Induction Of Adaptive Response Research Articles

A study on the radiosensitivity and induction of adaptive response in peripheral blood lymphocytes of patients with secondary immunodeficiency syndrome

This study examined radiosensitivity at low and high dose exposure to X-rays in human lymphocytes and the ability of low and high dose radiation to induce radioadaptive response when the peripheral blood cells from patients with secondary immune deficiency syndrome and healthy donors of different ages were irradiated in vitro. The frequency of micronuclei in cytochalasin-blocked binuclear lymphocytes in culture served as an indication of cytogenetic damage. It was found that the spontaneous level of cytogenetic damage in blood lymphocytes of patients with secondary immune deficiency syndrome was 2.5 times greater than that of healthy young and older volunteers and there was also a substantial interindividual variability in outcome parameters as compared to the data of control groups. There were no differences in mean values for radiosensitivity at low and high dose exposure of X-rays between the groups. In all groups, no correlation was shown between the spontaneous level of micronuclei in lymphocytes and the radiosensitivity of individuals. The adaptive response was induced with the same frequency and to the same extent in lymphocytes in patients with secondary immune deficiency syndrome and in healthy donors of different ages.

A Study on the Radiosensitivity and Induction of Adaptive Response in Peripheral Blood Lymphocytes of Patients with Secondary Immunodeficiency Syndrome

A Study on the Radiosensitivity and Induction of Adaptive Response in Peripheral Blood Lymphocytes of Patients with Secondary Immunodeficiency Syndrome

Implication of Sodium Hypochlorite as a Sanitizer in Ready-to-Eat Salad Processing and Advantages of the Use of Alternative Rapid Bacterial Detection Methods.

The use of disinfection agents in the washing processing of ready-to-eat (RTE) vegetables, especially sodium hypochlorite, is a common industrial practice performed to enhance microbiological quality. However, some studies have reported a restart of bacterial growth and a substantial increase in bacterial load during early storage associated with the use of disinfection agents, which might represent a risk for consumers. We evaluated the effect of sodium hypochlorite on bacterial growth trends during the shelf-life in Lactuca sativa, simulating the industrial procedures for RTE vegetable packaging. Immediately after sodium hypochlorite treatment, an effective abatement of the bacterial load was observed, followed by a restart of growth throughout storage. After 5 days, the bacterial load was close to that reached by the control samples, indicating that the net increase in bacterial load was significantly higher in the treated samples. This might be ascribed to the reduction in competitive microflora and/or to the induction of adaptive responses by resting bacteria, which might select disinfectant-resistant bacteria. These findings elicit some concerns about the actual duration of the shelf-life; products might decrease their microbiological quality earlier during storage, pointing out the need to better clarify the impact of sodium hypochlorite as a sanitizer to closer consider its use in RTE vegetable processing. Furthermore, due to the importance of the rapid estimation of bacterial load and the early detection of foodborne pathogens throughout the food chain, the accuracy of the rapid bacteria detection method, the Micro Biological Survey (MBS), and its effectiveness for microbiological analyses of RTE vegetables were evaluated.

Multimodal control of dendritic cell functions by nociceptors.

It is known that interactions between nociceptors and dendritic cells (DCs) can modulate immune responses in barrier tissues. However, our understanding of the underlying communication frameworks remains rudimentary. Here, we show that nociceptors control DCs in three molecularly distinct ways. First, nociceptors release the calcitonin gene-related peptide that imparts a distinct transcriptional profile on steady-state DCs characterized by expression of pro-interleukin-1β and other genes implicated in DC sentinel functions. Second, nociceptor activation induces contact-dependent calcium fluxes and membrane depolarization in DCs and enhances their production of proinflammatory cytokines when stimulated. Finally, nociceptor-derived chemokine CCL2 contributes to the orchestration of DC-dependent local inflammation and the induction of adaptive responses against skin-acquired antigens. Thus, the combined actions of nociceptor-derived chemokines, neuropeptides, and electrical activity fine-tune DC responses in barrier tissues.

