King's College London

Research portal

Transient Receptor Potential Canonical Channels 4 and 5 Mediate Escherichia coli-Derived Thioredoxin Effects in Lipopolysaccharide-Injected Mice

Research output: Contribution to journalArticle

Standard

Transient Receptor Potential Canonical Channels 4 and 5 Mediate Escherichia coli-Derived Thioredoxin Effects in Lipopolysaccharide-Injected Mice. / Pereira, Domingos M.S.; Mendes, Saulo J.F.; Alawi, Khadija; Thakore, Pratish; Aubdool, Aisah; Sousa, Nágila C.F.; da Silva, João F.R.; Castro, José A.; P Pereira, Ione C.; Silva, Luís C.N.; Grisotto, Marcos A.G.; Monteiro-Neto, Valério; Costa, Soraia K.P.; da Costa, Robson; Calixto, João B.; Brain, Susan D.; Fernandes, Elizabeth S.

In: Oxidative Medicine and Cellular Longevity, Vol. 2018, 10.06.2018.

Research output: Contribution to journalArticle

Harvard

Pereira, DMS, Mendes, SJF, Alawi, K, Thakore, P, Aubdool, A, Sousa, NCF, da Silva, JFR, Castro, JA, P Pereira, IC, Silva, LCN, Grisotto, MAG, Monteiro-Neto, V, Costa, SKP, da Costa, R, Calixto, JB, Brain, SD & Fernandes, ES 2018, 'Transient Receptor Potential Canonical Channels 4 and 5 Mediate Escherichia coli-Derived Thioredoxin Effects in Lipopolysaccharide-Injected Mice', Oxidative Medicine and Cellular Longevity, vol. 2018. https://doi.org/10.1155/2018/4904696

APA

Pereira, D. M. S., Mendes, S. J. F., Alawi, K., Thakore, P., Aubdool, A., Sousa, N. C. F., ... Fernandes, E. S. (2018). Transient Receptor Potential Canonical Channels 4 and 5 Mediate Escherichia coli-Derived Thioredoxin Effects in Lipopolysaccharide-Injected Mice. Oxidative Medicine and Cellular Longevity, 2018. https://doi.org/10.1155/2018/4904696

Vancouver

Pereira DMS, Mendes SJF, Alawi K, Thakore P, Aubdool A, Sousa NCF et al. Transient Receptor Potential Canonical Channels 4 and 5 Mediate Escherichia coli-Derived Thioredoxin Effects in Lipopolysaccharide-Injected Mice. Oxidative Medicine and Cellular Longevity. 2018 Jun 10;2018. https://doi.org/10.1155/2018/4904696

Author

Pereira, Domingos M.S. ; Mendes, Saulo J.F. ; Alawi, Khadija ; Thakore, Pratish ; Aubdool, Aisah ; Sousa, Nágila C.F. ; da Silva, João F.R. ; Castro, José A. ; P Pereira, Ione C. ; Silva, Luís C.N. ; Grisotto, Marcos A.G. ; Monteiro-Neto, Valério ; Costa, Soraia K.P. ; da Costa, Robson ; Calixto, João B. ; Brain, Susan D. ; Fernandes, Elizabeth S. / Transient Receptor Potential Canonical Channels 4 and 5 Mediate Escherichia coli-Derived Thioredoxin Effects in Lipopolysaccharide-Injected Mice. In: Oxidative Medicine and Cellular Longevity. 2018 ; Vol. 2018.

Bibtex Download

@article{1db6514ebfb74ef587eb90998749ca58,
title = "Transient Receptor Potential Canonical Channels 4 and 5 Mediate Escherichia coli-Derived Thioredoxin Effects in Lipopolysaccharide-Injected Mice",
abstract = "Thioredoxin plays an essential role in bacterial antioxidant machinery and virulence; however, its regulatory actions in the host are less well understood. Reduced human Trx activates transient receptor potential canonical 5 (TRPC5) in inflammation, but there is no evidence of whether these receptors mediate bacterial thioredoxin effects in the host. Importantly, TRPC5 can form functional complexes with other subunits such as TRPC4. Herein, E. coli-derived thioredoxin induced mortality in lipopolysaccharide- (LPS-) injected mice, accompanied by reduction of leukocyte accumulation, regulation of cytokine release into the peritoneum, and impairment of peritoneal macrophage-mediated phagocytosis. Dual TRPC4/TRPC5 blockade by ML204 increased mortality and hypothermia in thioredoxin-treated LPS mice but preserved macrophage's ability to phagocytose. TRPC5 deletion did not alter body temperature but promoted additional accumulation of peritoneal leukocytes and inflammatory mediator release in thioredoxin-administered LPS mice. Thioredoxin diminished macrophage-mediated phagocytosis in wild-type but not TRPC5 knockout animals. TRPC5 ablation did not affect LPS-induced responses. However, ML204 caused mortality associated with exacerbated hypothermia and decreased peritoneal leukocyte numbers and cytokines in LPS-injected mice. These results suggest that bacterial thioredoxin effects under LPS stimuli are mediated by TRPC4 and TRPC5, shedding light on the additional mechanisms of bacterial virulence and on the pathophysiological roles of these receptors.",
author = "Pereira, {Domingos M.S.} and Mendes, {Saulo J.F.} and Khadija Alawi and Pratish Thakore and Aisah Aubdool and Sousa, {N{\'a}gila C.F.} and {da Silva}, {Jo{\~a}o F.R.} and Castro, {Jos{\'e} A.} and {P Pereira}, {Ione C.} and Silva, {Lu{\'i}s C.N.} and Grisotto, {Marcos A.G.} and Val{\'e}rio Monteiro-Neto and Costa, {Soraia K.P.} and {da Costa}, Robson and Calixto, {Jo{\~a}o B.} and Brain, {Susan D.} and Fernandes, {Elizabeth S.}",
year = "2018",
month = "6",
day = "10",
doi = "10.1155/2018/4904696",
language = "English",
volume = "2018",
journal = "Oxidative Medicine and Cellular Longevity",
issn = "1942-0900",
publisher = "Hindawi Publishing Corporation",

