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CORRECTION article

Front. Pharmacol., 26 November 2025

Sec. Neuropharmacology

Volume 16 - 2025 | https://doi.org/10.3389/fphar.2025.1733683

Correction: Lack of the Nlrp3 inflammasome improves mice recovery following traumatic brain injury

This article is a correction to:

  1. Lack of the Nlrp3 Inflammasome Improves Mice Recovery Following Traumatic Brain Injury

    1. Read original article
Natasha IrreraNatasha Irrera1Gabriele PizzinoGabriele Pizzino1Margherita CalMargherita Calò2Giovanni PallioGiovanni Pallio1Federica ManninoFederica Mannino1Fausto FamFausto Famà3Vincenzo ArcoraciVincenzo Arcoraci1Vincenzo FodaleVincenzo Fodale3Antonio DavidAntonio David3Francesca CosentinoFrancesca Cosentino3Letteria MinutoliLetteria Minutoli1Emanuela MazzonEmanuela Mazzon4Placido BramantiPlacido Bramanti4Francesco Squadrito Francesco Squadrito1*Domenica AltavillaDomenica Altavilla5Alessandra BittoAlessandra Bitto1
  • 1Department of Clinical and Experimental Medicine, AOU Policlinico G. Martino, University of Messina, Messina, Italy
  • 2Department of Veterinary Sciences, University of Messina, Messina, Italy
  • 3Department of Human Pathology, AOU Policlinico G. Martino, University of Messina, Messina, Italy
  • 4IRCCS Centro Neurolesi “Bonino-Pulejo”, Messina, Italy
  • 5Department of Biomedical and Dental Sciences and Morphological and Functional Sciences, AOU Policlinico G. Martino, University of Messina, Messina, Italy

A Correction on
Lack of the Nlrp3 inflammasome improves mice recovery following traumatic brain injury

by Irrera N, Pizzino G, Calò M, Pallio G, Mannino F, Famà F, Arcoraci V, Fodale V, David A, Cosentino F, Minutoli L, Mazzon E, Bramanti P, Squadrito F, Altavilla D and Bitto A (2017). Front. Pharmacol. 8:459. doi: 10.3389/fphar.2017.00459

In the published article, there was an error in Figures 3B,D, 5B,D,G,I as published. The previously published images were erroneously labeled in the source file. The corrected Figures 3B,D, 5B,D,G,I and their captions appear below.

Figure 3
Histological images of brain sections showing comparisons across Sham-WT, WT-TBI, and WT-TBI with BAY 11-7082 groups. Each row corresponds to a condition, with sections from cortex (A, F, K), hippocampus CA1 (B, G, L), CA3 (C, H, M), and stratum lacunosum moleculare (E, J, O). Differences, including tissue damage indicated by arrows, are visible between conditions.

Figure 3. Representative H&E staining of brain tissue from WT animals 24 h following TBI. (A) Cortex of Sham-WT animal. Original magnification X5. (B) Hippocampus of Sham-WT animal. The rectangle indicates the Ca1, Ca3, and stratus lacunosum moleculare areas used for enlargement. Original magnification X5. (C) Ca1 area of Sham-WT animal. Original magnification X40. (D) Ca3 area of Sham-WT animal. Original magnification X40. (E) Stratus lacunosum moleculare of Sham-WT animal. Original magnification X20. (F) Cortex of WT-TBI animal, the arrow indicates the impact point, hemorrhage and edema are markedly visible. Original magnification X5. (G) Hippocampus of WT-TBI animal. The rectangle indicates the Ca1 and Ca3 areas used for enlargement. Original magnification X5. (H) Ca1 area of WT-TBI animal, showing loss of normal architecture, presence of hemorrhage and edema, with shrank neurons. Original magnification X40. (I) Ca3 area of WT-TBI animal, showing diffused neuronal loss and presence of eosinophil neurons (arrows). Original magnification X40. (J) Stratus lacunosum moleculare of WT-TBI animal, showing hemorrhage and edema. Original magnification X20. (K) Cortex of WT-TBI + BAY 11-7082 animal, the arrow indicates the impact point, hemorrhage and edema are markedly visible. Original magnification X5. (L) Hippocampus of WT-TBI + BAY 11-7082 animal. The rectangle indicates the Ca1, Ca3, and stratus lacunosum moleculare areas used for enlargement. Original magnification X5. (M) Ca1 area of WT-TBI + BAY 11-7082 animal, showing a more preserved architecture, without hemorrhage or edema. Original magnification X40. (N) Ca3 area of WT-TBI + BAY 11-7082 animal, showing slight neuronal loss and presence of shrank and eosinophil neurons (arrows). Original magnification X40. (O) Stratus lacunosum moleculare of WT-TBI + BAY 11-7082 animal, showing a more preserved architecture. Original magnification X20.

