Infection and Immunity Program

Mallorca, Spain

Infection and Immunity Program

Mallorca, Spain
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News Article | May 23, 2017
Site: www.eurekalert.org

Inflammation is the process by which the body responds to injury or infection but when this process becomes out of control it can cause disease. Monash Biomedicine Discovery Institute (BDI) researchers, in collaboration with the Monash Institute of Pharmaceutical Sciences (MIPS), have shed light on a key aspect of the process. Their findings may help guide the development of new treatments of inflammatory diseases such as atherosclerosis, which can lead to heart attack or stroke, and type 2 diabetes. Published today in the journal Science Signaling, the research reveals how certain proteins cause the white blood cells that play a central role in inflammatory responses to behave in different ways. White blood cells are beneficial in helping to eliminate invading microorganisms or repair damaged tissue, but they can prolong the response and damage healthy tissues, leading to disease. The proteins, called chemokines, are secreted into blood vessels and activate chemokine receptors embedded in the outer membranes of the white blood cells. While it was previously thought that this occurred like an on-off switch, the scientists found that the chemokine receptor can behave more like a 'dimmer switch' with one chemokine giving a strong signal and another giving a weaker signal. They found that different responses can be caused by different chemokines activating the same receptor. This explained for the first time the mechanism by which white blood cells produced varying responses: a strong short-lived response (acute inflammation) or a steady, longer-lived response (chronic inflammation). "Until now, we did not understand how this was possible," said co-lead author Associate Professor Martin Stone. "Our work has identified the specific features of chemokines and receptors that are involved in their inflammatory activity," Associate Professor Stone said. "The ultimate goal is to develop anti-inflammatory drugs that target these molecules," he said. The findings, which Associate Professor Stone presented at an international conference on cell signalling last week, will have wide implications as the proteins involved are essential to all inflammatory diseases. Associate Professor Stone, who heads a laboratory in the Infection and Immunity Program at the Monash BDI collaborated closely with co-lead author Dr Meritxell Canals from MIPS. First author was PhD student Mrs Zil E. Huma. This research was supported by the Australian National Health and Medical Research Council, the Australian Research Council, Monash University and ANZ Trustees. Read the full paper titled Key determinants of selective binding and activation by the monocyte chemoattractant proteins at the chemokine receptor CCR2 Committed to making the discoveries that will relieve the future burden of disease, the newly established Monash Biomedicine Discovery Institute at Monash University brings together more than 120 internationally-renowned research teams. Our researchers are supported by world-class technology and infrastructure, and partner with industry, clinicians and researchers internationally to enhance lives through discovery.


News Article | May 24, 2017
Site: www.medicalnewstoday.com

Inflammation is the process by which the body responds to injury or infection but when this process becomes out of control it can cause disease. Monash Biomedicine Discovery Institute (BDI) researchers, in collaboration with the Monash Institute of Pharmaceutical Sciences (MIPS), have shed light on a key aspect of the process. Their findings may help guide the development of new treatments of inflammatory diseases such as atherosclerosis, which can lead to heart attack or stroke, and type 2 diabetes. Published in the journal Science Signaling, the research reveals how certain proteins cause the white blood cells that play a central role in inflammatory responses to behave in different ways. White blood cells are beneficial in helping to eliminate invading microorganisms or repair damaged tissue, but they can prolong the response and damage healthy tissues, leading to disease. The proteins, called chemokines, are secreted into blood vessels and activate chemokine receptors embedded in the outer membranes of the white blood cells. While it was previously thought that this occurred like an on-off switch, the scientists found that the chemokine receptor can behave more like a 'dimmer switch' with one chemokine giving a strong signal and another giving a weaker signal. They found that different responses can be caused by different chemokines activating the same receptor. This explained for the first time the mechanism by which white blood cells produced varying responses: a strong short-lived response (acute inflammation) or a steady, longer-lived response (chronic inflammation). "Until now, we did not understand how this was possible," said co-lead author Associate Professor Martin Stone. "Our work has identified the specific features of chemokines and receptors that are involved in their inflammatory activity," Associate Professor Stone said. "The ultimate goal is to develop anti-inflammatory drugs that target these molecules," he said. The findings, which Associate Professor Stone presented at an international conference on cell signalling last week, will have wide implications as the proteins involved are essential to all inflammatory diseases. Associate Professor Stone, who heads a laboratory in the Infection and Immunity Program at the Monash BDI collaborated closely with co-lead author Dr Meritxell Canals from MIPS. First author was PhD student Mrs Zil E. Huma. This research was supported by the Australian National Health and Medical Research Council, the Australian Research Council, Monash University and ANZ Trustees. Article: Key determinants of selective binding and activation by the monocyte chemoattractant proteins at the chemokine receptor CCR2, Martin J. Stone et al., Science Signaling, doi: 10.1126/scisignal.aai8529, published 23 May 2017.


