Evidence map›Paper›PMID 26255211›Full record

ArticleCytokine2015

Interleukin-6 inhibits apoptosis of exocrine gland tissues under inflammatory conditions.

Jing Zhou, Jun-O Jin, Ekta S Patel, Qing Yu

Abstract read
In one paragraph

Article in Cytokine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

6 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Strategy of Hepatic Metabolic Defects Induced byInternational journal of molecular sciences · 2020
    Article
  5. Article
  6. Article
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

4 authors at 1 institution in 1 country.

Jing ZhouDepartment of Immunology and Infectious Diseases, The Forsyth Institute, 245 First Street, Cambridge, MA 02142, USA; Department of Oral Medicine, Infection and Immunity, Harvard School of Dental Medicine, 188 Longwood Avenue, Boston, MA 02115, USA. Electronic address: jzhou@forsyth.org.
Jun-O JinDepartment of Immunology and Infectious Diseases, The Forsyth Institute, 245 First Street, Cambridge, MA 02142, USA. Electronic address: junojin1@gmail.com.
Ekta S PatelDepartment of Immunology and Infectious Diseases, The Forsyth Institute, 245 First Street, Cambridge, MA 02142, USA; Department of Oral Medicine, Infection and Immunity, Harvard School of Dental Medicine, 188 Longwood Avenue, Boston, MA 02115, USA. Electronic address: ektaspatel01@gmail.com.
Qing YuDepartment of Immunology and Infectious Diseases, The Forsyth Institute, 245 First Street, Cambridge, MA 02142, USA; Department of Oral Medicine, Infection and Immunity, Harvard School of Dental Medicine, 188 Longwood Avenue, Boston, MA 02115, USA. Electronic address: qyu@forsyth.org.
Harvard University · US

Funding

Regulation and Function of Interleukin-7 in Primary Sjogrens SyndromeR01DE023838 · NIDCR · ADA FORSYTH INSTITUTE, INC. · PI YU, QING · 2014 to 2018
$2.4M
The Forsyth Core Center for Discovery at the Host-Biofilm InterfaceP30DE020751 · NIDCR · ADA FORSYTH INSTITUTE, INC. · PI SMITH, DANIEL JAMES · 2009 to 2010
$1.8M
Mechanisms and Therapeutic Modulation of T Cell Autoimmune Responses in Sjogren's SyndromeR56DE023838 · NIDCR · ADA FORSYTH INSTITUTE, INC. · PI CHA, SEUNGHEE, YU, QING · 2020 to 2020
$532k
NIDCR NIH HHS P30 DE020751NIDCR NIH HHS R01 DE023838NIDCR NIH HHS R56 DE023838
6 · The paper itself

Abstract

Interleukin (IL)-6 is a multi-functional cytokine that can either promote or suppress tissue inflammation depending on the specific disease context. IL-6 is elevated in the exocrine glands and serum of patients with Sjögren's syndrome (SS), but the specific role of IL-6 in the pathogenesis of this disease has not been defined. In this study, we showed that IL-6 expression levels were increased with age in C56BL/6.NOD-Aec1Aec2 mice, a primary SS model, and higher than the control C57BL/6 mice. To assess the role of IL-6 during the immunological phase of SS development, a neutralizing anti-IL-6 antibody was administered into 16 week-old female C56BL/6.NOD-Aec1Aec2 mice, 3 times weekly for a consecutive 8 weeks. Neutralization of endogenous IL-6 throughout the immunological phase of SS development led to increased apoptosis, caspase-3 activation, leukocytic infiltration, and IFN-γ- and TNF-α production in the salivary gland. To further determine the effect of IL-6 on the apoptosis of exocrine gland cells, recombinant human IL-6 or the neutralizing anti-IL-6 antibody was injected into female C57BL/6 mice that received concurrent injection of anti-CD3 antibody to induce the apoptosis of exocrine gland tissues. Neutralization of IL-6 enhanced, whereas administration of IL-6 inhibited apoptosis and caspase-3 activation in salivary and lacrimal glands in this model. The apoptosis-suppressing effect of IL-6 was associated with up-regulation of Bcl-xL and Mcl-1 in both glands. Moreover, IL-6 treatment induced activation of STAT3 and up-regulated Bcl-xL and Mcl-1 gene expression in a human salivary gland epithelial cell line. In conclusion, IL-6 inhibits the apoptosis of exocrine gland tissues and exerts a tissue-protective effect under inflammatory conditions including SS. These findings suggest the possibility of using this property of IL-6 to preserve exocrine gland tissue integrity and function under autoimmune and inflammatory conditions.

Indexed as

ApoptosisAnimalsAntibodies, Neutralizingbcl-X ProteinCaspase 3Cell LineDisease Models, AnimalEnzyme ActivationExocrine GlandsFemaleHumansInflammationInterferon-gammaInterleukin-6Mice, Inbred C57BLMice, Inbred NODAntibodies, Neutralizingbcl-X ProteinCaspase 3Interferon-gammaInterleukin-6interleukin-6, mouseRecombinant ProteinsStat3 protein, mouseSTAT3 Transcription FactorTumor Necrosis Factor-alphaApoptosisExocrine glandInflammationInterleukin-6Sjögren’s syndrome

Identifiers

PMID26255211
PMCPMC4605873
OpenAlexW1054702922

What OpenQuestion holds

Textmetadata
LicenceTDM
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.