MCP-1 Signaling Disrupts Social Behavior by Modulating Brain Volumetric Changes and Microglia Morphology


Por: Maldonado-Ruiz, Roger, Trujillo-Villarreal, Luis A., Montalvo-Martinez, Larisa, Fabian Mercado-Gomez, Octavio, Arriaga-Avila, Virginia, Garza-Ocanas, Lourdes, Ortiz-Lopez, Rocio, Garza-Villarreal, Eduardo A., Guevara-Guzman, Rosalinda, Camacho-Morales, Alberto

Publicada: 1 feb 2022 Ahead of Print: 1 nov 2021
Resumen:
Autism spectrum disorder (ASD) is a disease characterized by reduced social interaction and stereotypic behaviors and related to macroscopic volumetric changes in cerebellar and somatosensory cortices (SPP). Epidemiological and preclinical models have confirmed that a proinflammatory profile during fetal development increases ASD susceptibility after birth. Here, we aimed to globally identify the effect of maternal exposure to high-energy dense diets, which we refer to as cafeteria diet (CAF) on peripheral and central proinflammatory profiles, microglia reactivity, and volumetric brain changes related to assisting defective social interaction in the mice offspring. We found a sex-dependent effect of maternal exposure to CAF diet or inoculation of the dsARN mimetic Poly (I:C) on peripheral proinflammatory and social interaction in the offspring. Notably, maternal exposure to CAF diet impairs social interaction and favors an increase in anxiety in male but not female offspring. Also, CAF diet exposure or Poly (I:C) inoculation during fetal programming promote peripheral proinflammatory profile in the ASD-diagnosed male but not in females. Selectively, we found a robust accumulation of the monocyte chemoattractant protein-1 (MCP-1) in plasma of ASD-diagnosed males exposed to CAF during fetal development. Biological assessment of MCP-1 signaling in brain confirms that systemic injection of MCP-1-neutralizing antibody reestablished social interaction and blocked anxiety, accompanied by a reduction in cerebellar lobule X (CbX) volume and an increase volume of the primary somatosensory (SSP) cortex in male offspring. These data highlight the contribution of diet-dependent MCP-1 signaling on volumetric brain changes and microglia morphology promoting ASD-like behavior in male mice.

Filiaciones:
Maldonado-Ruiz, Roger:
 Univ Autonoma Nuevo Leon, Coll Med, Dept Biochem, Calle Dr Eduardo Aguirre Pequeno S-N, Monterrey 64460, Nuevo Leon, Mexico

 Univ Autonoma Nuevo Leon, Ctr Res & Dev Hlth Sci, Neurometab Unit, San Nicolas De Los Garza, Nuevo Leon, Mexico

Trujillo-Villarreal, Luis A.:
 Univ Autonoma Nuevo Leon, Coll Med, Dept Biochem, Calle Dr Eduardo Aguirre Pequeno S-N, Monterrey 64460, Nuevo Leon, Mexico

 Univ Autonoma Nuevo Leon, Ctr Res & Dev Hlth Sci, Neurometab Unit, San Nicolas De Los Garza, Nuevo Leon, Mexico

Montalvo-Martinez, Larisa:
 Univ Autonoma Nuevo Leon, Coll Med, Dept Biochem, Calle Dr Eduardo Aguirre Pequeno S-N, Monterrey 64460, Nuevo Leon, Mexico

 Univ Autonoma Nuevo Leon, Ctr Res & Dev Hlth Sci, Neurometab Unit, San Nicolas De Los Garza, Nuevo Leon, Mexico

Fabian Mercado-Gomez, Octavio:
 Univ Nacl Autonoma Mexico, Coll Med, Dept Physiol, Mexico City, DF, Mexico

Arriaga-Avila, Virginia:
 Univ Nacl Autonoma Mexico, Coll Med, Dept Physiol, Mexico City, DF, Mexico

Garza-Ocanas, Lourdes:
 Univ Autonoma Nuevo Leon, Coll Med, Dept Pharmacol & Toxicol, San Nicolas De Los Garza, Nuevo Leon, Mexico

Ortiz-Lopez, Rocio:
 Tecnol Monterrey, Sch Med & Hlth Sci, Monterrey, Mexico

Garza-Villarreal, Eduardo A.:
 Univ Nacl Autonoma Mexico, Inst Neurobiol, Mexico City, DF, Mexico

Guevara-Guzman, Rosalinda:
 Univ Nacl Autonoma Mexico, Coll Med, Dept Physiol, Mexico City, DF, Mexico

Camacho-Morales, Alberto:
 Univ Autonoma Nuevo Leon, Coll Med, Dept Biochem, Calle Dr Eduardo Aguirre Pequeno S-N, Monterrey 64460, Nuevo Leon, Mexico

 Univ Autonoma Nuevo Leon, Ctr Res & Dev Hlth Sci, Neurometab Unit, San Nicolas De Los Garza, Nuevo Leon, Mexico
ISSN: 08937648





MOLECULAR NEUROBIOLOGY
Editorial
Humana Press Inc., 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA, Estados Unidos America
Tipo de documento: Article
Volumen: 59 Número: 2
Páginas: 932-949
WOS Id: 000720612100003
ID de PubMed: 34797523