Figure 5
Histological images showing cortex and hippocampus regions in WT-TBI (A-E) and NLRP3-/- TBI (F-J) mice. Panels illustrate different areas and a bar graph (K) compares histological scores on the seventh day between WT-TBI and NLRP3-/- TBI groups.

Figure 5. Representative H&E staining of brain tissue from WT and NLRP3−/− mice 7 days following TBI. (A) Cortex of WT-TBI animal, the arrow indicates the impact point, hemorrhage and edema are still markedly visible. Original magnification X5. (B) Hippocampus of WT-TBI animal. The rectangle indicates the Ca1, Ca3, and stratus lacunosum moleculare areas used for enlargement. Original magnification X5. (C) Ca1 area of WT-TBI animal, showing partial restoration of normal architecture with shrank neurons. Original magnification X40. (D) Ca3 area of WT-TBI animal, showing neuronal loss and presence of eosinophil neurons (arrows). Original magnification X40. (E) Stratus lacunosum moleculare of WT-TBI animal, showing partially restored architecture. Original magnification X20. (F) Cortex of NLRP3−/−-TBI animal, the arrow indicates the impact point, hemorrhage and edema are markedly visible. Original magnification X5. (G) Hippocampus of NLRP3−/−-TBI animal. The rectangle indicates the Ca1, Ca3, and stratus lacunosum moleculare areas used for enlargement. Original magnification X5. (H) Ca1 area of NLRP3−/−-TBI animal, showing a preserved architecture, absence of hemorrhage and edema, with few shrank neurons. Original magnification X40. (I) Ca3 area of NLRP3−/−-TBI animal, showing neuronal loss and presence of eosinophil neurons (arrows). Original magnification X40. (J) Stratus lacunosum moleculare of NLRP3−/−-TBI animal, showing an almost normal architecture. Original magnification X20. (K) The graph represents the cumulative histological score evaluated at 7 days from each group of animals. §p < 0.05 vs. WT-TBI. Each bar represents the mean and SD of seven animals.

Author Francesca Cosentino was incorrectly written as Cosentino Francesca.

The original article has been updated.

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All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

Keywords: NLRP3 inflammasome, traumatic brain injury, inflammation, cytokines, apoptosis

Citation: Irrera N, Pizzino G, Calò M, Pallio G, Mannino F, Famà F, Arcoraci V, Fodale V, David A, Cosentino F, Minutoli L, Mazzon E, Bramanti P, Squadrito F, Altavilla D and Bitto A (2025) Correction: Lack of the Nlrp3 inflammasome improves mice recovery following traumatic brain injury. Front. Pharmacol. 16:1733683. doi: 10.3389/fphar.2025.1733683

Received: 27 October 2025; Accepted: 03 November 2025;
Published: 26 November 2025.

Edited and reviewed by:

Jacob Raber, Oregon Health and Science University, United States

Copyright © 2025 Irrera, Pizzino, Calò, Pallio, Mannino, Famà, Arcoraci, Fodale, David, Cosentino, Minutoli, Mazzon, Bramanti, Squadrito, Altavilla and Bitto. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

*Correspondence: Francesco Squadrito, ZnNxdWFkcml0b0B1bmltZS5pdA==

Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.