A recent study by Nicole Powell et al. published in the October 8, 2013 issue of PNAS, suggests that stress hormones may contribute to pro-inflammation through selective expansion and/or recruitment of a specific subpopulation of immature, proinflammatory monocytes.
In the 1970s and 1980s stress was often considered immunosuppressive. Recent evidence, however, indicates that psychological stress influences immunity in a less monochromatic way, but at multiple levels and can be in either direction, in terms of its pro- or anti-inflammatory effects.
One mechanism of how stress may boost inflammation – is through the effects of stress hormones on the induction of migration and recruitment of immune cells.
In fact, stress hormones such as catecholamines (the end products of the sympathetic nervous system) are able to modify the circulation and cell trafficking of virtually all immune cells, such as lymphocytes, polymorphonuclear cells, monocytes, dendritic cells and NK cells.
The bone marrow is extensively innervated. Previous research indicates that in the bone marrow, catecholamines originate mostly from the sympathetic nerve fibers, and myelopoiesis is negatively affected by α1-adrenoreceptors expressed on bone marrow cells (Maestroni GJ et al., Blood. 1992, 80:1178).
The PNAS study of Powell et al. demonstrates the ability of the sympathetic nervous system, through a β-adrenoreceptor-mediated mechanism to increase the myelopoietic output of immature proinflammatory monocytes (Ly-6chigh in mice and CD14+/CD16− in humans).
According to the authors this mechanism may have evolved to help the immune system anticipate wound-related bacterial infections, however, in contemporary social environments, it may promote chronic inflammation.
Thus, taken as a whole, the study may identify an additional mechanism by which adverse social environments and stress can enhance the risk of inflammation-related diseases in susceptible individuals.
Source: Proc Natl Acad Sci U S A, 2013, 110:16574-9. doi: 10.1073/pnas.1310655110. Epub 2013 Sep 23
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