Most infections begin at mucosal surfaces. These surfaces are covered by the secretory proteins of the exocrine glands (eg, the salivary, respiratory, and gastrointestinal glands), which provide a first line of innate defense. The release of these secretory proteins is under neuroendocrine control and thus, in theory, sensitive to modulation by psychosocial stress. This was empirically tested by measuring the salivary secretion of cystatin S, lactoferrin, α-amylase, the mucins MUC5B and MUC7, and total salivary protein in response to stressors known to evoke distinct patterns of cardiac autonomic activity.
Thirty-two undergraduate volunteers were each subjected to two laboratory stressors and a control condition. Stressors were an active coping memory test and a passive coping video presentation showing surgical procedures. In the control condition participants viewed a didactic video presentation.
The stressors evoked the expected distinct patterns of cardiac autonomic activity. The memory test produced a strong increase in sympathetic activity (evidenced by a shortened preejection period), and a decrease in cardiac parasympathetic activity (evidenced by a decrease in heart rate variability). This active coping response was associated with an enhanced secretion (μg/min, controlling for salivary flow rate) of MUC7, lactoferrin, α-amylase, and total salivary protein. Conversely, the surgical video produced an increase in cardiac vagal tone and a modest increase in sympathetic activity. This passive coping response was associated with an enhanced secretion of all proteins studied. These secretory responses were generally larger than the secretory responses during the active coping memory test. Correlation analyses indicated that for both stressors autonomic and cardiovascular reactivity was positively associated with an enhanced and prolonged secretory activity.
Stress-induced modulation of innate secretory immunity may be a contributing factor in the observed relationship between stress and susceptibility to infectious diseases. We further propose a more differentiated approach to acute stress by distinguishing among stressors with distinct autonomic nervous system effects.