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<p>Nasal inflammation-induced olfactory dysfunction is caused by sensory processing alterations in and beyond the olfactory epithelium, likely through the spreading of peripheral inflammation into the olfactory bulb (OB), damaging its neuronal computations. Although the consequences of chronic nasal inflammation have extensively described in animal models, their presence upon acute inflammation has not been evaluated. Thus, we tested whether acute nasal inflammation induced by a single lipopolysaccharide (LPS) intranasal application swiftly spreads into the OB, focusing on its microglia, interleukin 1 beta (IL-1β) levels, neuronal network activity, and olfactory function. We found that a single intranasal LPS application leads to early microglial morphological changes at OB granule cell-layer, along with increased IL-1β staining, the following day. Intranasal LPS application decreases slow OB network activity and increases fast OB network activity, while uncoupling its slow activity from breathing. Moreover, acute LPS-induced nasal inflammation dampens odor-induced OB network activation, correlating with deficient olfactory detection and discrimination. We conclude that acute LPS-induced nasal inflammation quickly spreads into the OB, mildly activating its microglia and disrupting its network activity and odor response, which likely contribute to olfactory impairment. These acute central nervous system alterations, whose mechanism remain to be determined, should be considered when diagnosing and treating inflammation-induced olfactory dysfunctions.</p>

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Lipopolysaccharide-Induced Nasal Inflammation Swiftly Spreads Into the Olfactory Bulb, Accelerating its Network Activity and Uncoupling it from Breathing

  • 期刊论文

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  • 发表日期：

    2026年2月23日

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  • Armando Ortega-Xique,
  • Benito Ordaz,
  • Jonathan-Julio Lorea-Hernández,
  • Fernando Peña-Ortega

摘要

Nasal inflammation-induced olfactory dysfunction is caused by sensory processing alterations in and beyond the olfactory epithelium, likely through the spreading of peripheral inflammation into the olfactory bulb (OB), damaging its neuronal computations. Although the consequences of chronic nasal inflammation have extensively described in animal models, their presence upon acute inflammation has not been evaluated. Thus, we tested whether acute nasal inflammation induced by a single lipopolysaccharide (LPS) intranasal application swiftly spreads into the OB, focusing on its microglia, interleukin 1 beta (IL-1β) levels, neuronal network activity, and olfactory function. We found that a single intranasal LPS application leads to early microglial morphological changes at OB granule cell-layer, along with increased IL-1β staining, the following day. Intranasal LPS application decreases slow OB network activity and increases fast OB network activity, while uncoupling its slow activity from breathing. Moreover, acute LPS-induced nasal inflammation dampens odor-induced OB network activation, correlating with deficient olfactory detection and discrimination. We conclude that acute LPS-induced nasal inflammation quickly spreads into the OB, mildly activating its microglia and disrupting its network activity and odor response, which likely contribute to olfactory impairment. These acute central nervous system alterations, whose mechanism remain to be determined, should be considered when diagnosing and treating inflammation-induced olfactory dysfunctions.