megakaryocytes, a type of bone marrow cell that gives rise to blood-clotting platelets. "We used a suite of cell surface markers specific to these progenitor cells that allowed us to isolate and characterise the cells," she said.
The researchers were surprised to find that progenitor cells believed only to be able to produce megakaryocytes were also able to develop into red blood cells.
"We were able to clearly demonstrate that these mouse megakaryocyte progenitor cells have the potential to develop into either megakaryocytes or red blood cells in response to cytokines such as thrombopoietin and erythropoietin, which was quite unexpected," Dr Ng said. "In addition, we discovered that other progenitor populations thought to really only make neutrophils and monocytes [other immune cells], were capable of making red blood cell and platelets really well. In effect, we will have to redraw the map as to how red cells and platelets are made in the bone marrow."
Dr Kauppi said the researchers found they could regulate whether the progenitor cell became a megakaryocyte or a red blood cell by using different combinations of cytokines. "Now that we have properly identified the major cells and determined how they respond to cytokine signals involved in red blood cell and platelet production, the stage is set for understanding how these progenitors are affected in health and disease," she said. "We can also better understand, for instance, how genetic changes may lead to the development of certain blood diseases. "
Dr Ng said the findings would also help researchers discover new ways in which the progenitor cells can be controlled.
"This research is the first step in the future development of treatments for patients with blood diseases," Dr Ng said. "This may occur either by limiting blood cell production when too many are being made, as with myeloproliferative disorders, or stimulating blood production when the blood system is compromised, such as during cancer treatment or infection." Dr Ng said.
The research team, led by Drs Ashley Ng and Maria Kauppi from the institute's Cancer and Haematology division, investigated subsets of blood 'progenitor' cells and the signals that cause them to expand and develop into mature blood cells. Their results were recently published in the journal Proceedings of the National Academy of Sciences.
Dr Ng describes blood progenitor cells as the 'heavy lifters' of the blood system. "They are the targets for blood cell hormones, called cytokines, which Professor Don Metcalf and colleagues have shown to be critical for regulating blood cell production," Dr Ng said. "In times of stress, such as bleeding, during infection or after chemotherapy, it is really the progenitor cells that respond by replacing lost or damaged blood cells."
Dr Kauppi said the research team was particularly interested in myeloid progenitor cells, which produce megakaryocytes, a type of bone marrow cell that gives rise to blood-clotting platelets. "We used a suite of cell surface markers specific to these progenitor cells that allowed us to isolate and characterise the cells," she said.
The researchers were surprised to find that progenitor cells believed only to be able to produce megakaryocytes were also able to develop into red blood cells.
"We were able to clearly demonstrate that these mouse megakaryocyte progenitor cells have the potential to develop into either megakaryocytes or red blood cells in response to cytokines such as thrombopoietin and erythropoietin, which was quite unexpected," Dr Ng said. "In addition, we discovered that other progenitor populations thought to really only make neutrophils and monocytes [other immune cells], were capable of making red blood cell and platelets really well. In effect, we will have to redraw the map as to how red cells and platelets are made in the bone marrow."
Dr Kauppi said the researchers found they could regulate whether the progenitor cell became a megakaryocyte or a red blood cell by using different combinations of cytokines. "Now that we have properly identified the major cells and determined how they respond to cytokine signals involved in red blood cell and platelet production, the stage is set for understanding how these progenitors are affected in health and disease," she said. "We can also better understand, for instance, how genetic changes may lead to the development of certain blood diseases. "
Dr Ng said the findings would also help researchers discover new ways in which the progenitor cells can be controlled.
"This research is the first step in the future development of treatments for patients with blood diseases," Dr Ng said. "This may occur either by limiting blood cell production when too many are being made, as with myeloproliferative disorders, or stimulating blood production when the blood system is compromised, such as during cancer treatment or infection." Dr Ng said.
