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While modernization has dramatically increased lifespan, it has also witnessed that the nature of stress has changed dramatically. Chronic stress result failures of homeostasis thus lead to various diseases such as atherosclerosis, non-alcoholic fatty liver disease NAFLD and depression. Chronic inflammation is an essential component of chronic diseases. Additionally, accumulating evidence suggested that excessive inflammation plays critical roles in the pathophysiology of the stress-related diseases, yet the basis for this connection is not fully understood.

Here we discuss the role of inflammation in stress-induced diseases and suggest a common pathway for stress-related diseases that is based on chronic mild inflammation. This framework highlights the fundamental impact of inflammation mechanisms and provides a new perspective on the prevention and treatment of stress-related diseases. Stress is a state of threatened homeostasis provoked by a psychological, environmental, or physiological stressor.

With rapid development of science and technology, as well as economy and strong social competition, the nature of stress has changed dramatically Landsbergis, Stressful events engender multiple neurochemical, neurotransmitter and hormonal alterations by mainly activating the sympathetic nervous system SNS and the hypothalamic-pituitary-adrenal HPA axis.

When stress stimuli are under control, the body responds to these in the physiological way. For instance, catecholamines are elevated to increase heart rate and blood pressure, which help us to fight or flight. This state is beneficial to our survival and recovery. However, when stress stimuli are prolonged or over exaggerated, in another word, chronically increased allostasis lead to pathophysiology.

In the last two decades, accumulating evidence indicated that severe or prolonged chronic stress resulted in increased risk for physical and psychiatric disorders, which is called stress-related disease.

According to the former review, the most common stress-related diseases are cardiovascular diseases CVD, i. The traditional standpoint of mechanisms linking stress and disease has focused on the classical stress systems—the HPA axis and SNS. However, alterations in HPA axis and SNS mainly have indirect effects on target systems; thus the mechanisms link stress to stress-related diseases, and are still under debate.

Recently, inflammation as a new and promising biological mechanism is proposed Rohleder, Accumulating literatures showed that excessive inflammation directly contribute to pathophysiology of stress-related diseases.

In this review article, the search terms were combinations of the following literatures were selected from PubMed: We make a brief summary of stress and inflammation in the field of stress-related diseases. On the basis of these reports, we further hypothesize that inflammation may be one of the common pathways of stress-related diseases. Large bodies of evidence indicate that stress can activate inflammatory response in brain as well as peripherally Rohleder, ; Calcia et al.

There exists communication between the neuroendocrine and immune systems Jiang et al. Stress activates the HPA axis through the hypothalamic secretion of corticotropin-releasing hormone CRHwhich normally suppresses immune responses through the release of glucocorticoids GCs from the adrenals. GCs are one of the major stress hormones released during stress response that are well known for their immunosuppressive and anti-inflammatory properties.

Studies during the s and s revealed that GCs inhibited lymphocyte proliferation and cytotoxicity. Further, GCs reduce the expression of several pro-inflammatory cytokines e. However, recent researchers have proved that GCs also have pro-inflammatory impact on immune system Elenkov, This work demonstrates 110833 proinflammatory role for GCs, enhancing the activation of the innate immune system 18033 response to danger signals Busillo et al.

The interaction of immune system and HPA axis form the endocrine negative feedback loops. However, when cytokine is over-stimulated in some diseases, these negative feedback loops could be weakened by reduced cytoplasmic GC-receptor GR level and decreased expression of GR driven anti-inflammatory genes, thus leading to GC e Sterling and Eyer, Both pro-inflammatory and anti-inflammatory mechanisms depend on the type and intensity of stressors.

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Acute stressors seem to enhance immune function, whereas chronic stressors are suppressive. Intense stressors over-activate the immune system, leading to the imbalance of inflammation and anti-inflammation. Elevated pro-inflammatory cytokines, increased microglia activation and accumulation of peripherally-derived monocytes and macrophages were detected in the brain with psychological stress exposure Johnson et al.

As the brain-resident macrophages, microglia was considered to be the major pro-inflammatory cytokine source. Stress-elicited potentiate microglial activation is via both direct and indirect mechanisms. Microglia express both GC and mineralocorticoid receptors, thus microglia are likely to have direct response to corticosterone peak Calcia et al.

In ldi, GC receptors also are highly present in the hippocampus and prefrontal cortex, so stress-induced lej may have indirect effects on microglia. Activated microglia display hypertrophic branch morphology with an enlarged soma and produce an exaggerated cytokine to recruit peripheral monocytes. Increased brain macrophages and circulating monocytes, contribute to elevated levels of pro-inflammatory cytokine production i.

In common, over-activated immune system, increased activity through SNS pathways, and reduced GCs responsiveness may work tandemly in the activation of inflammatory responses during stress. GCs, catecholamines, cytokines and other mediators released by stress are thought to be the main mediators in stress-induced pro-inflammatory effect.

Classically, inflammation is classically known as the crucial response to microbe invasion or tissue injury to keep maintenance of tissue homeostasis. In recent years, our knowledge of the inflammation role is greatly enlarged. Inflammatory pathway has been recognized as a pivotal molecular basis in the pathogenesis of many chronic diseases. Accumulating researches suggested that excessive inflammation plays critical roles in relationship between stress and stress-related diseases.

Although stress and inflammation, or inflammation and diseases have been widely ej nicely discussed, there are few literatures concerned of all these three factors stress, inflammation and disease.

In this part, we will discuss inflammation in different stress-related diseases and explore the inside mechanism Table 1. CVD was considered to be a leading cause of death worldwide.

