Essential Role of p38 Mitogen-activated Protein Kinase in Contact Hypersensitivity

Takanami-Ohnishi, Yoko; Amano, Sadao; Kimura, Sadao; Asada, Sachie; Utani, Atsushi; Maruyama, Masumi; Osada, Hiroyuki; Tsunoda, Hajime; Irukayama-Tomobe, Yoko; Goto, Katsutoshi; Karin, Michael; Sudo, Tatsuhiko; Kasuya, Yoshitoshi

doi:10.1074/jbc.m207326200

Cited by 55 publications

(53 citation statements)

References 46 publications

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“…Among them, p38␣ and -␤ are expressed relatively ubiquitously, as shown by Northern blot analysis of adult tissues (4). Although targeted disruption of the p38␣ gene results in homozygous embryonic lethality because of defects in erythropoiesis and placental organogenesis (5,6), the p38␣ ϩ/Ϫ mouse is a useful tool for analyzing the in vivo role of p38 in disease models (7)(8)(9).…”

Section: Mice Platelets Of P38␣mentioning

confidence: 99%

Involvement of p38α Mitogen-activated Protein Kinase in Lung Metastasis of Tumor Cells

Matsuo

Amano

Furuya

et al. 2006

Journal of Biological Chemistry

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To study the role of p38 mitogen-activated protein kinase (p38) activity during the process of metastasis, p38␣؉/؊ mice were subjected to an in vivo metastasis assay. The number of lung colonies of tumor cells intravenously injected in p38␣ ؉/؊ mice was markedly decreased compared with that in wild-type (WT) mice. On the other hand, the time-dependent increase in tumor volume after subcutaneous tumor cells transplantation was comparable between WT and p38␣ mice. Platelets of p38␣؉/؊ mice were poorly bound to tumor cells in vitro and in vivo compared with those of WT mice. Eand P-selectin mRNAs were markedly induced in the lung after intravenous injection of tumor cells. However, the induction of these selectin mRNAs in p38␣ ؉/؊ mice was weaker than that in WT mice. Furthermore, the resting expression levels of E-selectin in lung endothelial cells and P-selectin in platelets of p38␣

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Section: Mice Platelets Of P38␣mentioning

confidence: 99%

Involvement of p38α Mitogen-activated Protein Kinase in Lung Metastasis of Tumor Cells

Matsuo

Amano

Furuya

et al. 2006

Journal of Biological Chemistry

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“…p38 MAPK are enzymes that play an important role in the signal transduction of TLR (Mehrotra et al, 2007). In mice treated with the specific p38 MAPK inhibitor SB202190 the ear swelling in response to DNFB was impaired (Takanami-Ohnishi et al, 2002). Further evidence for the importance of p38 MAPK was found in in vitro studies.…”

Section: The Role Of Tlrs In Skin Sensitizationmentioning

confidence: 62%

Keratinocytes, Innate Immunity and Allergic Contact Dermatitis - Opportunities for the Development of In Vitro Assays to Predict the Sensitizing Potential of Chemicals

Veen¹,

Vandebriel²,

Loveren³

et al. 2011

Contact Dermatitis

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“…Meanwhile, in the mesenteric lymph nodes, where pre-matured T cells expand and mature into cytotoxic T cells, donor-derived CD8 + and CD4 + lymphocytes are fewer in p38a +/--grafted mice. Several studies have reported that activated p38 up-regulates the expression of several cytokines, such as IL-12p40, IL-18, and IL-4 [16,17,27], and plays essential roles in T cell proliferation in vitro and in vivo [18][19][20]. The induction of Th1-dominant cytokines, such as IL-12p40 and IL-18, was suppressed in the MLNL of p38a +/--grafted mice, which may be one of the reasons why fewer lymphocytes infiltrated into the MLNL.…”

Section: Discussionmentioning

confidence: 99%

“…The B6 mice that carry the GFP transgene (B6-GFP mice) were a gift from Dr. Masaru Okabe (Osaka University, Osaka, Japan) [42]. Mice heterozygous for targeted disruption of the p38a gene in the B6 background (p38a +/-) were maintained in RIKEN BioResource Center (Tsukuba, Japan) [13,27]. GFP-WT and GFP-p38a +/-mice were generated as donor mice by mating B6-GFP and B6-p38a +/-mice.…”

Section: Discussionmentioning

confidence: 99%

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Reduced p38 mitogen-activated protein kinase in donor grafts accelerates acute intestinal graft-versus-host disease in mice

et al. 2005

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The gastrointestinal tract is a major target of graft-versus-host disease (GVHD), which constitutes a life-threatening complication of bone marrow transplantation. GVHD is mainly caused by the activation of donor-derived lymphocytes, in which cytokine cascades play essential roles. Since p38 MAPK (p38) has been identified as a regulator of cytokine reactions and proposed as a molecular target for anti-inflammatory therapy, we investigated the contribution of p38 to the severity of murine intestinal GVHD. Unexpectedly, p38a +/-donor graft induced more acute GVHD-related mortality and more severe gut injury. The survival of p38a +/-donor-derived intestinal intraepithelial lymphocytes (IEL) was prolonged in vitro and in vivo, and TNF-a expression in the p38a +/-donor-derived IEL was also increased compared with wild-type cells. In contrast, the p38a +/-grafted mice resulted in decreased expansion of donor lymphocytes in mesenteric lymph nodes, and the up-regulation of IL-12p40 and IL-18 was diminished. These findings suggest that p38 has dichotomous effects for inflammatory response in vivo; not only regulates inflammatory cytokine expression and lymphocyte expansion, but also has distinct regulatory functions for IEL in intestinal GVHD. In conclusion, the inhibition of p38 may not be a suitable antiinflammatory strategy for GVHD due to the associated intestinal injury.

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Essential Role of p38 Mitogen-activated Protein Kinase in Contact Hypersensitivity

Abstract: The present study was designed to elucidate the role of p38 mitogen-activated protein kinase (p38) in the pathogenesis of inflammation, using a mouse contact hypersensitivity (CHS) model induced by 2,4-dinitro-1-fluorobenzene (DNFB).

Cited by 55 publications

References 46 publications

Involvement of p38α Mitogen-activated Protein Kinase in Lung Metastasis of Tumor Cells

Involvement of p38α Mitogen-activated Protein Kinase in Lung Metastasis of Tumor Cells

Keratinocytes, Innate Immunity and Allergic Contact Dermatitis - Opportunities for the Development of In Vitro Assays to Predict the Sensitizing Potential of Chemicals

Reduced p38 mitogen-activated protein kinase in donor grafts accelerates acute intestinal graft-versus-host disease in mice

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