Daily Archives: June 25, 2012

The Gut Microbiota: your good germ friends to nurture to strengthen your immune system against “Allergy”


Your gut has both good microbes and sometimes, dangerous microbes. The trick is to know how to encourage the good microbes to grow inside your gut while creating a very difficult environment for the bad microbes inside your body. The good microbes codevelop inside your body since birth say a wonderful international group of physician and microbial scientists from five countries including Singapore, Sweden, USA, England and France. What germs your body can harbor depends firstly on your genes, and that means not everybody can tolerate all good microbes. Following your personal genes through your personal nutrition choices tailored to your specific lifestyle decides your microbiota. Believe it or not, your gut microbes control your brain, muscles, and your liver through your gut cells. Gives a whole new meaning to the term, “You are what you eat”. I would not add, “Your brain is what you eat”. These scientists strongly suggest that it is imperative to understand the individual gut microbiota, which means your good microbes, to get a better understanding of how to keep your brain and your muscles in peak performance by assisting your immune regulatory system. Apparently, your immune system is assisted by your good microbes. David Artis and his team at University of Pennsylvannia have become the leading scientists calling for an overhaul of the study of what is allergy and the immune system, based on gut microbiota research.

Have you ever wondered how that poor kid playing in the filth is healthier than your kid brought up in a sterilized home and school environment and playground? Well, the answer may lie in the good microbes that co-develop in the gut since birth. The articles below may be of interest to you. Your gut is “infested” fortunately by trillions of beneficial microbes that occupy their own favorite niches inside the intestine, as it folds its way inside your body. You might want to reconsider next time you have that antibiotic – it may indiscriminate and kill the bacteria that help you along with that single one that is harming you, currently. Have you ever wondered how some people are better able to “fight” off infection? They may actually have a stronger gut.  The term “my gut reaction” may not be that funny after all!

1)  Host-Gut Microbiota Metabolic Interactions
2) Crossover Immune Cells Blur the Boundaries
3) Innate Lymphoid Cells Promote Anatomical Containment of Lymphoid-Resident Commensal Bacteria
4) Immunology: Allergy challenged

1)  Host-Gut Microbiota Metabolic Interactions

Published Online June 6 2012
Science 8 June 2012:
Vol. 336 no. 6086 pp. 1262-1267
DOI: 10.1126/science.1223813
  • REVIEW

Host-Gut Microbiota Metabolic Interactions

  1. Jeremy K. Nicholson1,*,
  2. Elaine Holmes1,
  3. James Kinross1,
  4. Remy Burcelin2,
  5. Glenn Gibson3,
  6. Wei Jia4,
  7. Sven Pettersson5,*

+Author Affiliations


  1. 1Biomolecular Medicine, Department of Surgery and Cancer, Faculty of Medicine, Imperial College London, Exhibition Road, South Kensington, London SW7 2AZ, UK.

  2. 2Institut National de la Santé et de la Recherche Médicale, U1048, and Institut des Maladies Métaboliques et Cardiovasculaire I2MC, Rangueil Hospital, BP84225, 31432 Toulouse, France.

  3. 3Department of Food and Nutritional Sciences, The University of Reading, Whiteknights, Reading, UK.

  4. 4Department of Nutrition, University of North Carolina at Greensboro, North Carolina Research Campus, Kannapolis, NC 28081, USA.

  5. 5Department of Microbiology, Tumor, and Cell Biology (MTC), Karolinska Institutet, Stockholm 117 77, Sweden, and School of Biological Sciences and National Cancer Centre, 11 Hospital Drive, Singapore 169610.
  1. *To whom correspondence should be addressed. E-mail: j.nicholson@imperial.ac.uk (J.K.N.);sven.pettersson@ki.se (S.P.)

ABSTRACT

The composition and activity of the gut microbiota codevelop with the host from birth and is subject to a complex interplay that depends on the host genome, nutrition, and life-style. The gut microbiota is involved in the regulation of multiple host metabolic pathways, giving rise to interactive host-microbiota metabolic, signaling, and immune-inflammatory axes that physiologically connect the gut, liver, muscle, and brain. A deeper understanding of these axes is a prerequisite for optimizing therapeutic strategies to manipulate the gut microbiota to combat disease and improve health.

