Редактирование: IL1B (раздел)

==Publications==

{{medline-entry
|title=[[IL1B]] triggers inflammatory cytokine production in bovine oviduct epithelial cells and induces neutrophil accumulation via [[CCL2]].
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33099841
|abstract=The oviduct is essential for reproduction. We previously showed that oviduct epithelial cells (OECs) isolated from aged cows expressed higher levels of inflammatory cytokines, including interleukin (IL) 1A and [[IL1B]]. In addition, aging is associated with tissue dysfunction and cellular senescence via a senescence-associated secretory phenotype (SASP) and immune cell accumulation. We investigated whether [[IL1A]] or [[IL1B]] causes SASP production, cellular senescence, and inflammatory responses in bovine OECs. The OECs were isolated from bovine oviducts from young (mean 50.3 months) and aged cows (mean 157.0 months) and cultured. Treatment with [[IL1A]] or [[IL1B]] induced SASP production (IL8, [[IL6]], TNFA, and [[CCL2]]) and mRNA expression of cell adhesion molecules in bovine OECs, but both IL1s did not induce cellular senescence in OECs and migration of polymorphonuclear neutrophils (PMNs). Cultured medium of OECs treated with IL1s, especially [[IL1B]], dramatically induced PMN migration. Treatment with the [[CCL2]] inhibitor, but not IL8 or its receptor [[CXCR2]] inhibitors, significantly reduced immune cell migration in [[IL1B]]-treated OEC-cultured medium. Treatment with [[IL1B]] increased PMN adhesion to OECs, resulting in further SASP production in OECs due to a PMN-OEC interaction. We suggest that senescence-associated IL1s cause SASP production in bovine OECs and [[CCL2]] induced by [[IL1B]] is essential for the migration of immune cells to OECs. Specifically, [[IL1B]] regulates PMN migration and adhesion to bovine OECs, and PMNs accelerate inflammatory cytokine production from bovine OECs via a direct interaction. These phenomena may contribute to chronic oviductal inflammation, resulting in subfertility.

|keywords=* CCL2
* cellular senescence
* inflammaging
* senescence-associated secretory phenotype
|full-text-url=https://sci-hub.do/10.1111/aji.13365
}}
{{medline-entry
|title=A Small Molecule Stabilizer of the [[MYC]] G4-Quadruplex Induces Endoplasmic Reticulum Stress, Senescence and Pyroptosis in Multiple Myeloma.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33066043
|abstract=New approaches to target [[MYC]] include the stabilization of a guanine-rich, G-quadruplex (G4) tertiary DNA structure in the NHE III region of its promoter. Recent screening of a small molecule microarray platform identified a benzofuran, D089, that can stabilize the [[MYC]] G4 and inhibit its transcription. D089 induced both dose- and time-dependent multiple myeloma cell death mediated by endoplasmic reticulum induced stress. Unexpectedly, we uncovered two mechanisms of cell death: cellular senescence, as evidenced by increased levels of p16, p21 and γ-[[H2AX]] proteins and a caspase 3-independent mechanism consistent with pyroptosis. Cells treated with D089 exhibited high levels of the cleaved form of initiator caspase 8; but failed to show cleavage of executioner caspase 3, a classical apoptotic marker. Cotreatment with the a pan-caspase inhibitor Q-VD-OPh did not affect the cytotoxic effect of D089. In contrast, cleaved caspase 1, an inflammatory caspase downstream of caspases 8/9, was increased by D089 treatment. Cells treated with D089 in addition to either a caspase 1 inhibitor or siRNA-caspase 1 showed increased IC  values, indicating a contribution of cleaved caspase 1 to cell death. Downstream effects of caspase 1 activation after drug treatment included increases in [[IL1B]], gasdermin D cleavage, and [[HMGB1]] translocation from the nucleus to the cytoplasm. Drug treated cells underwent a 'ballooning' morphology characteristic of pyroptosis, rather than 'blebbing' typically associated with apoptosis. ASC specks colocalized with [[NLRP3]] in proximity ligation assays after drug treatment, indicating inflammasome activation and further confirming pyroptosis as a contributor to cell death. Thus, the small molecule [[MYC]] G4 stabilizer, D089, provides a new tool compound for studying pyroptosis. These studies suggest that inducing both tumor senescence and pyroptosis may have therapeutic potential for cancer treatment.

