Interleukin 1-beta but not the interleukin-1 receptor antagonist modulates inspiratory rhythm generation in vitro.

Interleukin 1-beta (IL-1β) is a cytokine that modulates breathing when applied systemically or directly into the brain. IL-1β is expressed, along with its receptors, in IL-1β-sensitive respiratory-related circuits, which likely include the inspiratory rhythm generator (the preBötzinger complex, preBötC). Thus, considering that IL-1β might directly modulate preBötC function, we tested whether IL-1β and its endogenous antagonist IL1Ra modulate inspiratory rhythm generation in the brainstem slice preparation containing the preBötC.

Microglial modulators reduce respiratory rhythm long-term facilitation in vitro.

Inflammation inhibits the expression of some, but not all forms of respiratory motor plasticity. For example, systemic application of lipopolysaccharide (LPS) inhibits the phrenic long-term facilitation induced by moderate-intermittent hypoxia in vivo. There are multiple pro-inflammatory processes triggered by the systemic application of LPS, including neuroinflammation in the CNS.

Hydrogen peroxide extracellular concentration in the ventrolateral medulla and its increase in response to hypoxia in vitro: Possible role of microglia.

Hydrogen peroxide (HO) is a messenger involved in both damaging neuroinflammatory responses and physiological cell communication. The ventrolateral medulla, which regulates several vital functions including breathing and blood pressure, is highly influenced by hydrogen peroxide, whose extracellular levels could be determined by hypoxia and microglial activity, both of which modulate ventrolateral medulla function. Therefore, in this study we aimed to test whether different patterns of hypoxia and/or putative microglial modulators change extracellular hydrogen peroxide in the ventrolateral medulla by using an enzymatic reactor online sensing procedure specifically designed for this purpose.