}

RIS (suitable for import to EndNote) Download

TY - JOUR

T1 - Transient Receptor Potential Canonical Channels 4 and 5 Mediate Escherichia coli-Derived Thioredoxin Effects in Lipopolysaccharide-Injected Mice

AU - Pereira, Domingos M.S.

AU - Mendes, Saulo J.F.

AU - Alawi, Khadija

AU - Thakore, Pratish

AU - Aubdool, Aisah

AU - Sousa, Nágila C.F.

AU - da Silva, João F.R.

AU - Castro, José A.

AU - P Pereira, Ione C.

AU - Silva, Luís C.N.

AU - Grisotto, Marcos A.G.

AU - Monteiro-Neto, Valério

AU - Costa, Soraia K.P.

AU - da Costa, Robson

AU - Calixto, João B.

AU - Brain, Susan D.

AU - Fernandes, Elizabeth S.

PY - 2018/6/10

Y1 - 2018/6/10

N2 - Thioredoxin plays an essential role in bacterial antioxidant machinery and virulence; however, its regulatory actions in the host are less well understood. Reduced human Trx activates transient receptor potential canonical 5 (TRPC5) in inflammation, but there is no evidence of whether these receptors mediate bacterial thioredoxin effects in the host. Importantly, TRPC5 can form functional complexes with other subunits such as TRPC4. Herein, E. coli-derived thioredoxin induced mortality in lipopolysaccharide- (LPS-) injected mice, accompanied by reduction of leukocyte accumulation, regulation of cytokine release into the peritoneum, and impairment of peritoneal macrophage-mediated phagocytosis. Dual TRPC4/TRPC5 blockade by ML204 increased mortality and hypothermia in thioredoxin-treated LPS mice but preserved macrophage's ability to phagocytose. TRPC5 deletion did not alter body temperature but promoted additional accumulation of peritoneal leukocytes and inflammatory mediator release in thioredoxin-administered LPS mice. Thioredoxin diminished macrophage-mediated phagocytosis in wild-type but not TRPC5 knockout animals. TRPC5 ablation did not affect LPS-induced responses. However, ML204 caused mortality associated with exacerbated hypothermia and decreased peritoneal leukocyte numbers and cytokines in LPS-injected mice. These results suggest that bacterial thioredoxin effects under LPS stimuli are mediated by TRPC4 and TRPC5, shedding light on the additional mechanisms of bacterial virulence and on the pathophysiological roles of these receptors.

AB - Thioredoxin plays an essential role in bacterial antioxidant machinery and virulence; however, its regulatory actions in the host are less well understood. Reduced human Trx activates transient receptor potential canonical 5 (TRPC5) in inflammation, but there is no evidence of whether these receptors mediate bacterial thioredoxin effects in the host. Importantly, TRPC5 can form functional complexes with other subunits such as TRPC4. Herein, E. coli-derived thioredoxin induced mortality in lipopolysaccharide- (LPS-) injected mice, accompanied by reduction of leukocyte accumulation, regulation of cytokine release into the peritoneum, and impairment of peritoneal macrophage-mediated phagocytosis. Dual TRPC4/TRPC5 blockade by ML204 increased mortality and hypothermia in thioredoxin-treated LPS mice but preserved macrophage's ability to phagocytose. TRPC5 deletion did not alter body temperature but promoted additional accumulation of peritoneal leukocytes and inflammatory mediator release in thioredoxin-administered LPS mice. Thioredoxin diminished macrophage-mediated phagocytosis in wild-type but not TRPC5 knockout animals. TRPC5 ablation did not affect LPS-induced responses. However, ML204 caused mortality associated with exacerbated hypothermia and decreased peritoneal leukocyte numbers and cytokines in LPS-injected mice. These results suggest that bacterial thioredoxin effects under LPS stimuli are mediated by TRPC4 and TRPC5, shedding light on the additional mechanisms of bacterial virulence and on the pathophysiological roles of these receptors.

UR - http://www.scopus.com/inward/record.url?scp=85055185180&partnerID=8YFLogxK

U2 - 10.1155/2018/4904696

DO - 10.1155/2018/4904696

M3 - Article

C2 - 29983857

AN - SCOPUS:85055185180

VL - 2018

JO - Oxidative Medicine and Cellular Longevity

JF - Oxidative Medicine and Cellular Longevity

SN - 1942-0900

ER -

View graph of relations

© 2018 King's College London | Strand | London WC2R 2LS | England | United Kingdom | Tel +44 (0)20 7836 5454