|keywords=* ASC and pannexin 1
* MYC G4-quadruplex stabilizer
* NLRP3
* caspase 1
* endoplasmic reticulum stress
* gasdermin D
* inflammasome
* pyroptosis
* senescence
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7650714
}}
{{medline-entry
|title=p53 and p53-related mediators PAI-1 and IGFBP-3 are downregulated in peripheral blood mononuclear cells of HIV-patients exposed to non-nucleoside reverse transcriptase inhibitors.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32272174
|abstract=The improved effectiveness and safety of the combined antiretroviral therapy (cART) has largely diminished mortality and AIDS-defining morbidity of HIV-patients. Nevertheless, chronic age-related diseases in these individuals are more common and their underlying pathogenic mechanisms of these actions seem to involve accelerated aging and enhanced inflammation. The present study explores markers of these processes in a heterogenous Spanish HIV cohort using peripheral blood samples of HIV-patients and matched uninfected controls. We isolated periheral blood mononuclear cells (PBMCs) and i) compared the expression of a panel of 14 genes related to inflammation and senescence in PBMCs of HIV-patients vs matched uninfected controls, ii) analyzed the expression in HIV-patients in association with a number of demographic, biochemical and immunological parameters and iii) in relation with the current cART they received. PBMCs of HIV-patients displayed significantly increased expression of general inflammatory genes ([[IL6]], [[IL18]] and [[CXCL10]]) and this occurs irrespectively of the antiviral therapy they have been receiving. Conversely, levels of senescence-associated genes [[TP53]], [[SERPINE1]]andIGFBP3 were slightly but significantly reduced in patients compared to uninfected matched individuals and this effect is related to NNRTI-containing treatments. The expression of the inflammatory markers [[IL6]], [[IL18]], [[IL1B]], TNFA, [[RELA]], [[CCL2]], [[[[CCL2]]0]] and [[CXCL10]] displayed correlation with certain demographic, morbidity- and HIV infection-related parameters. The levels of [[TP53]] mRNA were positively associated only with plasma LDL. Correlation analysis between the expressions of pairs of genes revealed a different pattern between HIV-patients and controls. The diminished expression of [[TP53]] and [[SERPINE1]] in HIV-patients was also observed at a protein level, and the correlation between the two proteins (p53 and PAI1) in patients and controls showed the opposite trend. In conclusion, HIV-patients show dysregulation of p53 and p53-related mediators, a phenomenon which may be of pathophysiological relevance and could be related to the shorter health- and/or life-span observed in these individuals.

|keywords=* Aging
* Antiretroviral drugs
* HIV
* Inflammation
* NNRTI
* Senescence
* p53
|full-text-url=https://sci-hub.do/10.1016/j.antiviral.2020.104784
}}
{{medline-entry
|title=Aged marrow macrophages expand platelet-biased hematopoietic stem cells via Interleukin1B.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30998506
|abstract=The bone marrow microenvironment (BMME) contributes to the regulation of hematopoietic stem cell (HSC) function, though its role in age-associated lineage skewing is poorly understood. Here we show that dysfunction of aged marrow macrophages (Mφs) directs HSC platelet-bias. Mφs from the marrow of aged mice and humans exhibited an activated phenotype, with increased expression of inflammatory signals. Aged marrow Mφs also displayed decreased phagocytic function. Senescent neutrophils, typically cleared by marrow Mφs, were markedly increased in aged mice, consistent with functional defects in Mφ phagocytosis and efferocytosis. In aged mice, Interleukin 1B ([[IL1B]]) was elevated in the bone marrow and caspase 1 activity, which can process pro-[[IL1B]], was increased in marrow Mφs and neutrophils. Mechanistically, [[IL1B]] signaling was necessary and sufficient to induce a platelet bias in HSCs. In young mice, depletion of phagocytic cell populations or loss of the efferocytic receptor Axl expanded platelet-biased HSCs. Our data support a model wherein increased inflammatory signals and decreased phagocytic function of aged marrow Mφs induce the acquisition of platelet bias in aged HSCs. This work highlights the instructive role of Mφs and [[IL1B]] in the age-associated lineage-skewing of HSCs, and reveals the therapeutic potential of their manipulation as antigeronic targets.