Induction of adaptive response in E. coli cells alkylating agents depend on their chemical structure

The most well–known alkylating agents (AA) used in mutational breeding of agricultural crops and microorganisms producing biologically active substances are methyl methanesulfonate (MMS) and ethylmethanesulfone (EMS). It is known that both of these substances effectively induce bacterial alkyltransferase, which leads to an adaptive response of bacteria, that is, to the development of resistance to toxic effects. Bacterial alkyltransferase is a homologue of O6-methylguanine-DNA-methyltransferase in human cells. The study of the induction of alkyltransferase in bacteria by various AA allows us to predict their ability to induce an adaptive response in human cells. Lux biosensors pColDp-lux and pAlkA-lux were used to study the ability of MMS, ECG and BPL to induce DNA damage and adaptive response in E.coli cells. MMS effectively elicited an SOS response in the ColD-lux biosensor, characterizing the level of DNA damage, and an adaptive response recorded in the AlkA-lux biosensor by inducing the expression of the alkyltransferase gene. Bifunctional ECG induced both SOS response and adaptive response less actively than monofunctional MMS. The BPL induced an SOS response only at low concentrations, and did not cause an adaptive response at the same concentrations. Thus, bifunctional ECG and BPL, whose activity depends on the reactivity of the products of the disclosure of their cyclic structures, alkylate DNA to a lesser extent than MMC. This is due to the fact that they form electrophilic methyl groups to a lesser extent than MMCs when the cycle is opened. Keywords: lux-biosensor, E.coli, SOS response, adaptive response, methyl methanesulfonate, epichlorohydrin, beta-propiolactone. &nbsp

The role of intrinsic radiosensitivity in the low-dose adaptive response induction in human peripheral blood mononuclear cells.

The role of intrinsic radiosensitivity in the low-dose adaptive response induction in human peripheral blood mononuclear cells.

Pre-Exposure to Radiofrequency Electromagnetic Fields and Induction of Radioadaptive Response in Rats Irradiated with High Doses of X-Rays

Background: Some evidence shows that a pre-exposure to RF can mitigate the effects of subsequent exposures to high doses of ionizing radiation.Objective: We aimed to assess the effect of a pre-exposure to non-ionizing RF radiation on survival, weight changes, food consumption, and water intake of lethally irradiated rats.Material and Methods: In this case-control study, we used a commercial mobile phone (GSM, 900/1800 MHz) as well as a 2.4 GHz Wi-Fi router as the sources of pre-exposure to RF radiation. Forty-eight rats were randomly divided into six groups of control, “8 Gy X-rays”, mobile phone, “mobile phone+8 Gy”, Wi-Fi, and “Wi-Fi+8 Gy”. Then, the survival fraction, weight loss, water, and food consumption changes were compared in different groups. Results: The survival analysis indicated that the survival rates in all of the exposed animals (“8 Gy X-rays”, “mobile phone+8 Gy”, “Wi-Fi+8 Gy”) were significantly lower than the control, “Wi-Fi”, and “mobile phone” groups. The changes in survival rates of “mobile+8 Gy”, “Wi-Fi+8 Gy”, and 8 Gy alone were not statistically significant. However, food and water intake were significantly affected by exposure to both RF pre-exposures and exposure to high dose ionizing radiation.Conclusion: To the best of our knowledge, the existence of a dose window for the induction of AR can be the cause of the lack of AR in our experiment. Our findings confirm that in a similar pattern with the adaptive responses induced by pre-exposure to ionizing radiation, the induction of adaptive response by RF-pre-exposures requires a minimum level of damage to trigger adaptive phenomena.

Induction of adaptive response in utero by ionizing radiation: A radiation quality dependent phenomenon

Investigation on possible induction of adaptive response (AR) by high-liner energy transfer (LET) particle radiation for protection against low-LET photon radiation-induced detrimental effects has not yet been performed <i>in utero</i>. This study verified if an AR could be induced by high-LET particle radiation from accelerated heavy ions against low-LET X-ray radiation-induced detrimental effects on fetal mice. Total body irradiation of pregnant C57BL/6J mice were performed by delivering a priming dose ranging from 10 mGy to 320 mGy of particle radiation on gestation day 11 followed one day later by a challenge dose at 3500 mGy from X-ray radiation. The monoenergetic beams of carbon, silicon and iron with the LET values of about 15, 55, and 200 KeV/μm, respectively, were examined. Significant suppression by the priming radiation of the detrimental effects (fetal death, malformation, or low body weight) was used as the endpoints for judgment of a successful AR induction on gestation day 18. Existence of AR was not observed. On the other hand, the priming dose of high-LET particle radiation, in some cases, even increased the detrimental effects induced by the challenge dose from low-LET X-ray radiation. Although existence of AR induced by high-LET radiation in cultured mammalian cells<i> in vitro </i> and in certain tissues of laboratory mice <i>in vivo</i> was demonstrated, the present study did not suggest that low dose of high-LET particle radiation could induce an AR in fetal mice <i>in utero</i> under the setup of our experimental system.