Large bodies of clinical trial pointed out that chronic stress, whether early life stress Su et al. Childhood adversity especially severe physical and sexual abuse in childhood was found 1083 strongly relate to higher morbidity of cardiovascular events in women Rich-Edwards et al.

Children who are less expressive and cohesive in their original family exhibited more problematic cardiovascular risk factor profiles Bleil et al. Those who experienced more family disruption events or early life family conflict had greater mean intima-media thickness IMTa subclinical eli of CVD risk Bleil et al.

In adulthood, work-related stressors such as low-income, high job demands combined with low control, shift work and workplace conflicts were mostly reported to be correlated to higher CVD risk Bleil et al. Besides that, poor sleep quality under stress, discrimination emotion stress, such as anger, hostility and aggressiveness were also involved in coronary artery disease Kop, On the contrast, effective stress management including positive emotions, optimism and life satisfaction were proved to have protective roles for CVD Bleil et al.

While the biological mechanisms of stress increasing CVD risk are not well-known, chronic low-grade inflammatory load may emerge as a possible link as it is both elevated by chronic stress and contributed to lwi process, progression and thrombotic complications of atherosclerosis.

IL-6 and CRP, the two important biomarkers of systematic inflammation, are considered indicative and potentially predictive for atherosclerosis Tsirpanlis, ; Nadrowski et al. Coincidently, these two inflammatory indicators were elevated in different types of life stress. For instance, severe levels of childhood abuse were associated with a more elevated acute stress-induced IL-6 response, possibly due to reduced methylation of the IL-6 promoter Janusek et al.

Adults who had greater childhood adversity was reported to have more depressive symptoms and elevated concentrations of CRP Janusek et al. In animal stress models social isolation, social disruption, cold stress, severe chronic unpredictable stressincreased plaque size, elevated serum IL-6, NPY levels were observed.

However, when single supplied with GC after 1833, plaque size and serum inflammatory factors were decreased or did not change.

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Noisy communities as life stressor induces significant increase in urine epinephrine and NE leading to hypertension Seidman and Lek, Inflammation has also been shown to correlate with endothelial dysfunction and relate to the renin-angiotensin system Li et lfi.

Overall, the possible mechanism could be summarized as follows. Anti-inflammatory drugs may have synergistic effect with conventional antihypertensive drugs on the prevention and treatment of stress-related CVD. Stressful events could motivate unhealthy food choices Kuo et al. These unhealthy foods are frequently associated with morbid obesity, type 2 diabetes mellitus, metabolic syndrome and NAFLD Mikolajczyk et al.

Stress enhances both post-meal peaks of triglycerides and delays lipids clearance Kiecolt-Glaser, A recent prospective study supported this view, and provided further evidence Cosgrove et al.

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Furthermore, effective stress management training or mindfulness-based lej reduction training has been proved to have clinically significant benefits on patients with type 2 diabetes. On the contrary, highly anxious patients did not obtain more improvement from the training Rosenzweig et al. Insulin resistance frequently develops during acute or chronic stress Tsuneki et al. Insufficient insulin secretion to compensate for insulin resistance is also the characteristic lie Type 2 1833.

Insulin resistance, visceral obesity, dyslipidemia, type 2 diabetes mellitus and metabolic syndrome are key risk factors in the development and progression of NAFLD. At the intersection of metabolism and immunity, inflammation may be an important link between stress and metabolic disease. Intense stress over-activates the immune system, leading to the imbalance between inflammation and anti-inflammation.

The activated stress pathways can initiate or exacerbate inflammation and culminate in hepatocyte cell death and liver damage by apoptosis Gentile et al. IL-1 family members might be involved in controlling insulin resistance and metabolic inflammation in various obesity-associated disorders Kamari et al. Chronic, low-grade inflammatory process is also the characteristic of diabetes.

Metabolism-controlling stress hormones, especially GCs and NE could exert anti-insulin effects, and in the long run induce insulin resistance. GC receptor antagonist RU and adrenalectomy reduce the occurrence of insulin resistance. lwi

High concentration of NE in plasma could raise fasting glucose and reduce glucose tolerance, possibly mediated by lipolysis and increased fatty acid concentrations Marangou et al. Adrenergic receptor activation may directly affect the insulin signaling pathway or cellular glucose transport Mulder et al.

Inflammation: The Common Pathway of Stress-Related Diseases

Additionally, GCs and NE could also regulate inflammation. In diabetes, elevated circulating levels of proinflammatory cytokines are originally thought to be the adipocytes themselves in response to obesity.

However, an increasing number of evidence suggests that obesity results in increased number of macrophages and changes in the activation status of these cells. Therefore, adipose tissue macrophages produce a significant proportion of the inflammatory factors that are upregulated by obesity Donath and Shoelson, Inflammatory cytokines produced by various cells such as Kupffer cells, macrophages, neutrophils, monocytes, adipocytes and hepatocytes, have critical roles in lipid metabolism and hepatic inflammation that promote liver damage.

Stressful experiences are fundamental in the provocation of major depression of disorder MDD.

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MAPK pathways have been proved to increase the activity of serotonin membrane transporters, the most important neurotransmitter associated with depression Zhu et al. The main idea of inflammatory depression is the activation of dm inflammatory immune response, particularly the synthesis of cytokines, which might influence neurochemicals and contribute to MDD Smith, Stress can facilitate the development of depressive-like behavior by promoting inflammatory cytokine expression Norman et al.

Additionally, a new pathway—kynurenine pathway KP has attracted much more attention in cytokine hypothesis. Proinflammatory cytokines activate KP to affect tryptophan metabolism and produce neurotoxin, which either reduces serotonin synthesis or fastens the reuptake of serotonin Miura et al.

Data from animal models and clinical patients prove the role of inflammation in depression.