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

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