Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “inflammatory response”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1979

Action of gold salts on the inflammatory response and inflammatory cell function.

Information relating to the effect and mechanism of action of gold salts on acute and chronic inflammatory processes has been reviewed. Gold salts are effective in suppressing various aspects of the acute inflammatory process although large gaps exist in the knowledge of the mechanisms involved. Available evidence indicates that gold salts affect many biochemical pathways and that interaction with enzymes plays a major role in their pharmacology. Because they are more difficult to investigate, the action of gold salts on various important aspects of chronic inflammation have not yet received much attention.

Animals↗
PubMed1978

[Variation of the inflammatory response of an autologus implant function and viability: mixed and unilateral inflammatory response].

The behaviour of an autologous grafted implant depends upon its viability. In our study, pericardial implants were used as cardiac valves. Results showed that when using fresh live pericardium, an inflammatory response developed destroying it within 8 days. When implants cells were killed without alteration of their antigenicity--in order to prevent rejection--cellular growth and neovascularisation from implantation site occurred leading to a secondary live graft. Controlled killing of the implant seems to be an essential step in order to get live grafts.

Animals↗
PubMed2026

The Differential Effects of Immunosuppressants on Hepatitis E Virus Replication and the Triggered Inflammatory Responses in Macrophages.

Organ transplant recipients are at high risk of developing chronic infection when exposed to hepatitis E virus (HEV), which can rapidly progress to liver fibrosis and cirrhosis. Macrophages play a key role in the response to the infection and disease progression. However, the interactions amongst immunosuppressants, macrophages, the course of HEV infection and activation of inflammatory response remain unclear. In this study, we generated M0, M1 and M2 macrophages from the human THP-1 cell line. These macrophages were then infected with HEV and treated with different immunosuppressants. We visualised viral infection using laser confocal microscopy, and quantitatively analysed viral replication and inflammatory responses by bulk sequencing, RT-qPCR, ELISA and Western blotting. We found that the M1 inflammatory macrophages exhibited the highest, while M2 macrophages had the lowest levels of viral RNA. Genome-wide transcriptome analysis indicated that viral, inflammation and immunity-related pathways were predominantly upregulated by HEV infection. Dexamethasone exerted potent inhibitory effects on inflammatory response in macrophages. Mycophenolic acid (MPA) demonstrated inhibitory effects on viral replication, IL-1β and TNF-α expression, whereas mTOR inhibitors had the opposite effects, and tacrolimus showed no clear effect. In conclusion, immunosuppressants can differentially affect HEV replication and the subsequent inflammatory responses in macrophages.

Humans↗
PubMed2025

Systematic acupuncture explains acupuncture at Baihui (GV20) and Fengchi (GB20) targeting the inflammatory response to regulate migraine.

OBJECTIVE: To take Baihui (GV20) and Fengchi (GB20) targeting inflammatory response to regulate migraine as an example to describe a new method for studying the mechanism of stimulating acupoints. METHODS: The target information of Baihui (GV20) and Fengchi (GB20) was retrieved, and after intersection with migraine, Kyoto Encyclopedia of Genes and Genomes (KEGG), Reactome, and UniProt Keywords were used for functional enrichment. After selecting the main pathway, rats were selected and nitroglycerin was used for modeling, and the behavioral scores, inflammatory factors, heme oxygenase 1 (HMOX1), protein kinase B (AKT1), signal transducer and activator of transcription 3 (STAT3), phosphorylated extracellular signal-regulated kinase 1/2 (P-ERK1/ERK2) and other states of the rats in the acupuncture, twisting, and electroacupuncture groups were compared. RESULTS: A total of 135 Baihui (GV20) targets and 27 Fengchi (GB20) targets were collected. A total of 73 target information were obtained after the intersection of these targets in migraine. These 73 targets have three main pathways: hypoxia-inducible factor 1 (HIF-1) signaling pathway, signaling by interleukins and inflammatory response. The main targets in the pathway were verified and found that interleukin-1 beta (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α) and HMOX1, AKT1, STAT3, P-ERK1/ERK2 can be regulated by Baihui (GV20) and Fengchi (GB20). CONCLUSION: Baihui (GV20) and Fengchi (GB20) can regulate migraine by regulating inflammatory factors and HMOX1, AKT1, STAT3, P-ERK1/ERK2 and other changes in HIF-1 signaling pathway, Signaling by Interleukins and Inflammatory response pathways. Based on systems biology and network pharmacology, and with the model of "acupoint-target-disease", explore the research methods of systematic acupuncture and moxibustion. We believe this is a usable research direction for exploring the mechanism of acupuncture stimulation.

