Stress induces the translocation of cutaneous and gastrointestinal microflora to secondary lymphoid organs of C57BL/6 mice

Bailey

Psychoneuroendocrinology

et al. 2008

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SummaryFrequent or chronic stress as a result of repeated or persistent exposure to social challenges has been shown to affect the glucocorticoid (GC) responsiveness of immune cells in mice. Lipopolysaccharide-stimulated splenocytes of mice that were repeatedly subjected to social disruption were less sensitive to the anti-inflammatory actions of GC as evident from an increased production of pro-inflammatory cytokines and enhanced cell survival. The development of functional GC resistance was accompanied by the accumulation of GC-insensitive CD11b + cells in the spleen. These cells were shown to exhibit impaired nuclear translocation of the GC receptor and lack of GCinduced suppression of NF-κB. Similar impairments in GC receptor function have been reported after in vitro treatment of various cell lines with interleukin (IL)-1. The aim of this study was to elucidate whether IL-1 is a critical factor for the development of GC resistance in socially stressed mice. In the first experiment, we investigated if repeated social stress alters plasma levels and tissue gene expression of IL-1α and IL-1β. It revealed that recurrent stressor exposure significantly increased splenic and hepatic mRNA expression and the plasma protein level of IL-1β, and hepatic mRNA expression of IL-1α. In the second experiment, IL-1 receptor type 1 (IL1R1)-deficient mice were subjected to the stressor and both the tissue distribution of CD11b + cells and the GC sensitivity of the splenocytes were compared to wildtype mice. Mice lacking the IL1R1 exhibited adrenal hypertrophy, thymic involution, and elevated serum corticosterone levels in response to the stressor but did not show splenic accumulation of CD11b + cells and failed to develop GC resistance. These findings suggest that IL-1 plays a critical role in the development of the social stress-associated GC resistance in the murine spleen.

Section: Discussionmentioning

confidence: 97%

Interleukin-1 receptor type 1-deficient mice fail to develop social stress-associated glucocorticoid resistance in the spleen

Bailey

Psychoneuroendocrinology

et al. 2008

Self Cite

“…Stress can reduce gastric emptying, slowing transit in the small intestine through stressor-induced increases in corticotrophin releasing hormone (Nakade et al, 2005). The collective message of this and the above research is that natural defences of mammals, such as those provided by the commensal microflora, stomach acid and normal GI motility can be significantly compromised by psychological and physical stress (Bailey et al, 2006). What might then be the response of an opportunistic enteropathogen to such stress induced changes in the GI tract of their bovine host?…”

Section: Microbial Endocrinologymentioning

confidence: 99%

“…Within the chambers the bacteria grew significantly better in the social conflict stressed mice compared with the control non-stressed mice, despite a fourfold increase in the anti-microbial phagocytic activity in the blood of the stressed animals (Dré au et al, 1999). In another rodent stress model, stressors such as social conflict and physical restraint (which have been similarly shown to be significant stressors of bovine species) caused translocation to systemic sites of both the gut and cutaneous microflora (Bailey et al, 2006 and. Significant spilling over of catecholamines from the systemic circulation into the gastrointestinal (GI) tract can occur during acute stress (Eisenhofer et al, 1997).…”

Section: Microbial Endocrinologymentioning

confidence: 99%

“…Any pathogens present might also respond to other signals produced by the intestinal microbial flora, such as the LuxS-dependent AI-3, which also activates transcription of genes involved in attaching and effacing lesion formation (Sperandio et al, 2003;Kendall et al, 2007). The increasing numbers of pathogens, and possibly also endogenous gut bacteria (Lyte and Bailey, 1997;Bailey et al, 2006 and, could affect gut integrity leading to bacterial translocation (iii) either to the mesenteric lymphatic tissue or, in a worst-case scenario, directly into the systemic circulation, where even commensal bacteria could lead to sepsis and multiple organ failure. Previous exposure to NA might also cause increased expression of E. coli virulence genes, leading to increased attachment of the pathogen to the gut mucosa, either through non-intimate attachments (Chen et al, 2006) (iv) or through espA-or locus of enterocyte effacement (LEE)-dependent intimate attachment (Vlisidou et al, 2004;Kendall et al, 2007) (v and vi), causing the attaching and effacing lesions characteristic of enteropathogenic and enterohaemorrhagic E. coli (note that this figure was adapted with permission from Freestone et al 2008). bacteria to the intestinal mucosa.…”