|mesh-terms=* Aging
* Animals
* Blood Platelets
* Bone Marrow
* Caspase 1
* Hematopoietic Stem Cells
* Humans
* Interleukin-1beta
* Macrophages
* Male
* Mice
* Mice, Inbred C57BL
* Mice, Knockout
* Neutrophils
* Phagocytosis
* Phenotype
* Proto-Oncogene Proteins
* Receptor Protein-Tyrosine Kinases
|keywords=* Aging
* Bone marrow
* Hematology
* Hematopoietic stem cells
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6542605
}}
{{medline-entry
|title=[[MEF2A]] alters the proliferation, inflammation-related gene expression profiles and its silencing induces cellular senescence in human coronary endothelial cells.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30885136
|abstract=Myocyte enhancer factor 2A ([[MEF2A]]) plays an important role in cell proliferation, differentiation and survival. Functional deletion or mutation in [[MEF2A]] predisposes individuals to cardiovascular disease mainly caused by vascular endothelial dysfunction. However, the effect of the inhibition of [[MEF2A]] expression on human coronary artery endothelial cells (HCAECs) is unclear. In this study, expression of [[MEF2A]] was inhibited by specific small interference RNA (siRNA), and changes in mRNA profiles in response to [[MEF2A]] knockdown were analyzed using an Agilent human mRNA array. Silencing of [[MEF2A]] in HCAECs accelerated cell senescence and suppressed cell proliferation. Microarray analysis identified 962 differentially expressed genes (DEGs) between the [[MEF2A]] knockdown group and the negative control group. Annotation clustering analysis showed that the DEGs were preferentially enriched in gene ontology (GO) terms and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways related to proliferation, development, survival, and inflammation. Furthermore, 61 of the 578 downregulated DEGs have at least one potential [[MEF2A]] binding site in the proximal promoter and were mostly enriched in the GO terms "reproduction" and "cardiovascular." The protein-protein interaction network analyzed for the downregulated DEGs and the DEGs in the GO terms "cardiovascular" and "aging" revealed that [[PIK3CG]], [[IL1B]], IL8, and [[PRKCB]] were included in hot nodes, and the regulation of the longevity-associated gene [[PIK3CG]] by [[MEF2A]] has been verified at the protein level, suggesting that [[PIK3CG]] might play a key role in [[MEF2A]] knockdown induced HCAEC senescence. [[MEF2A]] knockdown accelerates HCAEC senescence, and the underlying molecular mechanism may be involved in down-regulation of the genes related with cell proliferation, development, inflammation and survival, in which [[PIK3CG]] may play a key role.
|mesh-terms=* Cell Differentiation
* Cell Proliferation
* Cells, Cultured
* Cellular Senescence
* Class Ib Phosphatidylinositol 3-Kinase
* Coronary Vessels
* Endothelial Cells
* Gene Expression Profiling
* Gene Expression Regulation
* Humans
* Inflammation
* MEF2 Transcription Factors
|keywords=* Cardiovascular disease
* Human coronary artery endothelial cells
* Myocyte enhancer factor 2A
* PIK3CG
* Senescence
* Vascular endothelial dysfunction
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6423757
}}
{{medline-entry
|title=Measuring the Inflammasome in Oncogene-Induced Senescence.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30474840
|abstract=Inflammasomes are multimeric protein complexes that process IL-1β by cleaving the translated full-length protein into its active IL-1β mature fragment. In oncogene-induced senescence, inflammasomes play a crucial role by regulating IL1R signaling and consequently modulating proliferation and the senescence-associated secretory phenotype (SASP). Inflammasome activation requires two steps: (a) priming of the inflammasome by activation of [[IL1B]] expression, followed by (b) cleavage and release of mature IL-1β. In this chapter, we describe methods to detect both stages of inflammasome activation in cellular senescence.