Acupuncture Points↗
PubMed2025

Elucidation of the immunotoxicity of PEDOT: PSS on RAW264.7 macrophages by oxidative stress, inflammatory response, and NF-κB pathway activation.

Poly(3,4-ethylenedioxythiophene): poly(styrenesulfonate) (PEDOT: PSS) nanoparticles, widely used conductive polymers, pose environmental and health risks due to their nanoscale dispersion. However, the characteristics of PEDOT: PSS in aquatic systems and the underlying mechanisms of its toxicity in animal and cell models remain poorly understood. This study aimed to investigate the toxicological effects of PEDOT: PSS nanoparticles on macrophages, with a focus on RAW 264.7 cells. After an acute exposure to PEDOT: PSS nanoparticles at different concentrations (5, 10, 20 μg/mL), we observed significant impairments in cell viability, proliferation, migration, adhesion, and phagocytosis, as well as morphological alterations. Concurrently, there was a marked upregulation of inflammatory markers, including reactive oxygen species (ROS), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1 beta (IL-1β), indicating the induction of oxidative stress and inflammation. Mechanistically, PEDOT: PSS nanoparticles activated the nuclear factor kappa B (NF-κB) signaling pathway, a key regulator of inflammatory responses, suggesting that they may mediate inflammatory responses and cell damage via activation of the NF-κB signaling pathway. These findings reveal the toxic mechanism of PEDOT: PSS nanoparticles in macrophages and provide new insights into their biological safety implications.

Animals↗
PubMed1977

Comparison of the effects of alclofenac, flurbiprofen, and prednisolone on acute inflammatory response in the rat.

The fluid and cellular phases of the inflammatory response were measured using a technique employing subcutaneous implantation of polyurethane foam cubes impregnated with heat-killed Mycobacterium tuberculosis. Fluribiprofen and prednisolone were equipotent and were capable of almost completely suppressing fluid and cellular responses, while alclofenac was less potent at nontoxic dose levels. Study of the patterns of cellular exudation by image analysing computer showed that alcofenac appears unique in that it produces a well-defined cell-free zone between the edge of the implanted cubes and a band of neutrophil polymorphs within the cubes.

Animals↗
PubMed2026

Phosphoproteomic analysis in a mouse model reveals ERK signaling as a key modulator of inflammatory response in nasal mucosa associated with childhood allergic rhinitis.

Childhood allergic rhinitis (AR) is a multifactorial condition arising from the interplay between genetic predisposition and environmental exposures. Although protein phosphorylation is widely recognized as a key regulator of gene expression across various physiological and pathological states, its global alterations in the nasal mucosa of pediatric patients with AR and their subsequent impact on mucosal function and inflammatory pathways remain incompletely characterized. Our study aimed to elucidate the molecular mechanisms underlying nasal mucosa dysfunction induced by pediatric AR. Our analysis revealed 3,861 proteins encompassing a total of 15,491 phosphorylation sites. Specifically, we detected 441 downregulated phosphorylation sites on 584 proteins and 531 upregulated phosphorylation sites on 722 proteins in the nasal mucosa of the AR group. Our proteomics findings suggest that the dysregulation of immune activation and metabolic regulation may contribute to AR pathophysiology. Through pathway analysis of the identified phosphorylation sites, we found Extracellular Signal-Regulated Kinase (ERK) signaling emerged as an important pathway; notably, upregulation of ERK1/2 phosphorylation was observed as a significant marker associated with AR. Importantly, targeting ERK inhibitors presents a potential therapeutic strategy for modulating key inflammatory response signaling pathways in the context of AR, although this finding is derived from preclinical mouse models and requires rigorous validation in human pediatric nasal mucosal tissues before any clinical translation can be considered. Collectively, these findings highlight that elucidating the molecular mechanisms underlying AR-induced nasal mucosal dysfunction in the mouse model may inform the novel therapeutic targets for pediatric allergy-related diseases. Overall, elucidating these mechanisms has substantial implications for developing targeted interventions aimed at mitigating inflammation associated with allergic rhinitis.

