Human neutrophils synthesize IL-8 in an IgE-mediated activation

Monteseirı́n, Javier; Chacón, Pedro; Vega, Antonio Pereira; Bekay, Rajaa El; Álvarez, M. F.; Álba, Gonzalo; Conde, Manuel; Jiménez, Juan; Asturias, Juan A.; Martı́nez, Alberto; Condé, J.; Pintado, Elı́zabeth; Bedoya, Francisco J.; Sobrino, Francisco

doi:10.1189/jlb.0903441

Cited by 30 publications

(40 citation statements)

References 69 publications

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“…These findings are in agreement with previous studies reporting an IgE-dependent mechanism, elicited by allergens, of TNF-a [32] or IL-8 production [33] by mononuclear cells and neutrophils, respectively. Evidence for the implication of these mediators, whose levels have been found elevated in bronchoalveolar lavage fluid and airways of asthmatic patients, in the pathology of allergy has been reported [34].…”

Section: Discussionsupporting

confidence: 94%

“…Immunoglobulins were dissociated from the lymphocyte surfaces as described [33], and the obtained supernatants were used for specific IgE and IgG determinations (HYTEC 288).…”

Section: Dissociation Of Lymphocyte-bound Immunoglobulins and Ige Recmentioning

confidence: 99%

“…cDNA was amplified by PCR using specific primers for COX-2 [21], IL-8 [33], glyceraldehyde-3-phosphate dehydrogenase (GAPDH) [21], and TNF-a (5 0 -AAGCCTG-TAGCCCATGTTGT-3 0 and 5 0 -CCAGATAGATGGGCTCATAC-3 0 ). The reactions were performed by 25-30 cycles of 94 C for 1 min, 58-60 C for 1 min, and 72 C for 1 min.…”

Section: Rna Extraction and Rt-pcr Analysismentioning

confidence: 99%

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Induction of cyclooxygenase-2 expression by allergens in lymphocytes from allergic patients

et al. 2005

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Cyclooxygenase (COX) is a key enzyme in prostaglandin (PG) synthesis. Up-regulation of COX-2 expression is responsible for increased PG release during inflammatory conditions and is thought to be also involved in allergic states. In this study, we demonstrate that in human T, B and natural killer lymphocytes from allergic patients, COX-2 expression became induced upon cell challenge with specific allergens and that this process is presumably IgE dependent and occurs after CD23 receptor ligation. This induction took place at both mRNA and protein levels and was accompanied by PGD 2 release. IgE-dependent lymphocyte treatment elicited, in parallel, an activation of the MAPK p38 and extracellular signal-regulated kinase 1/2, an enhancement of calcineurin (CaN) activity, and an increase of the DNA-binding activity of the nuclear factor of activated T cells and of NF-jB, with a concomitant decrease in the levels of the cytosolic inhibitor of jB, IjB. In addition, specific chemical inhibitors of MAPK, such as PD098059 and SB203580, as well as MG-132, an inhibitor of proteasomal activity, abolished allergen-induced COX-2 up-regulation, suggesting that this process is mediated by MAPK and NF-jB. However, induction of COX-2 expression was not hampered by the CaN inhibitor cyclosporin A. We also examined the effect of a selective COX-2 inhibitor, NS-398, on cytokine production by human lymphocytes. Treatment with NS-398 severely diminished the IgE-dependently induced production of IL-8 and TNF-a. These results underscore the relevant role of lymphocyte COX-2 in allergy and suggest that COX-2 inhibitors may contribute to the improvement of allergic inflammation through the reduction of inflammatory mediator production by human lymphocytes.

