A murine model of stress controllability attenuates Th2-dominant airway inflammatory responses

Abstract

Epidemiological and experimental studies suggest a positive correlation between chronic respiratory inflammatory disease and the ability to cope with adverse stress. Interactions between neuroendocrine and immune systems are believed to provide insight toward the biological mechanisms of action. The utility of an experimental murine model was employed to investigate the immunological consequences of stress-controllability and ovalbumin-induced airway inflammation. Pre-conditioned uncontrollable stress exacerbated OVA-induced lung histopathological changes that were typical of Th2-predominant inflammatory response along respiratory tissues. Importantly, mice given the ability to exert control over aversive stress attenuated inflammatory responses and reduced lung pathology. This model represents a means of investigating the neuro-immune axis in defining mechanisms of stress and respiratory disease.

Abuse during childhood and adolescence and risk of adult-onset asthma in African American women

“…27 In a mouse model of allergic airway inflammation, stress was observed to worsen the histopathologic changes of inflammation in the airways. 28 Alternatively, stress in childhood could lead to long-lasting or even permanent alterations in the immune system, the airways, or the autonomic nervous system that predispose to the development of asthma decades after the abuse occurred. During infancy and early childhood, adaptive immunity is undergoing maturation and the airways are undergoing growth and epithelial changes.…”

Corticotropin-releasing hormone receptor-1 and 2 activity produces divergent resistance against stress-induced pulmonary Streptococcus pneumoniae infection

“…Mal-adaptation to external and perceived threats considered life stressors are considered to impact the susceptibility and severity of disease states including: infectious disease and non-infectious chronic disease (Cohen et al, 1991; Glaser et al, 1992; Vedhara et al, 1999; Joachim et al, 2003; Deshmukh et al, 2010). Because immune function is central to the resolution and progression of disease states, interactions between the immune and central nervous systems are proposed to be a defining link, which explains the role of stress on disease outcomes.…”

“…genetic, perception) and/or environmental factors (e.g. type or quality of the stressor) (Cohen et al, 1993; Gonzalez-Gay et al, 2003; Ziaian et al, 2006; Gonzales et al, 2008; Turyk et al, 2008; Wang et al, 2008; Bailey et al, 2009; Kimura et al, 2009; Schwabe et al, 2009; Deshmukh et al, 2010; Heffner, 2011). Elevations in glucocorticoids for example, have been shown to suppress cell-mediated immune responses resulting in susceptibility to infectious and non-infectious disease states (Ferrari, 2003; Schwabe et al, 2009; Solodushko et al, 2009; Elftman et al, 2010; Smets et al, 2010; Sommershof et al, 2011).…”

“…There is an increased awareness of the role that stressors play in the susceptibility and progression of respiratory diseases (Cohen et al, 1997, 1999; Chen and Miller, 2007; Gonzales et al, 2008; Bailey et al, 2009; Kimura et al, 2009; Deshmukh et al, 2010). In particular, Streptococcus pneumoniae infection accounts for a majority of community-acquired illnesses, (Pachon et al, 1990; File, 2004) and complications from pneumococcal infection are responsible for 1.1 million deaths annually (Hoskins et al, 2001) for which stress is a notable risk factor.…”

Childhood abuse and adult-onset asthma among Peruvian women

“…The mice demonstrated stress-induced narrowed airways and goblet cell hyperplasia, which are known features of human asthma pathogenesis. [32, 33] Regardless of the pathophysiologic processes involved, a small but growing literature supports the thesis that adversity during childhood, particularly, childhood physical and sexual abuse, may be associated with chronic lung disorders including adult-onset asthma. [18]…”