Immune-mediated impairment of tonic immobility defensive behavior in an experimental model of colonic inflammation.

Leda Menescal-de-Oliveira, Mariulza Rocha Brentegani, Fernanda Pincelli Teixeira, Humberto Giusti, Rafael Simone Saia

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Article in Pflugers Archiv : European journal of physiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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Leda Menescal-de-OliveiraDepartment of Physiology, Ribeirão Preto Medical School, University of São Paulo, Avenida Dos Bandeirantes, 3900, Ribeirão Preto, São Paulo, 14049-900, Brazil.

Mariulza Rocha BrenteganiDepartment of Physiology, Ribeirão Preto Medical School, University of São Paulo, Avenida Dos Bandeirantes, 3900, Ribeirão Preto, São Paulo, 14049-900, Brazil.

Fernanda Pincelli TeixeiraDepartment of Physiology, Ribeirão Preto Medical School, University of São Paulo, Avenida Dos Bandeirantes, 3900, Ribeirão Preto, São Paulo, 14049-900, Brazil.

Humberto GiustiDepartment of Physiology, Ribeirão Preto Medical School, University of São Paulo, Avenida Dos Bandeirantes, 3900, Ribeirão Preto, São Paulo, 14049-900, Brazil.

Rafael Simone SaiaDepartment of Physiology, Ribeirão Preto Medical School, University of São Paulo, Avenida Dos Bandeirantes, 3900, Ribeirão Preto, São Paulo, 14049-900, Brazil. rssaia@fmrp.usp.br.

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6 · The paper itself

Abstract

Ulcerative colitis has been associated with psychological distress and an aberrant immune response. The immunomodulatory role of systemic cytokines produced during experimental intestinal inflammation in tonic immobility (TI) defensive behavior remains unknown. The present study characterized the TI defensive behavior of guinea pigs subjected to colitis induction at the acute stage and after recovery from intestinal mucosa injury. Moreover, we investigated whether inflammatory mediators (tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-8, IL-10, and prostaglandins) act on the mesencephalic nucleus, periaqueductal gray matter (PAG). Colitis was induced in guinea pigs by intrarectal administration of acetic acid. The TI defensive behavior, histology, cytokine production, and expression of c-FOS, IBA-1, and cyclooxygenase (COX)-2 in PAG were evaluated. Colitis reduced the duration of TI episodes from the first day, persisting throughout the 7-day experimental period. Neuronal c-FOS immunoreactivity was augmented in both columns of the PAG (ventrolateral (vlPAG) and dorsal), but there were no changes in IBA-1 expression. Dexamethasone, infliximab, and parecoxib treatments increased the duration of TI episodes, suggesting a modulatory role of peripheral inflammatory mediators in this behavior. Immunoneutralization of TNF-α, IL-1β, and IL-8 in the vlPAG reversed all effects produced by colitis. In contrast, IL-10 neutralization further reduced the duration of TI episodes. Our results reveal that peripherally produced inflammatory mediators during colitis may modulate neuronal functioning in mesencephalic structures such as vlPAG.

Indexed as

ColitisAnimalsCyclooxygenase 2CytokinesDexamethasoneDisease Models, AnimalGuinea PigsImmobility Response, TonicInfliximabMalePeriaqueductal GrayProto-Oncogene Proteins c-fosCyclooxygenase 2CytokinesDexamethasoneInfliximabProto-Oncogene Proteins c-fosColitisCyclooxygenase-2CytokinesInflammatory responseInfliximabInterleukinMicrogliaNeuronal activationPeriaqueductal gray matterTumor necrosis factor

Identifiers

PMID39218820

DOI10.1007/s00424-024-03011-1

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