Proinflammatory cytokines like interleukin-1 beta (IL-1 beta) affect the
control of breathing. Our aim is to determine the effect of the
anti-inflammatory cytokine IL-10 on the control of breathing. IL-10
knockout mice (IL-10(-/-), n = 10) and wild-type mice (IL-10(+/+), n =
10) were exposed to the following test gases: hyperoxic hypercapnia 7%
CO2-93% O-2, normoxic hypercapnia 7% CO2-21% O-2, hypoxic hypercapnia
7% CO2-10% O-2, and hypoxic normocapnia 3% CO2-10% O-2. The
ventilatory function was assessed using whole body plethysmography.
Recombinant mouse IL-10 (rIL-10; 10 mu/kg) was administered
intraperitoneally to wild-type mice (n = 10) 30 min before the onset of
gas challenge. IL-10 was administered in neonatal medullary slices
(10-30 ng/ml, n = 8). We found that IL-10(-/-) mice exhibited
consistently increased frequency and reduced tidal volume compared with
IL-10(+/+) mice during room air breathing and in all test gases (by
23.62 to 33.2%, P < 0.05 and -36.23 to -41.69%, P < 0.05,
respectively). In all inspired gases, the minute ventilation of
IL-10(-/-) mice was lower than IL-10(+/+) (by -15.67 to -22.74%, P <
0.05). The rapid shallow breathing index was higher in IL-10(-/-) mice
compared with IL-10(+/+) mice in all inspired gases (by 50.25 to 57.5%,
P < 0.05). The intraperitoneal injection of rIL-10 caused reduction of
the respiratory rate and augmentation of the tidal volume in room air
and also in all inspired gases (by -12.22 to -29.53 and 32.18 to
45.11%, P < 0.05, respectively). IL-10 administration in neonatal rat
(n = 8) in vitro rhythmically active medullary slice preparations did
not affect either rhythmicity or peak amplitude of hypoglossal nerve
discharge. In conclusion, IL-10 may induce a slower and deeper pattern
of breathing