INFLAMMATION RESEARCH (IR) 发表有关炎症和相关领域各个方面的同行评审论文，包括组织病理学、免疫学机制、基因表达、介质、实验模型、临床研究和药物效果。相关领域定义广泛，包括例如过敏和哮喘、休克、疼痛、关节损伤、皮肤病以及相关药物的临床试验。

The journal "Agents and Actions" publishes peer-reviewed papers on various aspects of inflammation and related fields, including histopathology, immunological mechanisms, gene expression, mediators, experimental models, clinical research, and drug effects. The definition of related fields is broad, encompassing areas such as allergies and asthma, shock, pain, joint injuries, skin diseases, and clinical trials of related drugs.

《Agents and Actions》期刊发表关于炎症及相关领域的同行评审论文，涵盖组织病理学、免疫学机制、基因表达、介质、实验模型、临床研究和药物效果等多个方面。相关领域的定义广泛，包括过敏和哮喘、休克、疼痛、关节损伤、皮肤病以及相关药物的临床试验。

Agents and Actions

Neuroinflammation in the peripheral nervous system has been linked to cancer metastasis-induced bone pain. The stimulator of interferon genes (STING), an innate immune sensor for cytosolic DNA, plays an important role in inflammation and cancer metastasis and is reported to be a critical regulator of nociception. Here, we examined the role of STING in primary nociceptive neurons and chronic pain to determine if it could be a new target for treating bone cancer pain (BCP).Walker 256 cancer cells were injected intratibially to induce bone cancer pain in rats. STING and its downstream inflammatory factors in dorsal root ganglia (DRG) were detected using western blotting and immunofluorescent staining. Transmission electron microscopy and the BCL2-associated X (Bax) expression were used to detect the mitochondrial stress in DRG neurons. C-176, a specific inhibitor of STING, was used to block STING activation and to test the pain behavior.Mechanical hyperalgesia and spontaneous pain were observed in BCP rats, accompanied by the upregulation of the STING expression in the ipsilateral L4-5 DRG neurons which showed significant mitochondrion stress. The STING/TANK-binding kinase 1 (TBK1)/nuclear factor-kappa B (NF-κB) pathway activation was observed in the DRGs of BCP rats as well as increased IL-1β, IL-6, and TNF-α expression. C-176 alleviated bone cancer pain and reduced the STING and its downstream inflammatory pathway.We provide evidence that STING pathway activation leads to neuroinflammation and peripheral sensitization. Pharmacological blockade of STING may be a promising novel strategy for preventing BCP.

Yuxin Zhang

Wei Wang

Zhihao Gong

Yuan Peng

Xin Li

Zuojing Zhang

Xiaoxuan Zhang

Xingji You

Jingxiang Wu

Inflammation Research

Inflamm. Res.

Activation of the STING pathway induces peripheral sensitization via neuroinflammation in a rat model of bone cancer pain

STING通路的激活通过神经炎症在大鼠骨癌痛模型中诱导外周致敏

The purpose of the present study was to evaluate the potential therapeutic effects of NZ on lipopolysaccharide (LPS)-induced RAW264.7 cells and explore its underlying mechanisms.

Pengjun Xiang

Tong Chen

Yi Mou

Hui Wu

Peng Xie

Guo Lu

Xiaojian Gong

Qinghua Hu

Yihua Zhang

Hui Ji

Inflammation research : official journal of the European Histamine Research Society ... [et al.]

Inflamm Res

NZ suppresses TLR4/NF-κB signalings and NLRP3 inflammasome activation in LPS-induced RAW264.7 macrophages.

NZ抑制LPS诱导的RAW264.7巨噬细胞中TLR4/NF-κB信号通路和NLRP3炎症小体激活。

Abstract Objective and design This observational study investigated the regulatory mechanism of Pim-1 in inflammatory signaling pathways. Materials THP-1, RAW 264.7, BV2, and Jurkat human T cell lines were used. Treatment None. Methods Lipopolysaccharide (LPS) was used to induce inflammation, followed by PIM1 knockdown. Western blot, immunoprecipitation, immunofluorescence, and RT-PCR assays were used to assess the effect of PIM1 knockdown on LPS-induced inflammation. Results PIM1 knockdown in macrophage-like THP-1 cells suppressed LPS-induced upregulation of pro-inflammatory cytokines, inducible nitric oxide synthase, cyclooxygenase-2, phosphorylated Janus kinase, signal transducer and activator of transcription 3, extracellular signal-regulated kinase, c-Jun N-terminal kinase, p38, and nuclear factor kappa B p65 (NF-κB p65). It also suppressed upregulation of inhibitor of NF-κB kinase α/β and enhanced the nuclear translocation of NF-κB p65. Moreover, it inhibited the upregulation of Nod-like receptor family pyrin domain-containing 3 (NLRP3) and cleavage of caspase-1 induced by co-treatment of LPS with adenosine triphosphate. Additionally, p-transforming growth factor-β-activated kinase 1 (TAK1) interacted with Pim-1. All three members of Pim kinases (Pim-1, Pim-2, and Pim-3) were required for LPS-mediated inflammation in macrophages; however, unlike Pim-1 and Pim-3, Pim-2 functioned as a negative regulator of T cell activity. Conclusions Pim-1 interacts with TAK1 in LPS-induced inflammatory responses and is involved in MAPK/NF-κB/NLRP3 signaling pathways. Additionally, considering the negative regulatory role of Pim-2 in T cells, further in-depth studies on their respective functions are needed.