|mesh-terms=* Caspase 1
* Cells, Cultured
* Cellular Senescence
* Fibroblasts
* Humans
* Inflammasomes
* Interleukin-1beta
* Oncogenes
* Signal Transduction
|keywords=* Caspase-1
* IL-1β
* Inflammasome
* Oncogene-induced senescence
* SASP
* Senescence
|full-text-url=https://sci-hub.do/10.1007/978-1-4939-8931-7_7
}}
{{medline-entry
|title=Lower levels of interleukin-1β gene expression are associated with impaired Langerhans' cell migration in aged human skin.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/28777886
|abstract=Langerhans' cells (LC) play pivotal roles in skin immune responses, linking innate and adaptive immunity. In aged skin there are fewer LC and migration is impaired compared with young skin. These changes may contribute to declining skin immunity in the elderly, including increased skin infections and skin cancer. Interleukin-1β (IL-1β) and tumour necrosis factor-α ([[TNF]]-α) are mandatory signals for LC migration and previous studies suggest that IL-1β signalling may be dysregulated in aged skin. Therefore, we sought to explore the mechanisms underlying these phenomena. In skin biopsies of photoprotected young (< 30 years) and aged (> 70 years) human skin ex vivo, we assessed the impact of trauma, and mandatory LC mobilizing signals on LC migration and gene expression. Biopsy-related trauma induced LC migration from young epidermis, whereas in aged skin, migration was greatly reduced. Interleukin-1β treatment restored LC migration in aged epidermis whereas [[TNF]]-α was without effect. In uncultured, aged skin IL-1β gene expression was lower compared with young skin; following culture, IL-1βmRNA remained lower in aged skin under control and [[TNF]]-α conditions but was elevated after culture with IL-1β. Interleukin-1 receptor type 2 ([[IL1R2]]) gene expression was significantly increased in aged, but not young skin, after cytokine treatment. Keratinocyte-derived factors secreted from young and aged primary cells did not restore or inhibit LC migration from aged and young epidermis, respectively. These data suggest that in aged skin, IL-1β signalling is diminished due to altered expression of [[IL1B]] and decoy receptor gene [[IL1R2]].
|mesh-terms=* Adult
* Age Factors
* Aged
* Aged, 80 and over
* Aging
* Biomarkers
* Chemotaxis
* Cytokines
* Epidermis
* Gene Expression
* Humans
* Interleukin-1beta
* Keratinocytes
* Langerhans Cells
* RNA, Messenger
* Receptors, Interleukin-1 Type II
* Signal Transduction
* Skin
* Tissue Culture Techniques
* Young Adult
|keywords=* Langerhans’ cells
* ageing
* skin
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5721243
}}
{{medline-entry
|title=Age-dependent changes in inflammation and extracellular matrix in bovine oviduct epithelial cells during the post-ovulatory phase.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/27580129
|abstract=The mammalian oviduct is an essential site for sperm storage, the transport of gametes, fertilization, and embryo development-functions that are aided by cytokines secreted from oviduct epithelial cells (OECs). Aging leads to cellular and organ dysfunction, with infertility associated with advanced maternal age. Few studies have investigated age-dependent changes in the oviduct as a possible cause of infertility, so we compared OECs from young (30-50 months) versus aged (more than 120 months) cattle. Next-generation sequencing was first used to identify age-related differences in gene expression. Several proinflammatory-related genes (including [[IL1B]], [[IL1A]], [[IL17C]], IL8, [[S100A8]], [[S100A9]], and TNFA) were activated in OECs from aged (more than 120 months) compare to young (30-50 months) individuals, whereas genes associated with extracellular matrix-related factors (COLs, [[POSTN]], [[BGN]], and LUM) were down-regulation in aged OECs. Indeed, IL1 B and IL8 abundance was higher in aged OECs than in young OECs. Young OECs also tended to proliferate faster, and the revolution frequency of young, ciliated OECs was higher than that of their aged counterparts. In contrast, aged OECs possessed more F-actin, an actin cytoskeleton marker associated with reduced elasticity, and contained high levels of reactive oxygen species, which are mediators of inflammation and senescence. These different functional characteristics of bovine OECs during the post-ovulatory phase support the emerging concept of "inflammaging," that is, age-dependent inflammation. Mol. Reprod. Dev. 83: 815-826, 2016 © 2016 Wiley Periodicals, Inc.