К вопросу о формировании адаптивного ответа под действием природного и профессионального факторов хронического облучения. Обзор литературы

The paper summarizes results of medical examination of two groups of patients, the public members resided in high natural background radiation areas and occupationally irradiated nu-clear and health workers. Adaptive response to chronic exposure to radiation was found to last much time and, thus, its impact on the development of late health effects, including cancer, may be great. In vitro studies demonstrate that induction of adaptive response is the multistep process including the excision reparation of nucleotides, nonhomologous DNA ends joining, antioxidative system and cell cycle control factors. The review presents data on effects of low doses radiation of high or low relative radiation effectiveness(RBE). Some damaged peripheral blood lympho-cytes demonstrated increased radioresistance to high radiation doses, results of examinations of both the public members and professionals.

Cytoplasmic Radiation Induced Radio-Adaptive Response in Human Lung Fibroblast WI-38 Cells.

It has been reported that in cells exposed to low-dose radiation, radio-adaptive responses can be induced which make irradiated cells refractory to subsequent high-dose irradiation. However, whether adaptive responses are possible when only the cytoplasm, not the nucleus, of the cell is exposed to radiation is still unclear. In this study, using the proton microbeam facility at the National Institute of Radiological Sciences (Japan), we found that cytoplasmic irradiation activates radio-adaptive responses in normal human lung fibroblast WI-38 cells. Our results showed that when cells received cytoplasmic irradiation with 500 protons prior to 2 Gy or 6 Gy X-ray broad-beam irradiation, the DNA double-strand break levels were significantly reduced. In contrast, at cytoplasmic irradiation with less than 100 protons, the radio-adaptive response was not detected. Moreover, the time interval between cytoplasmic irradiation and whole-cell X-ray irradiation should be longer than 6 h for the induction of adaptive responses. In addition, cytoplasmic irradiation elevated the level of cellular mitochondrial superoxide, which enhanced the phosphorylation of extracellular signal-regulated kinases 1/2 (ERK 1/2) and its mediated nuclear accumulation of nuclear factor (erythroid-derived 2)-like 2 (NRF2). This signaling pathway contributed to cytoplasmic irradiation-induced adaptive response as supported by the observations that treatment with the mitochondrial superoxide scavenger mito-tempol, ERK 1/2 inhibitor U0126 or NRF2 inhibitor ML385 could repress the adaptive response. Overall, we showed that cytoplasmic irradiation induces radio-adaptive responses and that mitochondrial superoxide/ERK 1/2/NRF2 signaling is a mechanism. Our results provide new information on the biological effects induced by cytoplasm-targeted irradiation.

Interactions between the N- and C-termini of the mechanosensitive ion channel AtMSL10 are consistent with a three-step mechanism for activation.

Although a growing number of mechanosensitive ion channels are being identified in plant systems, the molecular mechanisms by which they function are still under investigation. Overexpression of the mechanosensitive ion channel MSL (MscS-Like)10 fused to green fluorescent protein (GFP) triggers a number of developmental and cellular phenotypes including the induction of cell death, and this function is influenced by seven phosphorylation sites in its soluble N-terminus. Here, we show that these and other phenotypes required neither overexpression nor a tag, and could also be induced by a previously identified point mutation in the soluble C-terminus (S640L). The promotion of cell death and hyperaccumulation of H2O2 in 35S:MSL10S640L-GFP overexpression lines was suppressed by N-terminal phosphomimetic substitutions, and the soluble N- and C-terminal domains of MSL10 physically interacted. We propose a three-step model by which tension-induced conformational changes in the C-terminus could be transmitted to the N-terminus, leading to its dephosphorylation and the induction of adaptive responses. Taken together, this work expands our understanding of the molecular mechanisms of mechanotransduction in plants.

