Leukocytes and epithelial cells are fundamental to antimi-crobial immunity. Their antimicrobial responses are an evolutionarily conserved component of the innate im-mune system and are influenced by the host’s response to external stimuli. The efficacy of host defense via anti-microbial responses derives from the ability of AMPs to rapidly identify and eradicate foreign microbes and acti-vate proinflammatory pathways, and from the capacity of later innate and adaptive immune responses to amplify protection through distinct biochemical mechanisms. Re-cent advances in neuroimmunology have identified a di-rect link between the neuroendocrine and immune sys-tems, where environmental stimuli are generally believed to promote a transient effect on the immune system in response to environmental challenges and are presum-ably brought back to baseline levels via neuroendocrine pathways. Stress is an environmental stimulus that flares from a variety of circumstances and has become en-grained in human society. Small bouts of stress are be-lieved to enhance the host’s immune response; however, prolonged periods of stress can be detrimental through excess production of neuroendocrine-derived mediators that dampen immune responses to invasive pathogens. Elucidation of the mechanisms behind stress-induced im-mune modulation of antimicrobial responses will ulti-mately lead to the development of more effective thera-peutic interventions for pathologic conditions. It is the in-tent of this review to broaden the existing paradigm of how stress-related molecules dampen immune re-sponses through suppression of antimicrobial mecha-nisms, and to emphasize that bacteria can use these fac-tors to enhance microbial pathogenesis during stress. J. Leukoc. Biol. 88: 000–000; 2010.

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We investigated whether inhalation of green odor (a mixture of equal amounts of trans-2-hexenal and cis-3-hexenol) prevents the skin-barrier disruption induced by chronic restraint stress in rats. To this end, transepidermal water loss (TEWL) was measured as an index of the disruption of skin-barrier function, whereas light- and electron-microscope examinations were performed to observe histological changes in the skin of the stressed animals. In addition, the effects on TEWL induced by chronic administration of a glucocorticoid, dexamethasone (DEX), were examined. Chronic restraint stress (8 h per day for 14 days) increased TEWL (vehicle + stress group). This effect (and the chronic stress–induced increase in adrenal weight) was prevented in rats that inhaled green odor at the beginning of each day’s restraint (2 h each day for 14 days; green odor + stress group). Electronmicroscope studies revealed that rats in the green odor + stress group possessed sufficient intercorneocyte lipids to create an effective skin barrier, although these had apparently been decreased in the vehicle + stress group. Daily administration of DEX for 14 days increased TEWL. The present results suggest that chronic stress–induced disruption of the skin barrier in rats can be reduced or prevented by green odor (possibly at least in part through an inhibitory effect on the stress-induced activation of the hypothalamo-pituitary-adrenocortical axis). Key words: adrenal gland, dexamethasone, hypothalamo-pituitary-adrenocortical axis, stratum corneum, transepidermal

Background: This study aimed to investigate the prevalence of temporomandibular disorder (TMD) among students of the University of Jordan. Methods: Information about the symptoms of TMD and the possible risk factors were collected using specifically designed questionnaires. The collected data sets were treated statistically using the SPSS release 14 package. Results: The results of the present investigation showed that pain in or about the ears or cheeks was the most prevalent symptom whereas locking of the temporomandibular joint (TMJ) was the least prevalent. Nearly one-third of the investigated sample (31.4%, 346/1103) had no symptoms of TMD whereas 68.6 % (757/1103) had at least one symptom. Students of health science studies had significantly the highest risk in developing TMJ clicking compared to students studying pure science or humanitarian studies. Conclusions: TMD is of a high prevalence among students of the

Objective: To examine the effect of a brief laboratory stressor and social support before the stressor on cardiovascular and cortisol responses, and skin barrier recovery after skin disruption. Methods: Eighty-five healthy participants (mean age 22.9 4.4 years) underwent a “tape-stripping ” procedure that disrupts normal skin barrier function, and were randomly assigned to a No Stress (reading task), Stress (Trier Social Stress Test), or Stress Social Support condition (support from a confederate before the stressor). Skin barrier recovery was assessed by measuring transepidermal water loss from up to 2 hours after skin disruption. Results: Compared with the No Stress condition, the stressor delayed skin barrier recovery by 10 % at 2 hours after skin disruption (effect size, r .29), and increased anxiety (r .24), negative affect (r .22), cardiovascular activity (r values from.4–.6), and among male participants, cortisol levels (r .40). Social support did not influence psychological or physiological responses or skin barrier recovery. Larger physiological responses to the tasks did not predict slower skin barrier recovery. Instead, larger systolic blood pressure responses predicted faster skin barrier recovery (r .26). Conclusions: This study replicated the effects of short-term laboratory stressors on skin barrier recovery, further establishing the relevance of skin barrier recovery for future research. The support manipulation did not influence physiological responses or skin barrier recovery, suggesting that future research on social support, physiology, and objective health outcomes should focus on naturalistic social interactions, relationships, and stressors. Key words: acute stress, social support, wound healing, cardiovascular reactivity, cortisol, skin barrier recovery. AUCI area under the curve with respect to increase; BMI body mass index; DBP diastolic blood pressure; GCRC General Clinical Research Center; HR heart rate; MAP mean arterial pressure; SBP systolic blood pressure; TSST Trier Social Stress Test; TEWL transepidermal water loss.

Abstract: Atopic dermatitis is a chronic inflammatory skin disease with a steadily increasing prevalence affecting 10-20 % of infants and 1-3 % of adults globally. It is often the first clinical manifestation of atopic disease preceding asthma and allergic rhinitis. Probably half of the children with atopic dermatitis devel-op some other form of atopic disease later in life. The pathogenesis involves a complex interplay of fac-tors including genetic predisposition due to altered immune or skin barrier function, interactions with the environment such as food and allergen exposures, and infectious triggers of inflammation. In this review, we summarize the recent advances in understanding the contribution of different factors in the pathophysiology

Copyright © 2015 Cody J. Connor et al.This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Psoriasis is a chronic, immune-mediated skin condition with a high rate of psychiatric comorbidity, which often goes unrecognized. Beyond the negative consequences of mood disorders like depression and anxiety on patient quality of life, evidence suggests that these conditions can worsen the severity of psoriatic disease. The mechanisms behind this relationship are not entirely understood, but inflammation seems to be a key feature linking psoriasis with mood disorders, and physiologic modulators of this inflammation, including the hypothalamic-pituitary-adrenal axis and sympathetic nervous system, demonstrate changes with psychopathology that may be contributory. Cyclical disruptions in the secretion of the sleep hormone, melatonin, are also observed in both depression and psoriasis, and with well-recognized anti-inflammatory and antioxidant activity, this aberration may represent a shared contributor to both conditions as well as common comorbidities like diabetes and cardiovascular disease. While understanding the complexities of the biological mechanisms at play will be key in optimizing the management of patients with comorbid psoriasis and depression/anxiety, one thing is certain: recognition of psychiatric comorbidity is an imperative first