Expression and functioning of glucocorticoid receptors

Chronic stress has been shown to and, ultimately, to worsen clinical symptoms of asthma (Chen and Miller, 2007, Haczku and Panettieri, 2010, Landeo- Gutierrez and Celedn, 2020, Rosenberg et al., 2014). a variety of and (Th) cells, such as Th-1 and Th-2 cells (Busse et al., 1993, Umetsu et al., 2002). Th-1 cells perpetuate cellular immune responses through the production of interferon- (IFN-) and interleukin-2 (IL-2), while Th-2 cells promote humoral responses through releasing cytokines such as IL-5 and IL-13 (Berger, 2000, Chen and Miller, 2007). One way chronic stress amplifies airway inflammation in asthma is by altering the glucocorticoid sensitivity of immune cells (Chen and Miller, 2007, Haczku and Panettieri, 2010). In the context of asthma, glucocorticoids are a class of steroid hormones that decrease the production of Th-1 (e.g., IFN-) and Th-2 (e.g., IL-5, IL-13) cytokines, thereby lowering the magnitude of airway inflammation (Banuelos and Lu, 2016). In humans, cortisol is the major glucocorticoid, and its release is regulated by the activation of the hypothalamicpituitaryadrenal axis. Persistent secretion of cortisol associated with repeated or chronic exposure to stressors may lead to reduced expression and functioning of glucocorticoid receptors (Miller et al., 2009). Dysfunctional glucocorticoid receptors are, thus, less sensitive to the immunosuppressive action of glucocorticoids (i.e., glucocorticoid resistance [GR]), contributing to the amplification of airway inflammation (Chen and Miller, 2007).

A few studies have linked low SES, as well as other chronic psychosocial stressors, to increased Th-1 and Th-2 cell resistance to glucocorticoids, which has been indexed by the capacity of cortisol to suppress Th-1 and Th-2 cytokine production by stimulated peripheral blood mononuclear cells (PBMCs) in vitro (Chen et al., 2016, Miller et al., 2009). For example, in a sample of children with asthma, Chen et al. (2016) found that lower family SES was associated with higher GR of Th-1 cytokines (e.g., IFN-) and Th-2 (e.g., IL-5, IL-13) cytokines in vitro. GR related to chronic stress may be particularly problematic for children with asthma, who, as a result, can exhibit resistance to corticosteroid medications, the most common therapy for asthma control (Barnes and Adcock, 2009). Identifying protective factors against the pernicious health consequences of stress-related GR is thus critical.

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A promising factor that may exert protective effects is positive parenting, which has been linked to multiple beneficial behavioral and psychological outcomes (Hoeve et al., 2009, McLeod et al., 2007) and more favorable health-related biological processes (Chen et al., 2011). Positive parenting

12/15/21, 5:09 PM Socioeconomic status, financial stress, and glucocorticoid resistance among youth with asthma: Testing the moderation effects o


is theorized to buffer the effects of SES primarily through its stress-buffering role that mitigates the toxic consequences of stress on health (Cohen and Wills, 1985). We investigated two forms of positive parenting, maternal involvement and warmth. Maternal involvement is a multifaceted construct that includes a broad range of behavioral, cognitive, and affective practices (e.g., monitoring, affective support) that mothers adopt to engage with childrens daily lives (Finzi- Dottan et al., 2016, Pleck, 2010). Maternal warmth refers to the acceptance, love, affection, comfort, nurturance, and care that mothers display towards their children (Khaleque and Rohner, 2012). Empirical evidence suggests that maternal involvement and warmth can act as stress- buffering factors in health outcomes (Chen et al., 2011, Cohen et al., 2020, Farrell et al., 2017, Figge et al., 2020). For example, maternal involvement reduced the risk of parent cultural stress on depressive and anxiety symptoms among children from low SES families (Figge et al., 2020). Similarly, maternal warmth was reported to buffer the risk of early socioeconomic disadvantage on adult health via reduced proinflammatory signaling (Chen et al., 2011).

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