Evidence map›Paper›PMID 42332095›Full record

ArticleCellular & molecular immunology2026

Fibroblast-derived CCL2 orchestrates immune responses and defends against Staphylococcus aureus skin infection.

Tatsuya Dokoshi, Marta Palomo-Irigoyen, Kazuki Dai, Terumi Hashimoto, Hiroaki Konishi, Lauriane Hivert, Michelle Bagood, Hung Chan, Samia Almoughrabie, Yoshiyuki Nakamura and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular & molecular immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. 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

14 authors.

Tatsuya DokoshiDepartment of Dermatology, University of California, La Jolla, CA, USA. ta1983@asahikawa-med.ac.jp.
Marta Palomo-IrigoyenDepartment of Dermatology, University of California, La Jolla, CA, USA.
Kazuki DaiDepartment of Internal Medicine, Division of Gastroenterology, Asahikawa Medical University, Asahikawa, Japan.
Terumi HashimotoDepartment of Internal Medicine, Division of Gastroenterology, Asahikawa Medical University, Asahikawa, Japan.
Hiroaki KonishiDepartment of Internal Medicine, Division of Gastroenterology, Asahikawa Medical University, Asahikawa, Japan.
Lauriane HivertDepartment of Dermatology, University of California, La Jolla, CA, USA.
Michelle BagoodDepartment of Dermatology, University of California, La Jolla, CA, USA.
Hung ChanDepartment of Dermatology, University of California, La Jolla, CA, USA.
Samia AlmoughrabieDepartment of Dermatology, University of California, La Jolla, CA, USA.
Yoshiyuki NakamuraDepartment of Dermatology, University of California, La Jolla, CA, USA.
Kellen J CavagneroDepartment of Dermatology, University of California, La Jolla, CA, USA.
Teruaki NakatsujiDepartment of Dermatology, University of California, La Jolla, CA, USA.
Mikihiro FujiyaDepartment of Internal Medicine, Division of Gastroenterology, Asahikawa Medical University, Asahikawa, Japan.
Richard L GalloDepartment of Dermatology, University of California, La Jolla, CA, USA.ORCID 0000-0002-1401-7861

Funding

Inflammatory cross-talk between skin and gutR01DK128787 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GALLO, RICHARD L, SALZMAN, NITA H · 2021 to 2024
$2.6M
NIDDK NIH HHS R01 DK128787U.S. Department of Health & Human Services | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (National Institute of Diabetes & Digestive & Kidney Diseases) R01DK128787
6 · The paper itself

Abstract

Host defense against invasive bacterial infections of the skin is essential for survival. It involves a complex yet incompletely understood process of microbial recognition followed by innate and adaptive systems for communication between resident and recruited cells to mount an effective defense. Stromal fibroblasts have not been classically considered immunocytes but are gaining recognition for their critical role in inflammation. Here, we identify fibroblast-derived C-C motif chemokine ligand 2 (CCL2) as a key mediator of host defense against invasive Staphylococcus aureus infection. Single-cell RNA sequencing revealed that fibroblasts are a predominant source of CCL2 under steady-state conditions in both human and mouse skin. The use of mice with a conditional deletion of CCL2 in fibroblasts demonstrated that the expression of CCL2 by fibroblasts alters macrophage cytokine production and antigen-presentation-associated responses and is important for monocyte recruitment. Additionally, we revealed a novel role for fibroblast-derived CCL2 in promoting fibroblast-to-adipocyte differentiation via ERK and p38 signaling, leading to reactive adipogenesis and enhanced production of the antimicrobial peptide cathelicidin. In mice with targeted deletion of Ccl2 in fibroblasts, these host immune responses are impaired, and S. aureus infection of the skin is greatly increased. These findings highlight fibroblast-derived CCL2 as a critical regulator of immunity and suggest its broader implications in inflammatory and infectious diseases.

Indexed as

Chemokine CCL2FibroblastsSkinStaphylococcal InfectionsStaphylococcal Skin InfectionsStaphylococcus aureusAdipocytesAnimalsCell DifferentiationHumansMacrophagesMiceMice, Inbred C57BLMice, KnockoutCcl2 protein, mouseChemokine CCL2CCL2FibroblastSkin infectionSpatial transcriptomicsStaphylococcus aureus

Identifiers

PMID42332095
PMCPMC13424308

What Socratic 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 Socratic graph.