ACKR2 contributes to pulmonary dysfunction by shaping CCL5:CCR5-dependent recruitment of lymphocytes during influenza A infection in mice

Inflammation triggered by influenza A virus (IAV) infection is important for viral clearance, induction of adaptive responses, and return to lung homeostasis. However, an exaggerated immune response, characterized by the overproduction of chemokines, can lead to intense lung injury, contributing to mortality. Chemokine scavenger receptors, such as ACKR2, control the levels of CC chemokines influencing the immune responses. Among the chemokine targets of ACKR2, CCL5 is important to recruit and activate lymphocytes. We investigated the role of ACKR2 during IAV infection in mice. Pulmonary ACKR2 expression was increased acutely after IAV infection preceding the virus-induced lung dysfunction. ACKR2-knockout (ACKR2-/-) mice were protected from IAV, presenting decreased viral burden and lung dysfunction. Mechanistically, the absence of ACKR2 resulted in augmented airway CCL5 levels, secreted by mononuclear and plasma cells in the lung parenchyma. The higher chemokine gradient led to an augmented recruitment of T and B lymphocytes, formation of inducible bronchus-associated lymphoid tissue and production of IgA in the airways of ACKR2-/- mice post-IAV. CCL5 neutralization in ACKR2-/- mice prevented lymphocyte recruitment and increased bronchoalveolar lavage fluid protein levels and pulmonary dysfunction. Finally, CCR5-/- mice presented increased disease severity during IAV infection, displaying increased neutrophils, pulmonary injury and dysfunction, and accentuated lethality. Collectively, our data showed that ACKR2 dampens CCL5 levels and the consequent recruitment of CCR5+ T helper 1 (Th1), T regulatory cells (Tregs), and B lymphocytes during IAV infection, decreasing pathogen control and promoting lung dysfunction in wild type mice. Therefore, ACKR2 is detrimental and CCR5 is protective during IAV infection coordinating innate and adaptive immune responses in mice.

Extracellular DNA Containing (dG)n Motifs Penetrates into MCF7 Breast Cancer Cells, Induces the Adaptive Response, and Can Be Expressed.

Background Oxidized human DNA or plasmid DNAs containing human ribosomal genes can easily penetrate into the breast cancer cells MCF7 and stimulate the adaptive response induction. Plasmid DNA containing a CMV promoter, gene EGFP, and the insertion of the human ribosomal genes can be expressed. A hypothesis is proposed: these features of the ribosomal DNA are due to the presence of dGn motifs that are prone to oxidize. Methods Cells of MCF7 line were cultured with plasmids which contained a CMV promoter and gene of fluorescent protein EGFP. Genetic construction pEGFP-Gn contains pEGFP vector and a small insertion with dG11 and dG13 motifs that are inclined to oxidation. The accumulation of pEGFP and pEGFP-Gn in MCF7 (qPCR), the levels of ROS in the cells, the content of 8-oxodG in plasmids and cellular DNA (flow cytometry, immunoassay, and fluorescent microscopy), the expression of NOX4 and EGFP, the localization of NOX4 and EGFP in MCF7 (qPCR, flow cytometry, and fluorescent microscopy), and the levels of the cell DNA damage (comet assay) were analyzed. Results (dG)n insertions in the plasmid pEGFP increase the levels of ROS, the cell DNA oxidation and DNA damage, and the level of transfection of plasmid into the MCF7 cells. NOX4 participates in the oxidation of pEGFP-Gn and pEGFP. The expression of EGFP gene in MCF7 is significantly increased in case of pEGFP-Gn. Stimulation of ROS synthesis (H2O2 40 μM or 10 cGy IR) increases the level of expression of EGFP. Conclusions GC-rich DNA fragments containing dGn motifs that are inclined to oxidation penetrate into MCF7 cancer cells, stimulate the adaptive response, and can be expressed. This property of GC-rich cell-free DNA should be considered and/or could potentially be used in therapy of tumors.

Inhibition of Virulence-Related Traits in Pseudomonas syringae pv. actinidiae by Gunpowder Green Tea Extracts.