**Source: Walter and Eliza Hall Institute
Según ABC, Mato presentará en el Congreso una tarjeta sanitaria única y una central de compras de fármacos
Ni copago, ni «medicamentazo», ni grandes medidas de recorte en las prestaciones sanitarias. En su bautizo en el Parlamento, como ministra de Sanidad, Asuntos Sociales e Igualdad, Ana Mato no pedirá , previsiblemente, grandes sacrificios ni medidas impopulares para atajar el gasto sanitario. Sí desgranará medidas de contención que permitan detener la sangría de la Sanidad, sin grandes sacrificios, por el momento. Ofrecerá una mano tendida a los grupos parlamentarios que le permitan llegar a acuerdos para garantizar la sostenibilidad del sistema sanitario y comprensión con una mayor colaboración público-privada en la gestión.
Se espera que Mato se limite a trazar en el Congreso el primer esbozo de lo que puede ser la reforma sanitaria cuando explique las principales líneas de su Departamento. Y habrá guiños para cada una de las responsabilidades que tiene bajo su ministerio: dependencia, discapacidad, mayores, consumo, igualdad o familia.
-Protocolos para ahorrar
Las medidas más duras de control del gasto sanitario se reservan para la próxima reunión con las comunidades autónomas, en el primer Consejo Interterritorial de Salud de esta nueva legislatura. Hoy se buscará el compromiso de los grupos para acordar una cartera de servicios básicos en la sanidad pública y protocolos de actuación para reducir los costes de la sanidad. Eso acabaría con la utilización indiscriminada de tratamientos y servicios. Cada patología tendrá definido el tratamiento más adecuado a cada edad y pronóstico. Por ejemplo, una prótesis de rodilla de última generación (casi siempre más cara) se reservará para un paciente activo y joven, no para alguien de 80 años.
-Agencia estatal de compras para hospitales
Se quiere acabar con la negociación directa de los laboratorios y empresas de tecnología sanitaria con cada hospital. Para reducir el agujero de las comunidades se adquirirán los productos más baratos a través de una central de compras, como ya se ha hecho con la vacuna de la gripe.
-Programa e-salud
Los ciudadanos que utilicen la Sanidad pública, vivan donde vivan, tendrán una tarjeta sanitaria única que será válida en cualquier comunidad autónoma. El nuevo equipo quiere vertebrar los 17 servicios de salud a través de un documento único que permitirá acceder a cualquier servicio de salud con independencia de la comunidad autónoma a la que pertenezca el paciente. Además relanzarán el programa de «e-salud» que informatizará las historias clínicas y hará realidad la receta electrónica para aligerar la presión de los centros de salud. Los enfermos crónicos podrán ir a la farmacia con su tarjeta electrónica y obtener su plan mensual de tratamiento, sin acudir periódicamente al centro de salud a por las recetas. La historia clínica del paciente también «viajará» en la tarjeta.
-Ley del aborto
Tampoco está previsto que Ana Mato aporte cambios sustanciales a lo que ya anunció el ministro de Justicia, Alberto Ruiz-Gallardón, como la existencia del consentimiento informado de los padres antes de que aborte una menor. Sanidad y Asuntos Sociales harán los estudios pertinentes para modificar la norma, mientras Justicia tramitará la reforma. Los cambios irán más en la línea de una ley de supuestos, en lugar de plazos, y defenderá los derechos del «nonato», siempre que estos no entren en colisión con otros derechos, siguiendo la doctrina fijada por el TC en 1985.
-Mayores y apoyo a la familia
En su toma de posesión Mato ya anunció que «lo esencial» para su departamento eran «las personas y su mayor bienestar», destacando a jóvenes, mayores, niños. Su departamento prepara un plan para mayores y medidas de apoyo a las familias.
-Dependencia y discapacidad
La intención en esta nueva legislatura es hacer cumplir la ley y que las empresas mantengan el 2% de reserva de plazas para discapacitados. La ministra puede anunciar cambios en la financiación de la ley de dependencia.
**Publicado e "ABC"
Se espera que Mato se limite a trazar en el Congreso el primer esbozo de lo que puede ser la reforma sanitaria cuando explique las principales líneas de su Departamento. Y habrá guiños para cada una de las responsabilidades que tiene bajo su ministerio: dependencia, discapacidad, mayores, consumo, igualdad o familia.