Hye Suk Baek

Nacksung Kim

Jong Wook Park

Taeg Kyu Kwon

Shin Kim

The role of Pim-1 kinases in inflammatory signaling pathways

Pim-1激酶在炎症信号通路中的作用

Sepsis-induced acute lung injury (ALI) is a complex and life-threatening condition lacking specific and efficient clinical treatments. Extracellular histones, identified as a novel type of damage-associated molecular patterns, have been implicated in the inflammatory process of ALI. However, further elucidation is needed regarding the precise mechanism through which extracellular histones induce inflammation. The aim of this study was to investigate whether extracellular histones can activate NLRP3 inflammasome-mediated inflammation in alveolar macrophages (AMs) by affecting TWIK2-dependent potassium efflux.

Jing Yu

Yu Fu

Nan Zhang

Jiameng Gao

Zhiyuan Zhang

Xuemei Jiang

Chang Chen

Zongmei Wen

Extracellular histones promote TWIK2-dependent potassium efflux and associated NLRP3 activation in alveolar macrophages during sepsis-induced lung injury.

在脓毒症诱导的肺损伤中，胞外组蛋白通过TWIK2依赖的钾外排促进肺泡巨噬细胞NLRP3的激活。

Delta neutrophil index (DNI) representing the number of immature granulocytes is an emerging marker used in diagnosis of infections and prediction of mortality in infected patients. The present study evaluated the diagnostic accuracy of DNI as a predictive and prognostic factor in infected patients.

Jae Hyon Park

Hyeong Ju Byeon

Keum Hwa Lee

Jong Wook Lee

Andreas Kronbichler

Michael Eisenhut

Jae Il Shin

Delta neutrophil index (DNI) as a novel diagnostic and prognostic marker of infection: a systematic review and meta-analysis.

Delta中性粒细胞指数（DNI）作为感染的新型诊断和预后标志物：一项系统评价和Meta分析。

This article is aims to provide an overview of studies reported in the literature to investigate the etiological role of IL-1/IL-1ra in various disease conditions and the different drug delivery systems developed to achieve IL-1ra as a possible therapeutic option.

Anand Ubhe

IL-1 receptor antagonist: etiological and drug delivery systems overview

IL-1受体拮抗剂：病因学与药物递送系统概述

G proteins are a class of important signal transducers in mammalians. G proteins can corpoarated with G proteincoupled receptors (GPCRs) and transmit signals from extracellular stimuli into intracellular response, which will regulate a series of biological functions. G-proteins are heterotrimeric proteins composed of Gα, Gβ, and Gγ subunits. Based on structural and functional similarity of their α-subunits, G proteins are typically grouped into four classes (Gi, Gs, Gq/11, and G12/13). The Gq/11 subfamily consists of Gq, G11, G14, and G15/16 proteins. Gαq is the α-subunit of Gq protein and encoded by GNAQ. Our previous studies revealed that Gαq play an important role in regulating T cell survival and T cell differentiation. Inflammasomes are multiprotein complexes that play a critical role in modulating innate inflammatory response. NLRP3 inflammasome is currently the most extensively studied inflammasome.

Ruixue Kong

Lijun Peng

Honggang Bao

Lulu Sun

Yan Feng

Hua Li

Dashan Wang

The role of Gαq in regulating NLRP3 inflammasome activation

Gαq在调节NLRP3炎症小体激活中的作用

Lidiane Isabel Filippin

María José Cuevas

Elena Lima

Norma Possa Marroni

Javier Gonzalez Gallego

Ricardo Machado Xavier

Retraction Note: The role of nitric oxide during healing of trauma to the skeletal muscle

撤稿说明：一氧化氮在骨骼肌创伤愈合中的作用

Vascularization after rib fracture is a crucial physiological process that is essential for the repair and healing of the rib. Studies have shown that CD90 plays a critical role in regulating rib fracture healing, but the underlying mechanism of its role has not been fully elucidated.

Lei Wang

Rui Hu

Pei Xu

Pengkai Gao

Bin Mo

Liya Dong

Fengqing Hu

CD90’s role in vascularization and healing of rib fractures: insights from Dll4/notch regulation

CD90在肋骨骨折血管化和愈合中的作用：来自Dll4/notch调控的见解

Abstract Introduction Pentoxifylline (PTX) affects most blood components and the blood vessels, potentially modulating various conditions. Due to its impact on markers linked to COVID-19 severity, research has explored PTX for acute COVID-19. Following the widespread administration of COVID-19 vaccinations, there has been a notable and consistently growing increase in research focusing on long COVID. Consequently, our examination of relevant acute COVID-19 data shall additionally be contextualized into long COVID research. Methods Various Databases were searched until July 2024 for all primary clinical studies on Pentoxifylline (PTX) in COVID-19. Results Studies were on acute infection with SARS-CoV-2 where PTX was an adjuvant to standard therapy for ethical and practical reasons under the circumstance. PTX generally reduced hospitalization duration and improved some inflammatory markers, but its impact on mortality was inconsistent. Adverse events were minimal. Meta-analysis revealed a significant reduction in hospitalization duration. Conclusion This systematic review and meta-analysis suggest that adding pentoxifylline (PTX) to standard COVID-19 therapy may significantly reduce hospitalization duration and improve some inflammatory markers. However, its impact on mortality rates is inconclusive. Adverse events are minimal. PTX can be favorable as an add-on in managing acute COVID-19 and could reduce the risk of long COVID, as well as assist in managing many of its most common symptoms.

短名	Inflamm. Res.
Journal Impact	4.75
国际分区	IMMUNOLOGY(Q2)
期刊索引	SCI Q2中科院 3 区

ISSN	0065-4299, 1023-3830, 1420-908X
h-index	107
国内分区	医学(3区)医学细胞生物学(3区)医学免疫学(3区)

出版信息	出版商: Birkhauser Verlag Basel，出版周期: ，期刊类型: journal，开源期刊: 否
基本数据	创刊年份: 1969，原创研究文献占比: ，自引率:， Gold OA占比:

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