Animals↗
PubMed1976

Effect of virus infection on the inflammatory response. Depression of macrophage accumulation in influenza-infected mice.

To better define the mechanisms by which viruses depress immune function, the effect of influenza infection on the ability of macrophages to accumulate at sites of inflammation was determined. Mice were inoculated with virus, and their inflammatory response measured in vivo by counting the number of leukocytes which accumulated in the peritoneal cavity 2 days after an intraperitoneal injection of phytohemagglutinin. Mice infected with influenza had a 57% and 65% depression of total leukocyte and macrophage accumulation, respectively, as compared to the response of uninfected mice. In contrast, bacterial pneumonia did not produce a decrease in the macrophage response. This indicated that the depression was produced by the virus infection rather than being a nonspecific phenomenon accompanying any inflammatory focus in the lung. The in vitro chemotactic responsiveness of normal peritoneal macrophages incubated with infectious influenza virus was 53% of normal. These experiments suggest that influenza infection may depress a host's ability to mobilize macrophages to inflammatory sites in vivo by inhibiting their chemotactic responsiveness.

Animals↗
PubMed2026

Anti-inflammatory activity of an IL-6 missense variant against crystal-induced inflammatory response.

Interleukin-6 (IL-6) has an important modulator effect on inflammation and immunity and is involved in the progression of nephrolithiasis (kidney stone). However, whether IL-6 genetic variants affect the pathogenesis of kidney stones remains unclear. The present study conducted a combined investigation of candidate gene-driven screening and systematic screening on whole exome sequencing data from 28 patients of calcium oxalate stones, identifying a non-synonymous single nucleotide polymorphism (SNP) rs13306435 in IL-6 as a candidate research locus, which was further validated using HRM genotyping in an expanded cohort comprising 241 cases and 229 healthy subjects. Western blotting and qRT-PCR were used to assess the effects of this variant on crystal-induced inflammation, while molecular dynamics simulation was employed to analyze structural alterations in the receptor binding complex. In individuals aged ≤40 years, the A allele of rs13306435 was nominally associated with a reduced risk of stone formation, but no association was observed for the whole population. This missense variant causes an aspartate-to-glutamate substitution (D/E), inhibiting calcium oxalate monohydrate (COM)-triggered JAK2/STAT3 activation and inflammatory responses. However, it decreased the binding energy of IL-6/IL-6R/gp130 complex by increasing hydrogen bonds and salt brigdge at remote interfaces, suggesting that enhanced receptor binding does not necessarily translate to increased downstream signaling. Although this variant is not associated with general stone susceptibility, it exhibits notable anti-inflammatory activity by attenuating COM-induced JAK2/STAT3 activation and may influence the progression of stones through this pathway. These findings provide new insights into the role of anti-inflammatory mechanisms in nephrolithiasis.

Humans↗
PubMed1977

Inflammatory responses of the rabbit eye to prostaglandins.

A modified Draize scoring procedure has been used to quantify the vascular effects of prostaglandins on the rabbit eye. Topical application of 100 microgram of PGE1 caused conjunctival redness (erythema due to vasodilatation), swelling (oedema due to increased capillary permeability), discharge, lids closure (decrease in palpebral aperture) and occasionally miosis, though no corneal or iridial damage was detected up to three hours. PGE1 and GE2 produced practically identical dose-related increases in scores for most of the inflammation parameters, though oedema responses were consistently lower after PGE2. The neutral, triethanolamine salt of PGE1 was as inflammatory as PG1 itself. PGF2alpha was 10-50 times less inflammatory than PGE1. It produced relatively greater erythema responses than oedema responses, when compared to PGE1. The novel prostaglandins, 19-OH PGE1 and 19-OH PGE2, recently identified as major prostaglandin constituents of human semen, were respectively 71 and 78 times inflammatory than PGE1. The 19-OH PGEs produced much greater erythema responses, relative to oedema, lids closure or discharge responses.