-Protocolos para ahorrar
Las medidas más duras de control del gasto sanitario se reservan para la próxima reunión con las comunidades autónomas, en el primer Consejo Interterritorial de Salud de esta nueva legislatura. Hoy se buscará el compromiso de los grupos para acordar una cartera de servicios básicos en la sanidad pública y protocolos de actuación para reducir los costes de la sanidad. Eso acabaría con la utilización indiscriminada de tratamientos y servicios. Cada patología tendrá definido el tratamiento más adecuado a cada edad y pronóstico. Por ejemplo, una prótesis de rodilla de última generación (casi siempre más cara) se reservará para un paciente activo y joven, no para alguien de 80 años.
-Agencia estatal de compras para hospitales
Se quiere acabar con la negociación directa de los laboratorios y empresas de tecnología sanitaria con cada hospital. Para reducir el agujero de las comunidades se adquirirán los productos más baratos a través de una central de compras, como ya se ha hecho con la vacuna de la gripe.
-Programa e-salud
Los ciudadanos que utilicen la Sanidad pública, vivan donde vivan, tendrán una tarjeta sanitaria única que será válida en cualquier comunidad autónoma. El nuevo equipo quiere vertebrar los 17 servicios de salud a través de un documento único que permitirá acceder a cualquier servicio de salud con independencia de la comunidad autónoma a la que pertenezca el paciente. Además relanzarán el programa de «e-salud» que informatizará las historias clínicas y hará realidad la receta electrónica para aligerar la presión de los centros de salud. Los enfermos crónicos podrán ir a la farmacia con su tarjeta electrónica y obtener su plan mensual de tratamiento, sin acudir periódicamente al centro de salud a por las recetas. La historia clínica del paciente también «viajará» en la tarjeta.
-Ley del aborto
Tampoco está previsto que Ana Mato aporte cambios sustanciales a lo que ya anunció el ministro de Justicia, Alberto Ruiz-Gallardón, como la existencia del consentimiento informado de los padres antes de que aborte una menor. Sanidad y Asuntos Sociales harán los estudios pertinentes para modificar la norma, mientras Justicia tramitará la reforma. Los cambios irán más en la línea de una ley de supuestos, en lugar de plazos, y defenderá los derechos del «nonato», siempre que estos no entren en colisión con otros derechos, siguiendo la doctrina fijada por el TC en 1985.
-Mayores y apoyo a la familia
En su toma de posesión Mato ya anunció que «lo esencial» para su departamento eran «las personas y su mayor bienestar», destacando a jóvenes, mayores, niños. Su departamento prepara un plan para mayores y medidas de apoyo a las familias.
-Dependencia y discapacidad
La intención en esta nueva legislatura es hacer cumplir la ley y que las empresas mantengan el 2% de reserva de plazas para discapacitados. La ministra puede anunciar cambios en la financiación de la ley de dependencia.
**Publicado e "ABC"
Honey could be effective at treating and preventing wound infections
Manuka honey could help clear chronic wound infections and even prevent them from developing in the first place, according to a new study published in Microbiology. The findings provide further evidence for the clinical use of manuka honey to treat bacterial infections in the face of growing antibiotic resistance. Streptococcus pyogenes is a normal skin bacterium that is frequently associated with chronic (non-healing) wounds. Bacteria that infect wounds can clump together forming 'biofilms', which form a barrier to drugs and promotes chronic infection. Researchers at Cardiff Metropolitan University have shown that manuka honey can not only destroy fully-formed S. pyogenes biofilms in vitro but also prevent the bacteria initially binding to components of wound tissue.
Honey has long been acknowledged for its antimicrobial properties. Traditional remedies containing honey were used in the topical treatment of wounds by diverse ancient civilisations. Manuka honey is derived from nectar collected by honey bees foraging on the manuka tree found growing in New Zealand and parts of Australia. It is included in modern licensed wound-care products around the world. Manuka honey has been reported to inhibit more than 80 species of bacteria, yet the antimicrobial properties of honey have not yet been fully exploited by modern medicine as its mechanisms of action are not fully understood.
