Induction of interleukin 8 by American cockroach allergens from human airway epithelial cells via extracellular signal regulatory kinase and jun N-terminal kinase but not p38 mitogen-activated protein kinase

Lee, Mey Fann; Wang, Nancy M.; Liu, Szu Wei; Lin, Shyh Jye; Chen, Yi Hsing

doi:10.1016/j.anai.2010.07.008

Cited by 17 publications

(19 citation statements)

References 26 publications

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“…We have recently demonstrated that activation of PAR-2 regulated TNFα production by NF-κB and ERK, but not p38, in alveolar macrophages [10]. Other reports have also shown that PAR-2 activation leads to increased ERK and IκBα/NF-κB signal transduction pathway activation [14-16]. In our study, we report that the major consequence of PAR-2 activation on neutrophils is the release of TNFα in the airways.…”

Section: Discussionsupporting

confidence: 58%

The role of protease-activated receptor-2 on pulmonary neutrophils in the innate immune response to cockroach allergen

Lutfi¹,

Lewkowich

Zhou³

et al. 2012

J Inflamm

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BackgroundSerine proteases in German cockroach (GC) have been shown to mediate allergic airway inflammation through the activation of protease activated receptor (PAR)-2. Neutrophils play an important role in regulating the innate immune response, and are recruited into the airways following GC frass exposure. As such, we investigated the role of PAR-2 in airway neutrophil recruitment, activation and cytokine production following allergen exposure.MethodsWild type and PAR-2-deficient mice were administered a single intratracheal instillation of PBS or GC frass and neutrophil recruitment, expression of PAR-2, CD80, CD86, and MHC class II were assessed by flow cytometry and levels of tumor necrosis factor (TNF)α was assessed by ELISA. Uptake of AlexaFluor 405-labeled GC frass by neutrophils was performed by flow cytometry.ResultsNeutrophil recruitment in the lung and airways following GC frass exposure was significantly decreased in PAR-2-deficient mice compared to wild type mice. GC frass exposure increased the level of PAR-2 on pulmonary neutrophils and increased numbers of PAR-2-positive neutrophils were found in the lungs; however PAR-2 did not play a role in meditating allergen uptake. Comparing wild type and PAR-2-deficient mice, we found that a single exposure to GC frass increased levels of CD80 and CD86 on pulmonary neutrophils, an effect which was independent of PAR-2 expression. Neutrophils isolated from the whole lungs of naïve PAR-2-deficient mice treated ex vivo with GC frass produced significantly less TNFα than in similarly treated wild type neutrophils. Lastly, neutrophils were isolated from the bronchoalveolar lavage fluid of wild type and PAR-2-deficient mice following a single intratracheal exposure to GC frass. Airway neutrophils from PAR-2-deficient mice released substantially decreased levels of TNFα, suggesting a role for PAR-2 in neutrophil-derived cytokine production.ConclusionsTogether these data suggest PAR-2 expression can be upregulated on lung neutrophils following allergen exposure and the consequence is altered release of TNFα which could drive the early innate immune response.

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Section: Discussionsupporting

confidence: 58%

The role of protease-activated receptor-2 on pulmonary neutrophils in the innate immune response to cockroach allergen

Lutfi¹,

Lewkowich

Zhou³

et al. 2012

J Inflamm

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“…PI3K/Akt and ERK1/2 pathways were found to be activated in lung cancer (Lu et al, 2010) Down regulation of PI3K/Akt pathway may inhibit the migration and invasion in NSCLC cells (Lee et al, 2010b). Our study demonstrated that the phosphorylation of Atk and Erk was involved in the inhibition of EGFR, Akt phosphorylation mainly in the inhibition of PI3K, and Erk phosphorylation mainly in ERK1/2 inhibitor.…”

Section: Discussionmentioning

confidence: 78%

Potential mechanism of interleukin‐8 production from lung cancer cells: An involvement of EGF–EGFR–PI3K–Akt–Erk pathway