Animals↗
PubMed2026

Single nucleus multiomics reveals an early inflammatory response to high-fat diet in mouse islets.

In periods of sustained hyper-nutrition, pancreatic β-cells undergo functional compensation through transcriptional upregulation of gene programs driving insulin secretion. This adaptation is essential for maintaining systemic glucose homeostasis and metabolic health. Using single nuclei multiomics, we have mapped the early transcriptional adaptive mechanisms in murine islets of Langerhans exposed to high-fat diet (HFD) for 1 and 3 wk. We show that β-cells exhibit the largest transcriptional response to HFD, characterized by early activation of pro-inflammatory eRegulons and down-regulation of β-cell identity genes, particularly in a distinct subset of β-cells. These observations extend to humans, where the prevalence of an β-cells with a high inflammatory signature is increased in diabetes. Collectively, these observations point to cellular crosstalk through pro-inflammatory signaling as a central and early driver of β-cell dysfunction that limits the compensatory capacity of β-cells, which is closely linked to the development of diabetes.

Animals↗
PubMed1977

The role of cell-mediated immunity in the induction of inflammatory responses. Parke-Davis Award Lecture, 1977.

Reactions of cell-mediated immunity fall into two broad categories: those that involve direct participation of intact lymphocytes in the effector mechanism of the reaction and those that involve mediation by soluble lymphocyte-derived factors known as lymphokines. The first kind of reaction is essentially limited to lymphocyte-dependent cytotoxicity, although certain aspects of T cell-B cell cooperation may fall into this category as well. The second category appears to comprise the bulk of the so-called cell-mediated immune response and provides a link between this system and the inflammatory system. Various lymphokines have been shown to exert profound influence upon inflammatory cell metabolism, cell surface properties, patterns of cell migration, and the activation of cells for various biologic activities involved in host defense. Although substantial information is now available about various physicochemical as well as biologic properties of lymphokines, purification and characterization data are as yet too incomplete to allow us to ascribe all of these activities to discrete mediator molecules. Current work involving the development of antibody-based techniques for mediator assay may shed light on this issue. Information on the kinds of cells capable of lymphokine production is now available. Contrary to prior expectation, T cells are not unique in their capacity for lymphokine production. Under appropriate circumstances, B cells and even nonlymphoid cells can do so as well. The unique property of lymphocytes in this regard appears to relate to their ability to respond to certain specialized signals such as specific antigen or an appropriate mitogen. Mediator production per se may represent a general biologic phenomenon. Although lymphokines have been defined mainly in terms of in vitro assays, early speculations about their in vivo importance are proving correct. Evidence for the role of lymphokines comes from studies involving detection of lymphokines in tissues, studies involving injection of exogenous lymphokines, and studies involving suppression of in vivo reactions by various techniques. The use of antilymphokine antibodies has proven useful in the latter kinds of experiments. Work in many laboratories is beginning to relate these findings to clinically relevant situations. A major unsolved problem relates to the regulation and control of lymphokine production and activity. At present only a limited body of information is available on this point. This is a potentially fruitful area for future investigation since it may provide techniques for manipulating the immune system in ways that are clinically useful.

Animals↗
PubMed2026

Pre-transport dietary chitosan improves the physiological robustness of juvenile largemouth bass (Micropterus salmoides) by modulating antioxidant and inflammatory responses.