News Article | May 25, 2017
Site: www.sciencedaily.com

Inflammation is the process by which the body responds to injury or infection but when this process becomes out of control it can cause disease. Monash Biomedicine Discovery Institute (BDI) researchers, in collaboration with the Monash Institute of Pharmaceutical Sciences (MIPS), have shed light on a key aspect of the process. Their findings may help guide the development of new treatments of inflammatory diseases such as atherosclerosis, which can lead to heart attack or stroke, and type 2 diabetes. Published today in the journal Science Signaling, the research reveals how certain proteins cause the white blood cells that play a central role in inflammatory responses to behave in different ways. White blood cells are beneficial in helping to eliminate invading microorganisms or repair damaged tissue, but they can prolong the response and damage healthy tissues, leading to disease. The proteins, called chemokines, are secreted into blood vessels and activate chemokine receptors embedded in the outer membranes of the white blood cells. While it was previously thought that this occurred like an on-off switch, the scientists found that the chemokine receptor can behave more like a 'dimmer switch' with one chemokine giving a strong signal and another giving a weaker signal. They found that different responses can be caused by different chemokines activating the same receptor. This explained for the first time the mechanism by which white blood cells produced varying responses: a strong short-lived response (acute inflammation) or a steady, longer-lived response (chronic inflammation). "Until now, we did not understand how this was possible," said co-lead author Associate Professor Martin Stone. "Our work has identified the specific features of chemokines and receptors that are involved in their inflammatory activity," Associate Professor Stone said. "The ultimate goal is to develop anti-inflammatory drugs that target these molecules," he said. The findings, which Associate Professor Stone presented at an international conference on cell signalling last week, will have wide implications as the proteins involved are essential to all inflammatory diseases. Associate Professor Stone, who heads a laboratory in the Infection and Immunity Program at the Monash BDI collaborated closely with co-lead author Dr Meritxell Canals from MIPS. First author was PhD student Mrs Zil E. Huma.


Gorrell R.J.,Infection and Immunity Program | Gorrell R.J.,Monash Biomedicine Discovery Institute | Zwickel N.,Infection and Immunity Program | Zwickel N.,Monash Biomedicine Discovery Institute | And 6 more authors.
Journal of Infectious Diseases | Year: 2016

Previous studies suggest overrepresentation of particular polymorphisms within the Helicobacter pylori CagL hypervariable motif (CagLHM) in gastric cancer-associated isolates. However, these disease correlations were geographically variable and ambiguous. We compared the disease correlation of several hundred geographically diverse CagL sequences and identified 33 CagLHM sequence combinations with disparate geographical distribution, revealing substantial worldwide CagLHM diversity, particularly within Asian countries. Notably, polymorphisms E59 and I60 were significantly overrepresented, whereas D58 and E62 were underrepresented, in gastric cancer-associated H. pylori isolates worldwide. Thus, CagLHM regional diversity may contribute to the varied prevalence of H. pylori-related gastric cancer observed in diverse populations. © The Author 2016. Published by Oxford University Press for the Infectious Diseases Society of America. All rights reserved.


Tomas A.,Infection and Immunity Program | Tomas A.,Institute Investigacion Sanitaria Of Palma Idispa | Tomas A.,Research Center Biomedica en Red Enfermedades Respiratorias | Lery L.,Institute Pasteur Paris | And 28 more authors.
Journal of Biological Chemistry | Year: 2015

Background: There is limited knowledge of Klebsiella pneumoniae determinants implicated in the blocking of the NF-κB signaling pathway. Results:Ahigh-throughput genetic screen led to the identification of 114 putative K. pneumoniae genes that are associated with suppression of NF-κB activation. Conclusion: CPS, LPS, and the T2SS-secreted PulA are needed for immune evasion. Significance: A new therapeutic approach to treat Klebsiella infections will be the prevention of immune evasion. © 2015 by The American Society for Biochemistry and Molecular Biology, Inc.

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