Previous research established a relationship between circulating sulfoconjugated norepinephrine (NE-SO4) and oxygen consumption at various exercise intensities. In this study, the stability of the NE-SO4 response was examined during sustained exercise at a constant relative intensity. Seven trained men bicycled at 78 +/- 3% of their maximal O2 consumption for 28 min and then rested on the ergometer for a comparable duration. After a 30-min rest, plasma samples were collected through an indwelling catheter at 7-min intervals during the exercise and recovery periods. Free NE and epinephrine increased sixfold during exercise. These changes were accompanied by increases in sulfoconjugated catecholamines, but only NE-SO4 achieved statistical significance (rest, 712 +/- 602; exercise, 1,329 +/- 1,163 pg/ml). This occurred at three collection periods (14, 21, and 28 min). Approximately 35, 52, and 95% of NE, epinephrine, and dopamine, respectively, existed as sulfoconjugated during exercise. Subject variation was present in the sulfoconjugated catecholamine response that could not be attributed to corresponding differences in circulating free catecholamine release. These findings implicate blood flow as a factor in the sulfoconjugation of NE, but not epinephrine or dopamine.
In the current study of MPXV infection in rhesus macaques, we analyzed the NK cell responses in absolute cell numbers, cell proliferation, chemokine receptor expression, and function. Our results showed that the absolute number of total NK cells in the blood increased in response to MPXV infection at a magnitude of 23-fold, manifested by similar increases in CD56+, CD16+ and CD16-CD56- double negative (DN) NK cells. Similarly, the frequency and NK cell number in the lymph nodes also largely increased with total NK cell number increasing nearly 50-fold. Ki67 staining showed that NK cells both in the blood and lymph nodes proliferated during acute infection. Chemokine analysis revealed an early reduction of CXCR3, CCR7 and CCR6 on NK cells, followed with an increased expression of CXCR3 and CCR5 at later time points (day 7). Furthermore, MPXV infection impaired NK cell degranulation and ablated secretion of IFN-g and TNF-a. Taken together, MPXV infection induced massive NK cell proliferation, but suppressed NK cell function.
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