Thursday, March 3, 2011

3 The Friday Four

In this issue of the Friday Four: USDA studies on herbal tea, how bacteria uses nanotubes to communicate and cause antibiotic resistance, studying white blood cells and mechanisms to eliminate inflammation after infections, and a study suggests ALS may be caused by a retrovirus.

1) In The Something We Knew All Along Department: Herbal Teas May Provide Health Benefits

Those who enjoy the caffeinated lift that comes from drinking traditional coffees and teas may tend to overlook the benefits of drinking herbal infusions. Now, as explained in this month's issue of Agricultural Research magazine, the idea that herbal teas may provide a variety of health benefits is no longer just folklore.

ScienceDaily. Retrieved March 3, 2011,

Original Source Publication: USDA/Agricultural Research Service (2011, March 2). Herbal teas may provide health benefits.

2) Bacteria Can Communicate With Each Other Through Nanotubes, Researchers Discover

A pathway whereby bacteria communicate with each other has been discovered by researchers at the Hebrew University of Jerusalem. The discovery has important implications for efforts to cope with the spread of harmful bacteria in the body.

ScienceDaily. Retrieved March 3, 2011,
from­ /releases/2011/03/110302080003.htm

Original Source Publication:
Gyanendra P. Dubey, Sigal Ben-Yehuda. Intercellular Nanotubes Mediate Bacterial Communication. Cell, 2011; 144 (4): 590 DOI: 10.1016/j.cell.2011.01.015

3) How Much Can a Cell Uptake? On White Blood Cells and Healing from Inflammation

Immunological research at the University of Haifa, Israel, has made a new breakthrough, revealing a critical component in the "decision-making" process of white blood cells that play a role in the healing process from bacterial inflammation. "The process that we have discovered can assist in the development of drugs that are based on the natural processes that take place in the human body, unlike most of the existing drugs that attempt to curb inflammation by artificial means," explains Dr. Amiram Ariel of the Department of Biology at the University of Haifa, who headed the study.

ScienceDaily. Retrieved March 11, 2011,
from­ /releases/2011/03/110302101656.htm

Original Source Publication:
Sagie Schif-Zuck, Nufar Gross, Simaan Assi, Ran Rostoker, Charles N. Serhan, Amiram Ariel. Saturated-efferocytosis generates pro-resolving CD11blow macrophages: Modulation by resolvins and glucocorticoids. European Journal of Immunology, 2011; 41 (2): 366 DOI: 10.1002/eji.201040801

4) Amyotrophic Lateral Sclerosis (ALS) Could Be Caused by a Retrovirus, Study Suggests

A retrovirus that inserted itself into the human genome thousands of years ago may be responsible for some cases of the neurodegenerative disease amyotrophic lateral sclerosis (ALS), also known as Lou Gherig's disease. The finding, made by Johns Hopkins scientists, may eventually give researchers a new way to attack this universally fatal condition.

ScienceDaily. Retrieved March 3, 2011,

Original Source Publication:
Renée Douville, Jiankai Liu, Jeffrey Rothstein, Avindra Nath. Identification of active loci of a human endogenous retrovirus in neurons of patients with amyotrophic lateral sclerosis. Annals of Neurology, 2011; 69 (1): 141 DOI: 10.1002/ana.22149


  1. About #3: gotta love those macrophages...what busy little bees they are! So, what happens when Bb infects a macrophage--seems I've heard this is one of Bb's tricks. One can imagine this might disrupt their organized way of keeping inflammation in check. Any clues in the article as to what this substance that redirects the macrophages behavior from consuming neutrophils to modulating the immune system is composed of?


  2. It is fascinating, Anonymous, and I was thinking about that when I read it...

    If you want to refer to the original abstract, it's this one:

    In reference to that abstract, CD11b is expressed on monocytes and neutrophils, in which it mediates margination and migration of these leukocytes to areas of inflammation, and these particular macrophages convert from CD11b low to CD11b phenotypes when facing dead cells (ex vivo).

    The abstract states, "In addition, we found that the pro-resolving lipid mediators resolvin E1 and D1, and the glucocorticoid dexamethasone regulated pro-resolving macrophage functions in vivo" - so RvE1 and PD1 are involved - sorry I can't tell you more without access, but here's older citations for those if you weren't previously familiar:

    On RvE1 (resolvin E1):

    On PD1 (resolvin D1):>

    I need to get a copy of the full text - I don't have access to it right now, but if you have a way to look it up, let me know. I'm curious, too. Otherwise, I have to truck up to the university library.

  3. Correction: That should have said, "and these particular macrophages convert from CD11b low to CD11b high phenotypes when facing dead cells (ex vivo)."


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