Green tea is a widely-consumed healthy drink produced from the leaves of Camellia sinensis. It is renowned for its antioxidant and anticarcinogenic properties, but also displays significant antimicrobial activity against numerous human pathogens. Here we analyzed the antimicrobial activity of Gunpowder green tea against Pseudomonas syringae pv. actinidiae (Psa), the agent that causes kiwifruit bacterial canker. At the phenotypic level, tea extracts strongly inhibited Psa growth and swimming motility, suggesting it could reduce Psa epiphytic survival during plant colonization. The loss of bacterial virulence-related traits following treatment with tea extracts was also investigated by large-scale transcriptome analysis, which confirmed the in vitro phenotypes and revealed the induction of adaptive responses in the treated bacteria allowing them to cope with iron deficiency and oxidative stress. Such molecular changes may account for the ability of Gunpowder green tea to protect kiwifruit against Psa infection.

Intermediate frequency magnetic field at 250.8 kHz does not induce DNA damage or “Adaptive Response” in vitro

The aim of this study was to examine whether intermediate frequency (IF)magnetic field (MF) induces genotoxic effects or play a role in the induction ofadaptive response after combined exposure to IF MF and ionizing radiation inleukocytes and in adrenocortical carcinoma cell line H295R. Cells were exposedto 250.8 kHz at the magnetic field strength of 80 A/m (equivalent to 100 µTmagnetic flux density) for 20 hours, or exposed to IF MF for 20 hours and 24hours later challenged with ionizing radiation (1.5 Gy X-ray). Evaluation of theDNA damage was performed with alkaline comet assay. Our results showed thatthere was no significant genotoxic effect of IF MF exposure compared to thecontrols in both cell types. Furthermore, results did not indicate a statisticallysignificant change in DNA strand breaks in IF MF pre-exposed cells when theywere subsequently exposed to 1.5 Gy. Consequently no adaptive response wasdetected.

Is Telomere Length a Biomarker of Adaptive Response in Space? Curious Findings from NASA and Residents of High Background Radiation Areas.

Telomere length and stability is a biomarker of aging, stress, and cancer. Shortening of telomeres and high level of DNA damages are known to be associated with aging. Telomere shortening normally occurs during cell division in most cells and when telomeres reach a critically short length, DNA damage signaling and cellular senescence can be triggered. The induction of an adaptive response by space radiation was first documented in 2003. Telomere length alterations are among the most fascinating observations in astronauts and residents of high background radiation areas. While study of the chronic exposure to high levels of background ionizing radiation in Kerala, India failed to show a significant influence on telomere length, limited data about the NASA astronaut Scott Kelly show that exposure to space radiation can induce telomeres to regain length. Interestingly, his telomeres shortened again only a couple of days after returning to Earth. The difference between these situations may be due to the differences in radiation dose, dose-rate, and/or type of radiation. Moreover, Scott Kelly’s spacewalks (EVA) could have significantly increased his cumulative radiation dose. It is worth noting that the spacewalks not only confer a higher dose activity but are also characterized by a different radiation spectrum than inside the space craft since the primary particles would not interact with the vehicle shell to generate secondary radiation. Generally, these differences can possibly indicate the necessity of a minimum dose/dose-rate for induction of adaptive response (the so called Window effect).

Hormesis: A Compelling Platform for Sophisticated Plant Science.

The field of dose-response has received attention from the early modern period in the history of science. While it was thought that linear dose-response is the rule of thumb, significant efforts revealed that biphasic dose-response commonly occurs when the experimental design permits its detection. This phenomenon is called hormesis and suggests that a basal stress level is needed for optimum health. Extensive evidence has accumulated showing the occurrence of hormesis in numerous plant species and the induction of adaptive responses by low stress doses that precondition plants for a following massive environmental challenge. However, the ecological consequences of low-level stress remain underexplored. In this Opinion article, we propose that hormesis can provide a compelling platform for sophisticated, next-generation plant science.