|mesh-terms=* Aging
* Animals
* Cattle
* Cytokines
* Epithelial Cells
* Extracellular Matrix
* Extracellular Matrix Proteins
* Female
* Gene Expression Regulation
* Inflammation
* Oviducts
* Ovulation

|full-text-url=https://sci-hub.do/10.1002/mrd.22693
}}
{{medline-entry
|title=Differential Matrix Metalloprotease (MMP) Expression Profiles Found in Aged Gingiva.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/27391467
|abstract=The periodontium undergoes age-related cellular and clinical changes, but the involved genes are not yet known. Here, we investigated age-related genetic changes in gingiva at the transcriptomic level. Genes that were differentially expressed between young and old human gingiva were identified by RNA sequencing and verified by real-time PCR. A total of 1939 mRNA transcripts showed significantly differential expression between young and old gingival tissues. Matrix metalloprotease (MMP) regulation was the top pathway involved in gingival aging. [[MMP3]], [[MMP9]], [[MMP12]], and [[MMP13]] were upregulated in old gingival tissues, concomitantly with interleukin-1 beta ([[IL1B]]) expression. In vitro experiments using human gingival fibroblasts (hGFs) showed that [[MMP12]] was upregulated in old hGFs compared to young hGFs. Moreover, the [[MMP3]], [[MMP9]] and [[IL1B]] levels were more highly stimulated by infection with the oral bacterium, Fusobacterium nucleatum, in old hGFs compared to young hGFs. Collectively, these findings suggest that, in gingiva, the upregulation of [[MMP12]] may be a molecular hallmark of natural aging, while the upregulations of [[MMP3]], MMM9, and [[IL1B]] may indicate externally (e.g., infection)-induced aging. These findings contribute to our understanding of the molecular targets involved in gingival aging. 
|mesh-terms=* Adolescent
* Adult
* Aged
* Aged, 80 and over
* Aging
* Female
* Fibroblasts
* Fusobacterium Infections
* Fusobacterium nucleatum
* Gelatinases
* Gene Expression Profiling
* Gene Expression Regulation, Enzymologic
* Gingiva
* Gingivitis
* Humans
* Interleukin-1beta
* Male
* Middle Aged

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4938517
}}
{{medline-entry
|title=Gene expression of inflammasome components in peripheral blood mononuclear cells (PBMC) of vascular patients increases with age.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/26448778
|abstract=Chronic low-grade inflammation is considered a driver of many age-related disorders, including vascular diseases (inflammaging). Inhibition of autophagic capacity with ageing was postulated to generate a pro-inflammatory condition via activation of inflammasomes, a group of Interleukin-1 activating intracellular multi-protein complexes. We thus investigated gene expression of inflammasome components in PBMC of 77 vascular patients (age 22-82) in association with age. Linear regression of real-time qRT-PCR data revealed a significant positive association of gene expression of each of the inflammasome components with age (Pearson correlation coefficients: [[AIM2]]: r = 0.245; P = 0.032; [[NLRP3]]: r = 0.367; P = 0.001; ASC (PYCARD): r = 0.252; P = 0.027; [[CASP1]]: r = 0.296; P = 0.009; [[CASP5]]: r = 0.453; P = 0.00003; [[IL1B]]: r = 0.247; P = 0.030). No difference in gene expression of [[AIM2]], [[NLRP3]], ASC [[CASP1]], and [[CASP5]] was detected between PBMC of patients with advanced atherosclerosis and other vascular patients, whereas [[IL1B]] expression was increased in PBMC of the latter group (P = 0.0005). The findings reinforce the systemic pro-inflammatory phenotype reported in elderly by demonstrating an increased phase-1 activation of inflammasomes in PBMC of vascular patients.