Section: Stress Hormone Modulation Of Bovine Enteropathogen Virulencementioning

confidence: 99%

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Stress and microbial endocrinology: prospects for ruminant nutrition

Freestone

Lyte

2010

Animal

The feed efficiency of ruminant meat and dairy livestock can be significantly influenced by factors within their living environments. In particular, events perceived by the animals as stressful (such as parturition, transport or handling) have been found to affect susceptibility to infection. It has been well documented that even minor stress such as weighing can result in an increase in colonisation and faecal shedding of enteric pathogens such as Salmonella enterica and Escherichia coli O157:H7. Such infections affect both ruminant overall health and therefore performance, and are a particular problem for the meat production industries. Prior explanations for stress enhancing the likelihood of infection is that activation of the sympathetic nervous system under stress leads to the release of neuroendocrine mediators such as the catecholamine stress hormones noradrenaline and adrenaline, which may impair innate and adaptive immunity. More recently, however, another equally compelling explanation, viewed through the lens of the newly recognised microbiological discipline of microbial endocrinology is that the myriad of bacteria within the ruminant digestive tract are as responsive to the hormonal output of stress as the cells of their host. Work from our laboratories has shown that enteric pathogens have evolved systems for directly sensing stress hormones. We have demonstrated that even brief exposure of enteric pathogens to physiological concentrations of stress hormones can result in massive increases in growth and marked changes in expression of virulence factors such as adhesins and toxins. Happy, less stressed ruminants may therefore be better-nourished animals and safer sources of meat. This article reviews evidence that stress, as well as affecting nutrition, in ruminants is correlated with increased risk of enteric bacterial infections, and examines the molecular mechanisms that may be at work in both processes.

Jundishapur J Microbiol

“…When eliminated in the environment together with feces it contaminates water, soil and food (1)(2)(3). Based on the particular present strain, it can provide resistance against pathogenic organisms or can itself be pathogenic, causing diseases at intestinal and extra-intestinal sites (4). Particularly, urban rivers have been often reported as having fecal contamination associated with antibiotic-resistant E. coli which threatens drinking water quality and public health (5)(6)(7).…”

Section: Introductionmentioning

confidence: 99%

Investigating the Resistance of Escherichia coli Against Some Selected Antimicrobials in Bam

Ayatollahi¹,

Vahidi²,

Shahcheraghi³

et al. 2013

Background: Antibiotics and corresponding resistance genes and resistant bacteria have been considered as emerging pollutants worldwide. Excessive and incorrect use of antimicrobials in human and veterinary medicine, as well as their metaphylactic application in livestock are considered to be key aspects of this current situation. Objectives: The current study aimed to investigate the resistance of Escherichia coli against six antibiotics, in Bam. Materials and Methods: This descriptive study was performed on 300 samples with positive cultures of E. coli in 2006-2007 at the Central Laboratory and the Pasteur hospital in Bam city. Information related to this study was first collected by visiting the above laboratories and completing questionnaires and then recorded in the Excel program and analyzed using the SPSS software and chi-square statistical method. Results: In this study, high resistances were found to nalidixic acid (59.7%) and gentamicin (52.3%) but high susceptibilities were found to ciprofloxacin (59.3%) and ceftriaxone (36.3%). Conclusions: According to the results obtained in this study ciprofloxacin is an effective antibiotic in E.coli infections.