Glutamine suppresses dinitrophenol fluorobenzene-induced allergic contact dermatitis and itching: Inhibition of contact dermatitis by glutamine

Jin, Zhe Wu; Kim, Haekyoung; Lee, Chang‐Hoon; Jung, Sung-Won; Shin, Sook-Jeong; Im, Suhn-Young; Cho, Baik-Hwan; Lee, Hern-Ku

doi:10.1016/j.jdermsci.2012.05.012

Cited by 8 publications

(13 citation statements)

References 29 publications

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“…It has been reported that Gln attenuates itch evoked by DNFB-induced CD (Jin et al, 2012). In this study, we further examined the effects of Gln on itch evoked by histamine and CQ.…”

Section: Grk2 Knockdown Inhibits the Anti-itch Activity Of Glnmentioning

confidence: 97%

“…The nonessential amino acid L-glutamine (Gln) is abundant in plasma (Haussinger, 1998) and is an energy substrate for most cells (Encarnacion et al, 1998;Fox et al, 1996). We recently reported that Gln inhibited itching evoked by dinitrochlorobenzene (DNFB)-induced contact dermatitis (CD) in mice (Jin et al, 2012). We have shown that Gln has an anti-inflammatory ability by deactivating p38 MAPK and cytosolic phospholipase A2 via rapid induction of MAPK phosphatase (MKP)-1 (Ko et al, 2009;Lee et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

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GPCR Kinase (GRK)-2 Is a Key Negative Regulator of Itch: l-Glutamine Attenuates Itch via a Rapid Induction of GRK2 in an ERK-Dependent Way

Lee

Park

et al. 2018

Journal of Investigative Dermatology

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Many itch mediators activate GPCR and trigger itch via activation of GPCR-mediated signaling pathways. GPCRs are desensitized by GPCR kinases (GRKs). The aim of this study is to explore the role of GRKs in itch response and the link between GRKs and glutamine, an amino acid previously shown to be an itch reliever. Itch responses were evoked by histamine, chloroquine, and dinitrochlorobenzene-induced contact dermatitis (CD). Phosphorylation and protein expression were detected by immunofluorescent staining and Western blotting. GRK2 knockdown using small interfering RNA enhanced itch responses evoked by histamine, chloroquine, and dinitrochlorobenzene-induced CD, whereas GRK2 overexpression using GRK2-expressing adenovirus reduced the itch responses. Glutamine reduced all itch evoked by histamine, chloroquine, and dinitrochlorobenzene-induced CD. Glutamine-mediated inhibition of itch was abolished by GRK2 knockdown. Glutamine application resulted in a rapid and strong expression of GRK2 in not only dinitrochlorobenzene-induced CD (within 10 minutes) but also cultured rat dorsal root ganglion cells, F11 (within 1 minute). ERK inhibitor abrogates glutamine-mediated GRK2 expression and inhibition of itch in dinitrochlorobenzene-induced CD. Our data indicate that GRK2 is a key negative regulator of itch and that glutamine attenuates itch via a rapid induction of GRK2 in an ERK-dependent way.

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“…It has been reported that Gln attenuates itch evoked by DNFB-induced CD (Jin et al, 2012). In this study, we further examined the effects of Gln on itch evoked by histamine and CQ.…”

Section: Grk2 Knockdown Inhibits the Anti-itch Activity Of Glnmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

GPCR Kinase (GRK)-2 Is a Key Negative Regulator of Itch: l-Glutamine Attenuates Itch via a Rapid Induction of GRK2 in an ERK-Dependent Way

Lee

Park

et al. 2018

Journal of Investigative Dermatology

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“…Like glucose, glutamine levels in standard medias are also supraphysiologic. However, many more in vitro and in vivo studies have examined the effects of supplementation, as have been discussed . Why disparate effects of blood glucose and exogenous glutamine have been observed is somewhat puzzling, but speaks to an as yet unclarified importance of glutamine in potentially limiting allergic disease.…”

Section: A Spoonful Of Sugar…cause or Cure For Allergy?mentioning

confidence: 99%

“…As suggested in previous mouse models, CARD11 mutant T cells cultured in the presence of exogenous glutamine demonstrated improvement in mTORC1 activation and partial restoration of defective proliferation and cytokine release. 51 Clinically, topical glutamine has been demonstrated to suppress allergic contact dermatitis, 60 while oral glutamine given in a controlled trial as supplemented infant formula to very low birth weight infants was shown to reduce the incidence of atopic dermatitis in early childhood. 61 These clinical findings raise the question as to how critical this particular pathway might be in the pathogenesis of atopic dermatitis or other allergic diseases in the general population.…”

Section: When Atopy Is In the C Ard (S)mentioning

confidence: 99%

“…However, many more in vitro and in vivo studies have examined the effects of supplementation, as have been discussed. 51,60,61,106 Why disparate effects of blood glucose and exogenous glutamine have been observed is somewhat puzzling, but speaks to an as yet unclarified importance of glutamine in potentially limiting allergic disease. A trial is currently being undertaken to prospectively study the efficacy of oral glutamine supplementation in patients with atopic dermatitis and evidence of impaired lymphocyte mTORC1 activation.…”

Section: A S P Oonful Of Sug Ar …C Aus E or Cure For Allergy ?mentioning

confidence: 99%

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The clinical and mechanistic intersection of primary atopic disorders and inborn errors of growth and metabolism

Lyons

Milner

2018

Immunological Reviews

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Summary Dynamic changes in metabolism have long been understood as critical for both the initiation and maintenance of innate and adaptive immune responses. A number of recent advances have clarified details of how metabolic pathways can specifically affect cellular function in immune cells. Critical to this understanding is ongoing study of the congenital disorders of glycosylation and other genetic disorders of metabolism that lead to altered immune function in humans. While there are a number of immune phenotypes associated with metabolic derangements caused by single gene disorders, several genetic mutations have begun to link discrete alterations in metabolism and growth specifically with allergic disease. This subset of primary atopic disorders is of particular interest as they illuminate how hypomorphic mutations which allow for some residual function of mutated protein products permit the “abnormal” allergic response. This review will highlight how mutations altering sugar metabolism and mTOR activation place similar constraints on T lymphocyte metabolism to engender atopy, and how alterations in JAK/STAT signaling can impair growth and cellular metabolism while concomitantly promoting allergic diseases and reactions in humans.

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Atopic Dermatitis and Psoriasis: Similarities and Differences in Metabolism and Microbiome

Chen,

Peng,

Zhu

et al. 2024

Clinic Rev Allerg Immunol

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Glutamine suppresses dinitrophenol fluorobenzene-induced allergic contact dermatitis and itching: Inhibition of contact dermatitis by glutamine

Cited by 8 publications

References 29 publications

GPCR Kinase (GRK)-2 Is a Key Negative Regulator of Itch: l-Glutamine Attenuates Itch via a Rapid Induction of GRK2 in an ERK-Dependent Way

GPCR Kinase (GRK)-2 Is a Key Negative Regulator of Itch: l-Glutamine Attenuates Itch via a Rapid Induction of GRK2 in an ERK-Dependent Way

The clinical and mechanistic intersection of primary atopic disorders and inborn errors of growth and metabolism

Atopic Dermatitis and Psoriasis: Similarities and Differences in Metabolism and Microbiome

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