Evidence map›Paper›PMID 22292110›Full record

ArticleNutrients2011

Effect of probiotic bacteria on microbial host defense, growth, and immune function in human immunodeficiency virus type-1 infection.

Susanna Cunningham-Rundles, Siv Ahrné, Rosemary Johann-Liang, Rachel Abuav, Ann-Margaret Dunn-Navarra, Claudia Grassey, Stig Bengmark, Joseph S Cervia

Open access · goldAbstract read
In one paragraph

Article in Nutrients, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
6.1field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 95 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Trial
  5. Trial
  6. Trial
  7. Trial
  8. Trial
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Review
  19. Review
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 6 institutions in 3 countries.

Susanna Cunningham-RundlesWeill-Cornell Cellular Immunology Laboratory, Division of Hematology/Oncology, Host Defenses Program, Department of Pediatrics, Weill Medical College of Cornell University, New York, NY 10065, USA.
Siv Ahrné
Rosemary Johann-Liang
Rachel Abuav
Ann-Margaret Dunn-Navarra
Claudia Grassey
Stig Bengmark
Joseph S Cervia
Cornell University · USCedars-Sinai Medical Center · USCentre for Nursing Innovation · GBLund University · SEUniversity College London · GBYeshiva University · US

Funding

VENOGLOBULIN-I IN THE TREATMENT OF SEVERE STEROID DEPENDENT ASTHMAM01RR006020 · NCRR · WEILL MEDICAL COLLEGE OF CORNELL UNIV · PI GOTTO, ANTONIO M · 1990 to 2003
$11.7M
RETINOIDS AND EPITHELIAL DIFFERENTIATIONP30CA029502 · NCI · STRANG CANCER PREVENTION CENTER · PI RIVLIN, RICHARD S · 2002 to 2006
$4.1M
ZINC AS A BIOLOGICAL RESPONSE MODIFIERP01CA029502 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI ZHANG, ZUO · 1985 to 2000
$360k
NCI NIH HHS CA29502NCI NIH HHS P01 CA029502NCI NIH HHS P30 CA029502NCRR NIH HHS M01 RR 6020
6 · The paper itself

Abstract

The hypothesis that probiotic administration protects the gut surface and could delay progression of Human Immunodeficiency Virus type1 (HIV-1) infection to the Acquired Immunodeficiency Syndrome (AIDS) was proposed in 1995. Over the last five years, new studies have clarified the significance of HIV-1 infection of the gut associated lymphoid tissue (GALT) for subsequent alterations in the microflora and breakdown of the gut mucosal barrier leading to pathogenesis and development of AIDS. Current studies show that loss of gut CD4+ Th17 cells, which differentiate in response to normal microflora, occurs early in HIV-1 disease. Microbial translocation and suppression of the T regulatory (Treg) cell response is associated with chronic immune activation and inflammation. Combinations of probiotic bacteria which upregulate Treg activation have shown promise in suppressing pro inflammatory immune response in models of autoimmunity including inflammatory bowel disease and provide a rationale for use of probiotics in HIV-1/AIDS. Disturbance of the microbiota early in HIV-1 infection leads to greater dominance of potential pathogens, reducing levels of bifidobacteria and lactobacillus species and increasing mucosal inflammation. The interaction of chronic or recurrent infections, and immune activation contributes to nutritional deficiencies that have lasting consequences especially in the HIV-1 infected child. While effective anti-retroviral therapy (ART) has enhanced survival, wasting is still an independent predictor of survival and a major presenting symptom. Congenital exposure to HIV-1 is a risk factor for growth delay in both infected and non-infected infants. Nutritional intervention after 6 months of age appears to be largely ineffective. A meta analysis of randomized, controlled clinical trials of infant formulae supplemented with Bifidobacterium lactis showed that weight gain was significantly greater in infants who received B. lactis compared to formula alone. Pilot studies have shown that probiotic bacteria given as a supplement have improved growth and protected against loss of CD4+ T cells. The recognition that normal bacterial flora prime neonatal immune response and that abnormal flora have a profound impact on metabolism has generated insight into potential mechanisms of gut dysfunction in many settings including HIV-1 infection. As discussed here, current and emerging studies support the concept that probiotic bacteria can provide specific benefit in HIV-1 infection. Probiotic bacteria have proven active against bacterial vaginosis in HIV-1 positive women and have enhanced growth in infants with congenital HIV-1 infection. Probiotic bacteria may stabilize CD4+ T cell numbers in HIV-1 infected children and are likely to have protective effects against inflammation and chronic immune activation of the gastrointestinal immune system.

Indexed as

HIV-1Acquired Immunodeficiency SyndromeBacterial TranslocationBifidobacteriumCD4-Positive T-LymphocytesChildDietary SupplementsFemaleHIV InfectionsHIV Wasting SyndromeHumansInfantInfant FormulaInfectious Disease Transmission, VerticalInflammationIntestinal MucosaAIDSanti retroviral therapyanti-retroviral therapy (ART)BCMbody cellular massbody mass index (BMI)CD4+ CD25+ FoxP3+ T regulatory cellsCD4+ Th17 cellschildrenfailure-to-thrivegrowthgut associated lymphoid tissue (GALT)HIV-1immune developmentinflammationlactobacillusmicrobial translocationmicrofloramicronutrientmucosal barriernutritionprobiotic bacteriawomen

Identifiers

PMID22292110
PMCPMC3260491
OpenAlexW1976189867

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.