Zhang

Wang

Zhang

et al. 2011

Journal Cellular Physiology

106

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Tumor inflammatory microenvironment is considered to play the role in the sensitivity of tumor cells to therapies and prognosis of lung cancer patients. Interleukin-8 (IL-8) is one of critical chemo-attractants responsible for leukocyte recruitment, cancer proliferation, and angiogenesis. The present study aimed at investigating potential mechanism of IL-8 production from human non-small cell lung cancer (NSCLC) SPC-A1 cells. We initially found that EGF could directly stimulate IL-8 production, proliferation, and bio-behaviors of lung cancer cells through the activation of EGFR, PI3K, Akt, and Erk signal pathway. EGF-stimulated IL-8 production, phosphorylation of Akt and Erk, and cell proliferation and movement could be inhibited by EGFR inhibitor (Erlotinib), PI3K inhibitor (GDC-0941 BEZ-235 and SHBM1009), and ERK1/2 inhibitor (PD98059). Our data indicate that IL-8 production from lung cancer cells could be initiated by their own produced factors, leading to the recruitment of inflammatory cells in the cancer tissue, and the formation of inflammatory microenvironment. Thus, it seems that the signal pathway of EGFR-PI3K-Akt-Erk can be the potential target of therapies for inflammatory microenvironment in lung cancer.

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“…In addition, the activation of MAPKs has been shown to be associated with the expression of proinflammatory mediators, which can lead to pathogenesis of allergic inflammation in asthma and other allergic disorders [10,42]. Thus, we investigated whether ERK and p38 played a role in DEHP-induced ICAM-1 and IL-8 expression in HUVECs.…”

Section: Discussionmentioning

confidence: 99%

“…Vascular endothelial cells have been reported to secrete a variety of inflammatory mediators, such as cytokines (IL-6, IL-8, TNF-alpha, and IL-4) and the intercellular adhesion molecule-1 (ICAM-1), to participate in inflammation and immune reactions [9][10][11]. IL-8 is a soluble ELR (glutamic acid-leucine-arginine) CXC chemokine implicated in the environmentally induced pulmonary inflammation [12].…”

Section: Introductionmentioning

confidence: 99%

ICAM-1 and IL-8 Are Expressed by DEHP and Suppressed by Curcumin Through ERK and p38 MAPK in Human Umbilical Vein Endothelial Cells

Wang

Dong

2011

Inflammation

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The present study aimed to determine whether curcumin isolated from the rhizome of Curcuma longa Linn could inhibit di-(2-ethylhexyl) phthalate (DEHP)-induced allergic inflammatory responses in human umbilical vein endothelial cells (HUVECs). We found that DEHP dose-dependently elevated adhesion molecule-1 (ICAM-1) protein level within 15-30 min, which was independent of de novo protein synthesis. And a late-phase induction of ICAM-1 was observed within 8 h treatment of DEHP via de novo protein synthesis through transcription and translation. DEHP also increased the expression of interleukin (IL)-8 in a time- and dose-dependent manner. Pretreatment with curcumin dose-dependently decreased DEHP-induced expression of ICAM-1 and IL-8 as well as phosphorylation of ERK1/2 and p38. Preincubation with ERK1/2 inhibitor (PD98059) or p38 inhibitor (SB203580) markedly blocked DEHP-stimulated activation of ICAM-1 and IL-8. We suggest that curcumin inhibits DEHP-induced expression of ICAM-1 and IL-8 through ERK and p38 MAPK signaling pathways in HUVECs and may contribute to ameliorate pathologies of DEHP-related allergic disorders.

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Induction of interleukin 8 by American cockroach allergens from human airway epithelial cells via extracellular signal regulatory kinase and jun N-terminal kinase but not p38 mitogen-activated protein kinase

Cited by 17 publications

References 26 publications

The role of protease-activated receptor-2 on pulmonary neutrophils in the innate immune response to cockroach allergen

The role of protease-activated receptor-2 on pulmonary neutrophils in the innate immune response to cockroach allergen

Potential mechanism of interleukin‐8 production from lung cancer cells: An involvement of EGF–EGFR–PI3K–Akt–Erk pathway

ICAM-1 and IL-8 Are Expressed by DEHP and Suppressed by Curcumin Through ERK and p38 MAPK in Human Umbilical Vein Endothelial Cells

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