Activation of the body’s natural defenses reserve of mice treated with various physico-chemical agents

The purpose of this work is to reveal the activation of natural defenses reserve in mice after treatment with different physico-chemical agents in vivo using previously developed technology of adaptive response induction. Physical agents were represented by X-rays, carbon ions, infrared light, He-Ne laser light, famine and chemical agents – by immunomodulator CaCl2 and anti-inflammatory drug ibuprofen. The following tasks were set: assessment of cytogenetic damage using a micronucleus test, the weight index of lymphoid organs (thymus and spleen) and the level of ROS production in whole blood through the method of luminol-dependent zymosan-induced chemiluminescence. SHK mice were irradiated according to the scheme of adaptive response. Analysis of data on the number of cytogenetic damage in bone marrow showed that pretreatment of the animals with all investigated agents and subsequent exposure to X-rays or carbon ions at a dose of 1.5 Gy has led to a decrease in radiosensitivity compared to the nontreated animals. Similar results were observed when analyzing weight index of lymphoid organs. Determination of level of ROS production has shown that the activation index calculated according to the relation of induced to spontaneous light area, was significantly higher in all groups of mice, indicating activation of the natural defenses reserve as compared to the group exposed only at a dose of 1.5 Gy. The obtained results confirm the assumption of revealing activation of the natural defense of the organism with the help of the adaptive response induction technology.

The Possible Role of Nitric Oxide Pathway in Pentylenetetrazole Preconditioning Against Seizure in Mice.

Preconditioning is defined as an induction of adaptive response in organs against lethal stimulation provoked by subsequent mild sublethal stress. Several chemical agents have been demonstrated to cause brain tolerance through preconditioning. The aim of the present study is to test the hypothesis that preconditioning with pentylenetetrazole (PTZ) may have protective effect against seizure induced by i.v. infusion of PTZ. Mice were preconditioned by low-dose administration of PTZ (25mg/kg) for 5 consecutive days, and the threshold of seizure elicited by i.v. infusion of PTZ was measured. To investigate the possible role of nitric oxide, NOS inhibitor enzymes, including L-NG-nitro-L-arginine methyl ester hydrochloride (L-NAME) (10mg/kg), aminoguanidine (AG) (50mg/kg), 7-nitroindazole (7-NI) (15mg/kg), and L-arginine (L-arg) (60mg/kg), were administered concomitantly with PTZ in both acute and chronic phases. Determination of seizure threshold revealed significant enhancement after preconditioning with low dose of PTZ. While the protective effect of PTZ preconditioning was enhanced after the administration of L-arg, it was reversed following administration of L-NAME and 7NI, suggesting the involvement of nitric oxide pathway as an underlying mechanism of PTZ-induced preconditioning. Preconditioning with PTZ led to brain tolerance and adaptive response in animal model of PTZ-induced seizure. This effect is in part due to the involvement of nitric oxide pathway.

Adverse and beneficial effects in Chinese hamster lung fibroblast cells following radiofrequency exposure.

In this study, the effect of radiofrequency (RF) exposure to 1950 MHz, Universal Mobile Telecommunication System signal, was investigated in Chinese hamster lung fibroblast cell line (V79). Genotoxic and cytotoxic effects of 20-h exposure at specific absorption rate (SAR) values from 0.15 W/kg to 1.25 W/kg were measured by means of cytokinesis-block micronucleus (MN) assay. Exposure was carried out blinded under strictly controlled conditions of dosimetry and temperature. The effect of RF exposure alone at four SAR values was tested, that is, 0.15, 0.3, 0.6, and 1.25 W/kg. A statistically significant increase in MN frequency was found in cultures exposed to 0.15 and 0.3 W/kg (P < 0.05) compared to sham-exposed ones, in the absence of cytotoxicity. SAR values of 0.6 and 1.25 W/kg did not exert any effect. Moreover, to evaluate the ability of RF to exert protective effects with respect to a chemical mutagen, cell cultures were also pre-exposed for 20 h at 0.3 or 1.25 W/kg, and then treated with 500 ng/ml of mitomycin-C (MMC). A significant reduction in the frequency of MN was detected in cultures pre-exposed to 1.25 W/kg compared to cultures treated with MMC alone (P < 0.05), indicating induction of adaptive response. Such a decrease was not induced by pre-exposure at 0.3 W/kg SAR. Taken together, our results indicated that V79 is a sensitive cell model to evidence either adverse or beneficial effects of RF exposure, depending on experimental conditions applied. Bioelectromagnetics. 38:245-254, 2017. © 2017 Wiley Periodicals, Inc.