Evidence map›Paper›PMID 28982735›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2018

Acidosis exacerbates in vivo IL-1-dependent inflammatory responses and neutrophil recruitment during pulmonary Pseudomonas aeruginosa infection.

Iviana M Torres, Yash R Patankar, Brent Berwin

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

17 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Inhibition of proton sensor GPR68 suppresses endothelial dysfunction and acute lung injury caused by Staphylococcus aureus bacterial particles.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  4. Review
  5. Review
  6. RSC advances · 2022
    Article
  7. Airway acidification impaired host defense againstEmerging microbes & infections · 2022
    Article
  8. Article
  9. Engineered mesenchymal stromal cell therapy during human lungMolecular therapy. Methods & clinical development · 2021
    Article
  10. Article
  11. Article
  12. The Role of Innate Immunity in Pulmonary Infections.BioMed research international · 2021
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. 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

3 authors at 1 institution in 1 country.

Iviana M TorresDepartment of Microbiology and Immunology, Geisel School of Medicine at Dartmouth, Lebanon, New Hampshire.
Yash R PatankarDepartment of Microbiology and Immunology, Geisel School of Medicine at Dartmouth, Lebanon, New Hampshire.
Brent BerwinDepartment of Microbiology and Immunology, Geisel School of Medicine at Dartmouth, Lebanon, New Hampshire.
Dartmouth College · US

Funding

IMMUNOBIOLOGY OF MYELOID AND LYMPHOID CELLST32AI007363 · NIAID · DARTMOUTH COLLEGE · PI Claudia V Jakubzick · 1990 to 2026
$9.5M
TRANSLATIONAL RESEARCH COREP30GM106394 · NIGMS · DARTMOUTH COLLEGE · PI MADDEN, DEAN R · 2013 to 2017
$6.1M
CENTER FOR MOLECULAR, CELLULAR, AND TRANSLATIONAL IMMUNOLOGYP30RR032136 · NCRR · DARTMOUTH COLLEGE · PI GREEN, WILLIAM R · 2011 to 2011
$1.2M
The Role of Flagellar Motility to Innate Immune Recognition of BacteriaR21AI121820 · NIAID · DARTMOUTH COLLEGE · PI BERWIN, BRENT L · 2016 to 2017
$461k
Inducing effective phagocytic clearance of non-motile bacteriaR03AI135358 · NIAID · DARTMOUTH COLLEGE · PI O'TOOLE, GEORGE A. · 2018 to 2019
$164k
NCRR NIH HHS P30 RR032136NIAID NIH HHS R21 AI121820NIAID NIH HHS T32 AI007363NIGMS NIH HHS P30 GM106394
6 · The paper itself

Abstract

Acidic microenvironments commonly occur at sites of inflammation and bacterial infections. In the context of a Pseudomonas aeruginosa infection, we previously demonstrated that acidosis enhances the cellular proinflammatory interleukin (IL)-1β response in vitro. However, how pH alterations affect in vivo IL-1β responses and subsequent IL-1-driven inflammation during infection with P. aeruginosa is unclear. Here, we report that acidosis enhances in vivo IL-1β production and downstream IL-1 receptor-dependent responses during infection with P. aeruginosa in models of acute pneumonia and peritonitis. Importantly, we demonstrate that infection with P. aeruginosa within an acidic environment leads to enhanced production of a subset of proinflammatory cytokines, including chemokine (C-X-C) motif ligand 1, IL-6, and chemokine (C-C motif) ligand 2, and increased neutrophil recruitment. Furthermore, with the use of IL-1 receptor type 1-deficient mice, we identify the contribution of the IL-1 signaling pathway to the acidosis-enhanced inflammatory response and pathology. These data provide insights into the potential benefit of pH regulation during bacterial infections to control disease progression and immunopathology.

Indexed as

AcidosisAnimalsCytokinesFemaleInflammationInflammation MediatorsInterleukin-1MiceMice, Inbred C57BLMice, KnockoutNeutrophil InfiltrationPneumonia, BacterialPseudomonas aeruginosaPseudomonas InfectionsReceptors, Interleukin-1 Type ICytokinesIL1R1 protein, mouseInflammation MediatorsInterleukin-1Receptors, Interleukin-1 Type IacidosisinflammationPseudomonas aeruginosa

Identifiers

PMID28982735
PMCPMC5866503
OpenAlexW2763372634

What OpenQuestion holds

Textmetadata
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.