 2) Crossover Immune Cells Blur the Boundaries

NEWS FOCUSIMMUNOLOGYCrossover Immune Cells Blur the Boundaries

  • Mitch Leslie

Science 8 June 2012: 1228-1229.

3)

Published Online June 6 2012
Science 8 June 2012:
Vol. 336 no. 6086 pp. 1321-1325
DOI: 10.1126/science.1222551
  • REPORT

Innate Lymphoid Cells Promote Anatomical Containment of Lymphoid-Resident Commensal Bacteria

  1. Gregory F. Sonnenberg1,
  2. Laurel A. Monticelli1,
  3. Theresa Alenghat1,
  4. Thomas C. Fung1,
  5. Natalie A. Hutnick2,
  6. Jun Kunisawa3,4,
  7. Naoko Shibata3,4,
  8. Stephanie Grunberg1,
  9. Rohini Sinha1,
  10. Adam M. Zahm5,
  11. Mélanie R. Tardif6,
  12. Taheri Sathaliyawala7,
  13. Masaru Kubota7,
  14. Donna L. Farber7,
  15. Ronald G. Collman8,
  16. Abraham Shaked9,
  17. Lynette A. Fouser10,
  18. David B. Weiner2,
  19. Philippe A. Tessier6,
  20. Joshua R. Friedman5,
  21. Hiroshi Kiyono3,4,11,
  22. Frederic D. Bushman1,
  23. Kyong-Mi Chang8,12,
  24. David Artis1,13,*

+Author Affiliations


  1. 1Department of Microbiology and Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.

  2. 2Department of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.

  3. 3Division of Mucosal Immunology, Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan.

  4. 4Department of Medical Genome Science, Graduate School of Frontier Science, The University of Tokyo, Chiba 277-8562, Japan.

  5. 5Department of Pediatrics, Division of Gastroenterology, Hepatology, and Nutrition, Perelman School of Medicine, University of Pennsylvania, Children’s Hospital of Philadelphia, Philadelphia, PA 19104, USA.

  6. 6Centre de Recherche en Infectiologie, Centre Hospitalier de l’Université Laval, Faculty of Medicine, Laval University, Quebec, Canada.

  7. 7Department of Surgery and the Columbia Center for Translational Immunology, Columbia University Medical Center, New York, NY 10032, USA.

  8. 8Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.

  9. 9Department of Surgery, University of Pennsylvania, Philadelphia, PA 19104, USA.

  10. 10Inflammation and Immunology Research Unit, Biotherapeutics Research and Development, Pfizer Worldwide R&D, Cambridge, MA 02140, USA.

  11. 11Core Research for Evolutional Science and Technology, Japan Science and Technology Agency, Tokyo 102-0075, Japan.

  12. 12Philadelphia VA Medical Center, Philadelphia, PA 19104, USA.

  13. 13Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
  1. *To whom correspondence should be addressed. E-mail: dartis@mail.med.upenn.edu

ABSTRACT

The mammalian intestinal tract is colonized by trillions of beneficial commensal bacteria that are anatomically restricted to specific niches. However, the mechanisms that regulate anatomical containment remain unclear. Here, we show that interleukin-22 (IL-22)–producing innate lymphoid cells (ILCs) are present in intestinal tissues of healthy mammals. Depletion of ILCs resulted in peripheral dissemination of commensal bacteria and systemic inflammation, which was prevented by administration of IL-22. Disseminating bacteria were identified as Alcaligenes species originating from host lymphoid tissues. Alcaligenes was sufficient to promote systemic inflammation after ILC depletion in mice, and Alcaligenes-specific systemic immune responses were associated with Crohn’s disease and progressive hepatitis C virus infection in patients. Collectively, these data indicate that ILCs regulate selective containment of lymphoid-resident bacteria to prevent systemic inflammation associated with chronic diseases.

