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2024 Fiscal Year Final Research Report

Nursing care approach via group3 innate lymphoid cells to orchestrate pressure-related wounds with deep tissue injury repair.

Research Project

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Project/Area Number 20K10654
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Review Section Basic Section 58050:Fundamental of nursing-related
Research InstitutionYamagata University

Principal Investigator

Matsuda Yumi  山形大学, 医学部, 教授 (90444926)

Co-Investigator(Kenkyū-buntansha) 石田 陽子  山形大学, 医学部, 准教授 (60322335)
菅野 恵美  東北大学, 医学系研究科, 教授 (10431595)
三浦 奈都子 (小山奈都子)  岩手県立大学, 看護学部, 教授 (40347191)
Project Period (FY) 2020-04-01 – 2025-03-31
Keywords褥瘡 / 創傷治癒 / DTPI / ILC3 / 腸管粘膜上皮細胞 / 細胞間結合蛋白 / occludin / claudin2
Outline of Final Research Achievements

This study aimed to elucidate the mechanism of deep tissue pressure injury (DTPI) and to explore nursing interventions for early regulation of inflammatory responses.
We examined the localization of RORγt-positive cells, a marker of type 3 innate lymphoid cells (ILC3s), in the skin and intestinal tract of mice with pressure-induced wounds. While ILC3s were not observed at the wound center, their number in the intestine increased immediately after injury and decreased by day 3.Occludin, a tight junction protein supporting barrier integrity, showed a time-dependent increase, while claudin-2, involved in nutrient absorption, remained stable.
These findings indicate that skin wound healing may affect intestinal function, providing a basis for developing nursing interventions that modulate the healing process.

Free Research Field

基礎看護分野

Academic Significance and Societal Importance of the Research Achievements

本研究はILC3マーカーのRORγt陽性細胞の皮膚と腸管の局在と相関をみた。圧迫創中心部のILC3局在性は明確にできなかったが、皮膚の受傷は腸管の粘膜上皮細胞の結合を示す結合蛋白への影響を与えていた。特に、創傷の真皮や結合組織の修復時期以降にclaudin2が増加しており、腸管の形態・機能は創の治癒過程に必要なエネルギー吸収路が確保される可能性を明らかにした。さらに腸管粘膜上皮のILC3の免疫細胞数も増減したため、保護するケアとして創傷治癒等に必要な栄養吸収や、免疫力を上げる方策の開拓につながると言える。以上は、看護ケア上の根拠ともなり得る成果であり、学術的にも社会的にも意義があると考える。

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Published: 2026-01-16  

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