Social temperament and lymph node innervation

Abstract

Socially inhibited individuals show increased vulnerability to viral infections, and this has been linked to increased activity of the sympathetic nervous system (SNS). To determine whether structural alterations in SNS innervation of lymphoid tissue might contribute to these effects, we assayed the density of catecholaminergic nerve fibers in 13 lymph nodes from 7 healthy adult rhesus macaques that showed stable individual differences in propensity to socially affiliate (Sociability). Tissues from Low Sociable animals showed a 2.8-fold greater density of catecholaminergic innervation relative to tissues from High Sociable animals, and this was associated with a 2.3-fold greater expression of nerve growth factor (NGF) mRNA, suggesting a molecular mechanism for observed differences. Low Sociable animals also showed alterations in lymph node expression of the immunoregulatory cytokine genes IFNG and IL4, and lower secondary IgG responses to tetanus vaccination. These findings are consistent with the hypothesis that structural differences in lymphoid tissue innervation might potentially contribute to relationships between social temperament and immunobiology.

Health Psychology: Developing Biologically Plausible Models Linking the Social World and Physical Health

“…Analyses of animals experimentally infected with SIV and randomly assigned to chronically threatening social conditions versus less stressful stable social conditions showed that social stress did indeed simultaneously increase SNS regulation of immune cells, undermine expression of antiviral cytokines, and accelerate replication of SIV (Sloan et al 2006(Sloan et al , 2007b(Sloan et al , 2008. Additional analyses showed that constitutional individual differences in sensitivity to social threat were also associated with increased SNS regulation of the lymph node tissues in which immune responses are initiated (Sloan et al 2007a). Thus, experimental model systems and naturally occurring analogues of the original socioepidemiologic relationship both support the overarching hypothesis that relationships between social behavior and HIV-1 disease progression are mediated by psychological threat responses that increase SNS signaling to the immune system and thereby alter leukocyte gene expression in ways that facilitate viral replication and accelerate the progression of clinical disease.…”

“…Likewise, multiple studies link psychosocial risk factors to HIV-1 disease progression , Cole et al 1997, Sloan et al 2007c). This link provided researchers with a rationale for subsequent analyses of the upstream biological processes that drive clinical disease progression (e.g., viral replication, innate immune responses; Cole et al 2001Cole et al , 2003, which ultimately led to the identification of specific molecular mechanisms mediating the effects of stress-induced neuroendocrine dynamics on HIV-1 pathogenesis (Cole et al 1998(Cole et al , 1999(Cole et al , 2001Collado-Hidalgo et al 2006;Sloan et al 2006Sloan et al , 2007aSloan et al ,b, 2008. Thus, successful discovery of pathways mediating biobehavioral influences on disease depends critically on the availability of a good basic understanding of disease pathogenesis (to guide the bottom-up selection of specific pathophysiologic targets) and the identification of a robust clinical phenomenon (to guide the top-down targeting of specific psychobiologic pathways).…”

Changes in the content of neuropeptides in intestinal lymph nodes of pigs suffering from experimental Brachyspira hyodysenteriae infection

“…Lymph nodes from Low Sociable animals showed much higher density of adrenergic innervation than lymph nodes from High Sociable animals (Sloan et al, 2008). This phenomenon may be explained by the fact of the existence of beta-adrenergic receptors in the cells of the immune system present, among others, in lymph nodes .…”

“…Additionally, there is a possibility that SP and VIP are involved in the mechanism of sensitization of immune cells in the lymphatic tissue (Enzmann and Drossler, 1994), and VIP and PACAP specifically modulate the expression of different cytokines (Martinez et al, 1996). What more, evidences suggest that there is a strong psychoneurological influence on functions of the immune system (Weihe et al, 1991;Panuncio et al, 1999;Sloan et al, 2008). These findings open new questions on the role of biologically active substances being neurotransmitters or neuromodulators in pathological processes.…”

Neuroimmunology

“…Recently, it was reported that social stress (Sloan et al, 2007b(Sloan et al, , 2008a, simian immunodeficiency virus (Sloan et al, 2008b), and social temperament (Sloan et al, 2007a) are able to affect the level of sympathetic innervation within lymphoid tissue, suggesting that if a toxicant affects these factors, an indirect immune toxicity might develop due to changes in the amount of NE available for release during an immune reaction. Likewise, compounds such as carbon disulfide (Caroldi and De Paris, 1995;Mckenna and Distefano, 1977) affect the synthesis of NE.…”