Endotoxemia increases heart (HR) and respiratory (fR) rates and disrupts cardio‐respiratory coupling (CRC). We previously identified expression of proinflammatory cytokines in the nTS during endotoxemia which was associated with increases in HR and fR, as well as uncoupling of cardio‐respiratory patterns. We hypothesized that microinjection of the proinflammatory cytokine IL‐1β into the nTS would increase HR, fR, and alter cardio‐ventilatory coupling (CVC), defined as the significant tendency for a heartbeat to occur at a preferred latency prior to the next breath. To test this hypothesis, we injected IL‐1β (0.5 ng, n=8) bilaterally into the nTS of anesthetized (isoflurane) spontaneously breathing adult male Harlan Sprague‐Dawley rats (n=12) and recorded diaphragmatic electromyogram (EMG) and electrocardiogram (ECG). 2h after focal injections of IL‐1β, fR increased 32% (from 42.9 ± 2.2 to 57.0±15 brths/min; p<0.05). CVC was analyzed with custom software and χ2 from multi‐ordered histograms was calculated. 2h post IL1‐β injection, the average χ2 value reduced from 40.76 ± 5.9 to 15.91 ± 3.6 (p<0.001) indicating loss of CVC. We conclude that exogenous IL‐1β injections into the nTS (reduced model of brainstem inflammation) reproduces some of the cardiorespiratory changes observed in experimental endotoxemia, and may contribute to altered cardio‐respiratory coupling.