|keywords=* AIM2
* Aging
* Atherosclerosis
* Inflammation
* NLRP3
* Vascular disease
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4596365
}}
{{medline-entry
|title=Gene expression markers of age-related inflammation in two human cohorts.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/26087330
|abstract=Chronically elevated circulating inflammatory markers are common in older persons but mechanisms are unclear. Many blood transcripts (>800 genes) are associated with interleukin-6 protein levels ([[IL6]]) independent of age. We aimed to identify gene transcripts statistically mediating, as drivers or responders, the increasing levels of [[IL6]] protein in blood at older ages. Blood derived in-vivo RNA from the Framingham Heart Study (FHS, n=2422, ages 40-92 yrs) and InCHIANTI study (n=694, ages 30-104 yrs), with Affymetrix and Illumina expression arrays respectively (>17,000 genes tested), were tested for statistical mediation of the age-[[IL6]] association using resampling techniques, adjusted for confounders and multiple testing. In FHS, [[IL6]] expression was not associated with [[IL6]] protein levels in blood. 102 genes (0.6% of 17,324 expressed) statistically mediated the age-[[IL6]] association of which 25 replicated in InCHIANTI (including 5 of the 10 largest effect genes). The largest effect gene (SLC4A10, coding for NCBE, a sodium bicarbonate transporter) mediated 19% (adjusted CI 8.9 to 34.1%) and replicated by PCR in InCHIANTI (n=194, 35.6% mediated, p=0.01). Other replicated mediators included [[PRF1]] (perforin, a cytolytic protein in cytotoxic T lymphocytes and NK cells) and [[IL1B]] (Interleukin 1 beta): few other cytokines were significant mediators. This transcriptome-wide study on human blood identified a small distinct set of genes that statistically mediate the age-[[IL6]] association. Findings are robust across two cohorts and different expression technologies. Raised [[IL6]] levels may not derive from circulating white cells in age related inflammation.
|mesh-terms=* Adult
* Aged
* Aged, 80 and over
* Aging
* Biomarkers
* Cohort Studies
* Female
* Gene Expression Profiling
* Genetic Markers
* Humans
* Inflammation
* Inflammation Mediators
* Interleukin-6
* Male
* Middle Aged
|keywords=* Aging
* Blood
* Epidemiology
* Human
* Inflammation
* Transcriptome
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4600657
}}
{{medline-entry
|title=Prior infection exacerbates postoperative cognitive dysfunction in aged rats.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/25972458
|abstract=Older patients may experience persisting postoperative cognitive dysfunction (POCD), which is considered to largely depend on surgery-induced (neuro)inflammation. We hypothesize that inflammatory events before surgery could predispose patients to POCD. When part of our aged rats developed Mycoplasma pulmonis, this presented the unique opportunity to investigate whether a pulmonary infection before surgery influences surgery-induced neuroinflammation and POCD. Male 18-mo-old Wistar rats that had recovered from an active mycoplasma infection (infection) and control rats (healthy) were subjected to abdominal surgery and jugular vein catheterization under general anesthesia (surgery) or remained naïve (control). In postoperative week 2, behavioral tests were performed to assess cognitive performance and exploratory behavior. The acute systemic inflammatory response was investigated by measuring plasma IL-6 and IL-12. In the hippocampus, prefrontal cortex and striatum, microglial activity, neurogenesis, and concentrations of IL-6, IL-12, [[IL1B]], and brain-derived neurotropic factor on postoperative day 14 were determined. Rats still showed signs of increased neuroinflammatory activity, as well as cognitive and behavioral changes, 3 wk after the symptoms of infection had subsided. Rats that had experienced infection before surgery exhibited a more generalized and exacerbated postoperative cognitive impairment compared with healthy surgery rats, as well as a prolonged increase in systemic cytokine levels and increased microglial activation in the hippocampus and prefrontal cortex. These findings support the hypothesis that an infection before surgery under general anesthesia exacerbates POCD. Future studies are necessary to determine whether the found effects are aging specific and to investigate the magnitude and time course of this effect in a controlled manner. 
|mesh-terms=* Abdomen
* Age Factors
* Aging
* Anesthesia, General
* Animals
* Behavior, Animal
* Brain-Derived Neurotrophic Factor
* Cognition
* Cognition Disorders
* Disease Models, Animal
* Encephalitis
* Exploratory Behavior
* Grooming
* Hippocampus
* Inflammation Mediators
* Male
* Memory
* Microtubule-Associated Proteins
* Mycoplasma Infections
* Mycoplasma pulmonis
* Neuropeptides
* Postoperative Complications
* Prefrontal Cortex
* Rats, Wistar
* Risk Factors
* Time Factors
|keywords=* brain-derived neurotropic factor
* infection
* learning and memory
* neuroinflammation
* postoperative cognitive dysfunction
|full-text-url=https://sci-hub.do/10.1152/ajpregu.00002.2015
}}