The acute stress caused by long-distance transport can lead to oxidative damage, immune dysfunction, and health deterioration in fish. This study evaluated dietary chitosan as a pre-transport nutritional strategy for juvenile largemouth bass (Micropterus salmoides). Five experimental diets contained chitosan at 0, 2.5, 5.0, 7.5, or 10.0 g/kg, designated as p0, p25, p50, p75, and p100, respectively, for 56 d. The effects of dietary chitosan were evaluated using growth performance, feed utilization, digestive function, antioxidant capacity, nonspecific immunity, and resistance to Aeromonas hydrophila infection. Then, fish from the p0 and p50 groups underwent a 12-h transport stress test, with samples collected before, during, and 7 d after transport. Dietary chitosan improved most of these parameters. Among the treatment groups, p50 and p75 showed the best overall performance. The dose-response analysis further indicated that the appropriate dietary inclusion range was 5.0-7.5 g/kg. Under transport stress, fish in the p50 group exhibited more stable antioxidant enzyme responses and lower lipid peroxidation, as indicated by reduced MDA levels. Consistent with these enzyme responses, antioxidant-related genes remained relatively stable. At the same time, expression patterns related to the Nrf2-Keap1 and NF-κB signaling pathways suggested that 5.0 g/kg chitosan alleviated transport-induced oxidative damage and inflammation. Dietary chitosan also attenuated pro-inflammatory gene induction and altered the temporal expression patterns of anti-inflammatory genes. Overall, 5.0-7.5 g/kg dietary chitosan is suitable for juvenile largemouth bass, and 5.0 g/kg may serve as an effective pre-transport dietary inclusion level.

Animals↗
PubMed2026

Qingfei Dayuan granules alleviate the inflammatory response in lipopolysaccharide-induced acute lung injury mice by inhibiting the Nf-κB signaling pathway and regulating the complement pathway.

OBJECTIVES: The study aimed to explore the effects and mechanisms by which Qingfei Dayuan granules (QFDY) mitigate pulmonary inflammation in lipopolysaccharide (LPS)-induced acute lung injury (ALI). METHODS: We established an ALI mouse model by intraperitoneal injection of LPS. HE, Transmission electron microscopy, ELISA assay of inflammatory cytokines, and immunohistochemistry (IHC) were used to assess the degree of lung injury and inflammation. Utilizing network analysis and proteomics analysis, the potential targets and pathways of QFDY were identified. Western blot, IHC, and qRT-PCR analysis were used to evaluate the potential mechanism of QFDY. Additionally, the chemical composition of QFDY were performed using UPLC-MS/MS. KEY FINDINGS: QFDY reduced the pathologic changes and inflammatory cell infiltration in lung tissue inflammation. Network and proteomic analysis showed that the mechanism of QFDY protection against ALI is closely related to the Nuclear factor-kappa B (NF-κB) signaling pathway and complement pathway. Animal experiments showed that Qingfei Dayuan granules (QFDY) significantly reduced the levels of IL-1β, IL-6, TNF-α, and lung tissue F4/80-positive alveolar macrophages. Additionally, western blot and qRT-PCR analyses showed the inhibition of the NF-κB pathway. Notably, the levels of mannose-binding lectin (MBL2) were significantly increased, while complement C3a and complement C5a proteins were reduced in the QFDY group compared to the LPS group. CONCLUSIONS: QFDY suppressed the inflammation in LPS-induced ALI by inhibiting the NF-κB and complement pathway.

Animals↗
PubMed1978

Influence of hydrocortisone on the modulation of the inflammatory response.

In vitro hydrocortisone, in pharmacologically attainable concentrations, binds nonspecifically to rat peritoneal mast cells and amplifies the stimulating effects of PGE1 on membrane-bound adenylate cyclase. As a consequence, the intracellular concentration of cyclic AMP in the target cells increases and histamine release is markedly reduced. Deoxycorticosterone, at the same concentrations, has no effect. These findings may in part explain the mechanism of action of anti-inflammatory steroids, possibly related to the modulating effects of E-type prostaglandins.

Animals↗
PubMed1975

Slow encephalopathies, inflammatory responses and arachis oil.

There is much interest in the possibility that diets rich in some plant oils may be of prophylactic and curative value in certain clinical conditions. This is generally attributed to the immunosuppressive effects of polyunsaturated fatty acids. Arachis (peanut) oil injections can increase the incubation period of experimental scrapie in mice. In the late 1950s several workers showed that arachis and some other oils contained very potent anti-inflammatory components quite apart from the polyunsaturated fatty acids. This suggests that the supposed efficacy of these acids in some clinical situations could be due to trace substances rather than the lipid itself and that the apparent ability of scrapie agents to use the host's lymphoreticular system as a Trojan horse may involve elements of the inflammatory system rather than the B/T cell immune system.

Animals↗