Evidence map›Paper›PMID 19413900›Full record

ArticleRespiratory research2009

Macrophage CD74 contributes to MIF-induced pulmonary inflammation.

Koichiro Takahashi, Kiyokazu Koga, Helena M Linge, Yinzhong Zhang, Xinchun Lin, Christine N Metz, Yousef Al-Abed, Kaie Ojamaa, Edmund J Miller

Open access · goldAbstract read
In one paragraph

Article in Respiratory research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

69 citing papers in PubMed, 128 citations in OpenAlex.

  1. Article
  2. Single-cell transcriptomic analysis identifies a MIF-driven keratinocyte-macrophage-Th2 axis as a key inflammatory circuit in atopic dermatitis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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  9. In vivo synergistic enhancement of MIF-mediated inflammation in acute lung injury by the plant ortholog Arabidopsis MDL1.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
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  11. Crosstalk between CD64EMBO molecular medicine · 2024
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  20. Olfactory receptors contribute to progression of kidney fibrosis.NPJ systems biology and applications · 2022
    Article

9 more citing papers are in PubMed but not listed here.

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

9 authors at 1 institution in 1 country.

Koichiro TakahashiCenter for Heart and Lung Research, The Feinstein Institute for Medical Research, Manhasset, New York, USA. ktakahas.nshs@gmail.com
Kiyokazu Koga
Helena M Linge
Yinzhong Zhang
Xinchun Lin
Christine N Metz
Yousef Al-Abed
Kaie Ojamaa
Edmund J Miller
Feinstein Institute for Medical Research · US

Funding

The Lung as a Source of Inflammation in SepsisR01HL081655 · NHLBI · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI MILLER, EDMUND J · 2006 to 2009
$1.6M
NHLBI NIH HHS R01 HL 081655NHLBI NIH HHS R01 HL081655
6 · The paper itself

Abstract

backgroundMIF is a critical mediator of the host defense, and is involved in both acute and chronic responses in the lung. Neutralization of MIF reduces neutrophil accumulation into the lung in animal models. We hypothesized that MIF, in the alveolar space, promotes neutrophil accumulation via activation of the CD74 receptor on macrophages.

methodsTo determine whether macrophage CD74 surface expression contributes MIF-induced neutrophil accumulation, we instilled recombinant MIF (r-MIF) into the trachea of mice in the presence or absence of anti-CD74 antibody or the MIF specific inhibitor, ISO-1. Using macrophage culture, we examined the downstream pathways of MIF-induced activation that lead to neutrophil accumulation.

resultsIntratracheal instillation of r-MIF increased the number of neutrophils as well as the concentration of macrophage inflammatory protein 2 (MIP-2) and keratinocyte-derived chemokine (KC) in BAL fluids. CD74 was found to be expressed on the surface of alveolar macrophages, and MIF-induced MIP-2 accumulation was dependent on p44/p42 MAPK in macrophages. Anti-CD74 antibody inhibited MIF-induced p44/p42 MAPK phosphorylation and MIP-2 release by macrophages. Furthermore, we show that anti-CD74 antibody inhibits MIF-induced alveolar accumulation of MIP-2 (control IgG vs. CD74 Ab; 477.1 +/- 136.7 vs. 242.2 +/- 102.2 pg/ml, p < 0.05), KC (1796.2 +/- 436.1 vs. 1138.2 +/- 310.2 pg/ml, p < 0.05) and neutrophils (total number of neutrophils, 3.33 +/- 0.93 x 104 vs. 1.90 +/- 0.61 x 104, p < 0.05) in our mouse model.

conclusionMIF-induced neutrophil accumulation in the alveolar space results from interaction with CD74 expressed on the surface of alveolar macrophage cells. This interaction induces p44/p42 MAPK activation and chemokine release. The data suggest that MIF and its receptor, CD74, may be useful targets to reduce neutrophilic lung inflammation, and acute lung injury.

Indexed as

Disease Models, AnimalIntramolecular OxidoreductasesMacrophage Migration-Inhibitory FactorsAnimalsAntigens, Differentiation, B-LymphocyteHistocompatibility Antigens Class IIHumansMacrophagesMaleMiceMice, Inbred C57BLPneumoniaAntigens, Differentiation, B-LymphocyteHistocompatibility Antigens Class IIIntramolecular Oxidoreductasesinvariant chainMacrophage Migration-Inhibitory FactorsMif protein, mouse

Identifiers

PMID19413900
PMCPMC2681459
OpenAlexW2115488718

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.