  • Received for publication 28 March 2012.
  • Accepted for publication 24 April 2012.

Immunology: Allergy challenged

Nature

 484,

458–459

(26 April 2012)

doi:10.1038/484458a

Published online

 25 April 2012

An article suggesting that allergic responses may not be an accident of an off-target immune system, but rather a deliberate defence against potential harm, provokes the question of whether our understanding of allergy needs an overhaul. Immunologists provide their opinions. See Perspective p.465

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Author information

Affiliations

  1. David Artis is in the Department of Microbiology and the Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.

  2. Rick M. Maizels is at the Institute of Immunology and Infection Research, University of Edinburgh, Edinburgh EH9 3JT, UK.

  3. Fred D. Finkelman is in the Department of Medicine, Cincinnati Veterans Affairs Medical Center, Cincinnati, Ohio 45220, USA, and in the Department of Internal Medicine, University of Cincinnati College of Medicine, and the Division of Cellular and Molecular Immunology, Cincinnati Children’s Hospital Medical Center.

Corresponding authors

Correspondence to:

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The world’s top influenza (Flu) research laboratories decided to institute a self-imposed moratorium


Should research work that attempts to make the H5N1 virus more potent, virulent, dangerous and transmissible under laboratory conditions be allowed? A meeting will be held in New York in July that will discuss whether the voluntary ban should be lifted.

The controversy over influenza risky levels of research ban and non-publication issues began over research by Netherlands researchers. They took an influenza (flu) virus that previously could only infect birds. They selected mutations from Influenza (Flu) viruses that had caused human pandemics with millions of deaths in 1918, and other years. They combined these mutations with the bird (avian) flu virus and passed it through ferrets. The reason they passed it through ferrets was that these animals most closely resemble how a person behaves when they are sick with the flu – the ferrets sneeze. The flu virus changed a little bit with each passage helped by the scientist to pass it from one sick ferret to a healthy ferret. In the first passage the scientist had to help or assist the mutant bird virus to infect the ferret by actually introducing it into the ferret. It could not “fly” through the air when the infected ferret sneezed to infect a healthy ferret in the vicinity. However, by the fifth passage onwards, this bird flu virus had mutated or picked up the ability to infect a healthy ferret by “flying” through the air in a sneeze pellet released by a sick ferret. The Dutch scientists could show how a new dangerous flu virus could emerge to cause a pandemic in people by existing previously in birds only, but by picking up mutations in flu virus infecting other animals or people and becoming able to “fly” in the air and infect a population. The scientists feel that knowing this ability will help them arm in advance and better equip governments to prepare in advance for the next pandemic. None of the ferrets died from this infection, a result of genetic engineering and multiple ferret transmission.

This research, by Ron Fouchier, PhD, of Erasmus Medical Center in the Netherlands and colleagues, was announced in a meeting of scientists and along with other researchers announcing their research on similar topics. Click here to read the reaction of the other researchers and policy makers present. Derek Smith, of the University of Cambridge, coauthored the second science paper, on June 21, 2012 gave a press release saying that such a pandemic event was in the realm of reality. Yoshihiro Kawaoka at the University of Wisconsin–Madison, published online by Nature discovered how the flu virus recognizes and stabilizes on a host cell through a protein during an influenza attack process. (Every human being is made up of several cells, as are all living things like birds, ferrets and plants; just in case you did not have a biology class in school. Also, a virus is not a bacterium. Only bacterial diseases can be cured by antibiotics. Viral diseases cannot be fought or cured by antibiotics).

The Dutch people were pondering on not allowing publication of research that might be dangerous in the hands of the wrong scientist, who might want to hurt all people. This view was contested by other scientists, including Nobel prize winner and head of the National Institute of Health, USA, who believe that the Dutch scientists research and similar research by University of Wisconsin scientists should be published in full. Click here to read what proposals made the Dutch Government reconsider their decision on banning this pubication of a bird flu study.