Wounds that are infected with S. pyogenes often fail to respond to treatment. This is largely due to the development of biofilms which may be difficult for antibiotics to penetrate -- in addition to problems of antibiotic resistance. The results of the study showed that very small concentrations of honey prevented the start of biofilm development and that treating established biofilms grown in Petri dishes with honey for 2 hours killed up to 85% of bacteria within them.
The Cardiff team are working towards providing molecular explanations for the antibacterial action of honey. The latest study reveals that honey can disrupt the interaction between S. pyogenes and the human protein fibronectin, which is displayed on the surface of damaged cells. "Molecules on the surface of the bacteria latch onto human fibronectin, anchoring the bacteria to the cell. This allows infection to proceed and biofilms to develop," explained Dr Sarah Maddocks who led the study. "We found that honey reduced the expression of these bacterial surface proteins, inhibiting binding to human fibronectin, therefore making biofilm formation less likely. This is a feasible mechanism by which manuka honey minimizes the initiation of acute wound infections and also the establishment of chronic infections.
Ongoing work in Dr Maddocks' lab is investigating other wound-associated bacteria including Pseudomonas aeruginosa and meticillin-resistant Staphylococcus aureus (MRSA). Manuka honey has also been shown to be effective at killing these bacteria. "There is an urgent need to find innovative and effective ways of controlling wound infections that are unlikely to contribute to increased antimicrobial resistance. No instances of honey-resistant bacteria have been reported to date, or seem likely," said Dr Maddocks. "Applying antibacterial agents directly to the skin to clear bacteria from wounds is cheaper than systemic antibiotics and may well complement antibiotic therapy in the future. This is significant as chronic wounds account for up to 4% of health care expenses in the developed world."
**Source: Society for General Microbiology
Honey has long been acknowledged for its antimicrobial properties. Traditional remedies containing honey were used in the topical treatment of wounds by diverse ancient civilisations. Manuka honey is derived from nectar collected by honey bees foraging on the manuka tree found growing in New Zealand and parts of Australia. It is included in modern licensed wound-care products around the world. Manuka honey has been reported to inhibit more than 80 species of bacteria, yet the antimicrobial properties of honey have not yet been fully exploited by modern medicine as its mechanisms of action are not fully understood.
Wounds that are infected with S. pyogenes often fail to respond to treatment. This is largely due to the development of biofilms which may be difficult for antibiotics to penetrate -- in addition to problems of antibiotic resistance. The results of the study showed that very small concentrations of honey prevented the start of biofilm development and that treating established biofilms grown in Petri dishes with honey for 2 hours killed up to 85% of bacteria within them.
The Cardiff team are working towards providing molecular explanations for the antibacterial action of honey. The latest study reveals that honey can disrupt the interaction between S. pyogenes and the human protein fibronectin, which is displayed on the surface of damaged cells. "Molecules on the surface of the bacteria latch onto human fibronectin, anchoring the bacteria to the cell. This allows infection to proceed and biofilms to develop," explained Dr Sarah Maddocks who led the study. "We found that honey reduced the expression of these bacterial surface proteins, inhibiting binding to human fibronectin, therefore making biofilm formation less likely. This is a feasible mechanism by which manuka honey minimizes the initiation of acute wound infections and also the establishment of chronic infections.
Ongoing work in Dr Maddocks' lab is investigating other wound-associated bacteria including Pseudomonas aeruginosa and meticillin-resistant Staphylococcus aureus (MRSA). Manuka honey has also been shown to be effective at killing these bacteria. "There is an urgent need to find innovative and effective ways of controlling wound infections that are unlikely to contribute to increased antimicrobial resistance. No instances of honey-resistant bacteria have been reported to date, or seem likely," said Dr Maddocks. "Applying antibacterial agents directly to the skin to clear bacteria from wounds is cheaper than systemic antibiotics and may well complement antibiotic therapy in the future. This is significant as chronic wounds account for up to 4% of health care expenses in the developed world."
**Source: Society for General Microbiology
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