Indomethacin impairs LPS-induced  behavioral fever in toads

Bícego, Kênia C.; Steiner, Alexandre A.; Antunes‐Rodrigues, José; Branco, Luiz G.S.

doi:10.1152/japplphysiol.00121.2002

Cited by 32 publications

(15 citation statements)

References 29 publications

(50 reference statements)

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“…Samples were covered with aluminum foil to protect from light and incubated under agitation at 25°C for 35 min. A temperature of 25°C was chosen to run the phagocytic assay, as this is the mean thermal preference for R. schneideri according to the study of Bicego, Steiner, Antunes‐Rodrigues, and Branco (). Reactions were stopped by adding 2 mL of cold (4°C) EDTA solution (6 mM).…”

Section: Methodsmentioning

confidence: 99%

Captivity effects on immune response and steroid plasma levels of a Brazilian toad (Rhinella schneideri)

et al. 2017

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Stressors can increase plasma glucocorticoid (GC) levels and decrease plasma androgen levels in different species of vertebrates. GCs can have immune-enhancing or immunosuppressive effects, which are dependent upon stress duration and intensity. The worldwide decline in amphibian populations is strongly linked to an array of different stressors. The impacts of stress on GCs, androgens, and the immune response are important to clarify and should lead to the better development of conservation strategies. The present study in adult male toads of Rhinella schneideri investigated the effects of captivity (7, 30, and 60 days) on plasma corticosterone (CORT) and plasma testosterone (T), as well as innate immune responses, specifically humoral and cell mediated responses, as indicated by bacterial killing ability (BKA) and phagocytosis by peritoneal cells, respectively. Captivity increased CORT threefold and decreased T versus controls. CORT maintained a threefold elevation throughout the captivity period, while body mass and T gradually decreased with time in captivity. BKA was lower at day 30, versus days 7 and 60, while peritoneal cell phagocytic efficiency decreased after day 30, remaining low at day 60. Moreover, phagocytosis efficiency was positively associated with T and body condition, suggesting that the effects of chronic stress on reproductive potential and immune response might be associated with the state of energetic reserves.

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Section: Methodsmentioning

confidence: 99%

Captivity effects on immune response and steroid plasma levels of a Brazilian toad (Rhinella schneideri)

et al. 2017

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“…Whereas only homeothermic animals are capable of internally increasing the body temperature in response to infections, both homeotherms and poikilotherms develop behavioral fever in response to infection-like conditions such as those stimulated by injections of LPS (19). Using the nematode C. elegans, it has been demonstrated that heatshock boosts innate immunity against bacteria through the activation of HSF-1 (2).…”

Section: Hyperactivation Of Daf-16 By Heat Shock Makes C Elegansmentioning

confidence: 99%

Regulation of DAF-16-mediated Innate Immunity in Caenorhabditis elegans

Singh

Aballay

2009

Journal of Biological Chemistry

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Activation of the innate immune system results in a rapid microbicidal response against microorganisms, which needs to be fine-tuned because uncontrolled immune responses can lead to infection and cancer, as well as conditions such as Crohn disease, atherosclerosis, and Alzheimer disease. Here we report that excessive activity of the conserved FOXO transcription factor DAF-16 enhances susceptibility to bacterial infections in Caenorhabditis elegans. We found that increased temperature activates not only DAF-16 nuclear import but also a control mechanism involved in DAF-16 nuclear export. The nuclear export of DAF-16 requires heat shock transcription factor HSF-1 and Hsp70/HSP-1. Furthermore, we show that increased expression of the water channel Aquoporin-1 is responsible for the deleterious consequences of excessive DAF-16-mediated immune response. These studies reveal a stress-inducible mechanism involved in the regulation of DAF-16 and indicate that uncontrolled DAF-16 activity and water homeostasis are a cause of the deleterious effects of excessive immune responses.The inflammatory response is a physiological process that takes place in the presence of a variety of noxious stimuli, including bacterial infections. A hallmark of inflammation is the increased tissue permeability, which allows components of the innate immune system to execute an inflammatory response at the site of infection. In addition to cellular immune effectors, humoral factors such as antimicrobial peptides, lysozymes, and reactive oxygen species accumulate at the site of infection to control invading microorganisms. Whereas this myriad of immune effectors plays a key role in the control of infections, they have the potential to damage host tissues. To provide insights into the mechanisms by which excessive immune responses may be deleterious to an infected host, we have taken advantage of the simple innate immune system of the genetically tractable nematode Caenorhabditis elegans.Dauer formation abnormal (DAF) 2 -16 is a key FOXO transcription factor that controls innate immunity in C. elegans (1-3). DAF-16 is closely related to mammalian FOXO3a, which has been linked to inflammation in response to infection (4, 5). Like FOXO3a, the activity of DAF-16 is tightly regulated by a wide variety of external stimuli such as nutrients, oxidative stress, and heat stress (6 -9). The activity of DAF-16 is tightly controlled at the level of subcellular localization and posttranslational modifications of the protein, including phosphorylation (7,8,10,11). The presence of such tight control suggests that there may be a stress-inducible mechanism that prevents the deleterious consequences of a hyperactive DAF-16.Here we studied the effect of hyperactivation of DAF-16 in the context of C. elegans immunity. We found that while DAF-16 overexpression protects C. elegans from bacterial infections, its excessive activation has deleterious effects. Even though increased temperature promotes DAF-16 nuclear import, it also turns on a control mechanism that prom...

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“…[1][2][3][4][5] A number of studies have reported that besides homeotherms, such as rats that are capable of internally increasing the body temperature, poikilothermic vertebrates and invertebrates develop behavioral fever in response to injections of LPS. 6 In mammals, where the molecular mechanisms of fever initiation have been very well studied, it is known that endogenous pyrogens stimulate the production of prostaglandins which are the main mediators of increased temperature. [7][8][9][10][11][12][13] Indeed, the extensively used nonsteroidal anti inflammatory drugs reduce fever by targeting prostaglandin synthesis.…”

Section: Introductionmentioning

confidence: 99%