So, the question here is:
Is it better to be knowleadgeable and thus prearmed and prepared for the pandemic war that could possibly arise in the near future given the three deadly pandemics since the first one in 1918 last century?
Or,
is it better to just wait and see what hits the public with a severe health blow to millions of people (about 50 million are estimated to have died in 1918) and then figure out what flu combination is causing the pandemic and look for scientists available to find a vaccine to prevent further spread?
You may contact via email: r.fouchier@erasmusmc.nl This group did show that …”The transmissible viruses were sensitive to the antiviral drug oseltamivir”….

Related Articles about the controversial flu virus current research
Bird flu study published after terrorism debate ….could start a deadly pandemic among humans. These initial findings were presented last September in Malta at the European Scientific Working group on Influenza meeting to an auditorium packed with fellow scientists and policy makers…
Fouchier anticipates resuming H5N1 studies soon….said the voluntary 60-day moratorium on lab-modified H5N1 viruses expired Mar 20 and added that researchers are waiting for national governments to release their lab biosecurity assessments. These assessments were a component of a plan stemming from a World Health Organization (WHO) meeting of technical experts in February.

Fouchier made his comments during a live episode of virologist Vincent Racaniello’s “This Week in Virology” (TWiV), which was broadcast via webcast from the Society for General Microbiology conference in Dublin, Ireland. Racaniello, a virologist at Columbia University, authors Virology Blog and hosts the weekly virology podcast series.

Fouchier’s group at Erasmus and a University of Wisconsin team led by Yoshihiro Kawaoka, DVM, PhD, conducted experiments that involved engineering an H5N1 virus and an H1N1-H5N1 hybrid, respectively, that were transmissible in ferrets via airborne droplets.

The studies have been accepted for publication in Science and Nature, but advisors to the US government in December recommended against publishing the full details of the studies, due to bioterrorism concerns….
Debate Persists Over Publishing Bird Flu Studies – you may click to hear a NPR discussion on this subject by biosecurity expert D.A. Henderson on the risks of publishing the research.
N.Y. Times: H5N1 ferret research should not have been done – by virology blog shows the New York Times editorial on 8 January 2012, entitled ‘An Engineered Doomsday’.
Mutant-flu paper published: Controversial study shows how dangerous forms of avian influenza could evolve in the wild. By Ed Yong on 02 May 2012 in Nature.com …Kawaoka found that the hybrid virus could spread between ferrets in separate cages after acquiring just four mutations. Three of these allow the HA protein to stick to receptor molecules on mammalian cells, and the fourth stabilizes the protein. “Before we initiated this experiment, we knew that receptor specificity is important,” says Kawaoka. “We didn’t know what else was needed.”…

Related Articles: The Controversial Flu virus papers being discussed above
1. Airborne Transmission of Influenza A/H5N1 Virus Between Ferrets in Science 22 June 2012: Vol. 336 no. 6088 pp. 1534-1541
by Sander Herfst and colleagues – A report. (…..The genetically modified A/H5N1 virus acquired mutations during passage in ferrets, ultimately becoming airborne transmissible in ferrets. None of the recipient ferrets died after airborne infection with the mutant A/H5N1 viruses. Four amino acid substitutions in the host receptor-binding protein hemagglutinin, and one in the polymerase complex protein basic polymerase 2, were consistently present in airborne-transmitted viruses. ……)
2. Pathogenesis and Transmission of Swine-Origin 2009 A(H1N1) Influenza Virus in Ferrets / http://www.sciencexpress.org / 2 July 2009 / Page 1 / 10.1126/science.1177127
3. Severity of Pneumonia Due to New H1N1 Influenza Virus in Ferrets Is Intermediate between That Due to Seasonal H1N1 Virus and Highly Pathogenic Avian Influenza H5N1 Virus. J Infect Dis. (2010) 201 (7): 993-999. doi: 10.1086/651132

Related Articles about the history of the Flu virus and vaccine development
History of the 1918 pandemic and the search for a vaccine
Should I get a flu vaccine this year?
Why am I feeling fatigued after getting the flu vaccine?

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