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Section: Discussionsupporting

confidence: 94%

“…Immunoglobulins were dissociated from the lymphocyte surfaces as described [33], and the obtained supernatants were used for specific IgE and IgG determinations (HYTEC 288).…”

Section: Dissociation Of Lymphocyte-bound Immunoglobulins and Ige Recmentioning

confidence: 99%

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Induction of cyclooxygenase-2 expression by allergens in lymphocytes from allergic patients

et al. 2005

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“…from four separate experiments performed in triplicate. NFAT expression in human neutrophils hypothesis is supported by three main facts: (i) we have previously reported the presence of specific IgE on the surface of neutrophils from allergic patients (Monteseirín et al, 2003;Monteseirín et al, 2004); (ii) anti-IgE Ab challenge triggered an equivalent response to that obtained with the antigens; and (iii) ligation of IgE receptors (mainly galectin-3 and Fc⑀RI) with specific Abs evoked NFAT2 activation. In line with our data, the liberation of IL8 by these cells following the stimulation by Fc⑀RI has been demonstrated previously (Gounni et al, 2001), and the challenge of neutrophils by galectin-3 stimulates superoxide production (Yamaoka et al, 1995).…”

Section: Discussionmentioning

confidence: 60%

Expression of the transcription factor NFAT2 in human neutrophils: IgE-dependent, Ca2+- and calcineurin-mediated NFAT2 activation

Vega

Chacón

Monteseirı́n

et al. 2007

Journal of Cell Science

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NFAT (nuclear factors of activated T cells) proteins constitute a family of transcription factors involved in mediating signal transduction. The presence of NFAT isoforms has been described in all cell types of the immune system, with the exception of neutrophils. In the present work we report for the first time the expression in human neutrophils of NFAT2 mRNA and protein. We also report that specific antigens were able to promote NFAT2 protein translocation to the nucleus, an effect that was mimicked by the treatment of neutrophils with anti-immunoglobulin E (anti-IgE) or anti-Fcϵ-receptor antibodies. Antigens, anti-IgE and anti-FcϵRs also increased Ca2+ release and the intracellular activity of calcineurin, which was able to interact physically with NFAT2, in parallel to eliciting an enhanced NFAT2 DNA-binding activity. In addition, specific chemical inhibitors of the NFAT pathway, such as cyclosporin A and VIVIT peptide, abolished antigen and anti-IgE-induced cyclooxygenase-2 (COX2) gene upregulation and prostaglandin (PGE2) release, suggesting that this process is through NFAT. Our results provide evidence that NFAT2 is constitutively expressed in human neutrophils, and after IgE-dependent activation operates as a transcription factor in the modulation of genes, such as COX2, during allergic inflammation.

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“…IL-8 is also secreted by neutrophils. The functional role of neutrophils in IgEmediated diseases has been demonstrated [116]. Antigen-dependent IL-8 release has been suggested to occur through IgEdependent mechanisms [116].…”

Section: Il-9mentioning

confidence: 99%

Food Protein–Induced Enterocolitis Syndrome

Nowak‐Węgrzyn

Jarocka-Cyrta

Castro

2017

J Investig Allergol Clin Immunol

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Food protein-induced enterocolitis syndrome (FPIES) is a non-IgE-, cell-mediated food allergy of unknown prevalence and pathophysiology. Onset is typically during the first year of life; seafood-induced FPIES may start in adulthood. Acute FPIES manifests within 1-4 hours after ingestion with repetitive emesis, pallor, and lethargy progressing to dehydration and hypovolemic shock in 15% of cases. Chronic FPIES manifests with intermittent emesis, watery diarrhea, and poor growth progressing to dehydration and hypovolemic shock over a period of days to weeks. Chronic FPIES has been only reported in infants aged less than 3 months fed with cow milk (CM) or soy formula. The most common triggers are CM, soy, rice, and oat. Diagnosis of FPIES relies on recognition of a pattern of clinical symptoms and may be missed owing to the absence of typical allergic symptoms (eg, urticaria, wheezing) and delayed onset in relation to food ingestion. Physician-supervised food challenge is recommended if diagnosis or the trigger food is not clear and to evaluate for resolution. Testing for food-specific IgE is usually negative, although a subset of patients, usually with CM-induced FPIES may develop sensitization to foods. Such atypical FPIES tends to have a more prolonged course. Despite the potential severity of the reactions, no fatalities have been reported, and FPIES has a favorable prognosis. In most cases, FPIES resolves by age 3-5 years, although persistence of CM-induced FPIES and soy FPIES into adulthood has been reported. The first international consensus guidelines on diagnosis and management of FPIES were published in 2017. Given that the pathophysiology of FPIES is poorly understood, there are no diagnostic biomarkers and no therapies to accelerate resolution. These unmet needs warrant future investigations to improve the care of patients with FPIES. Key words: FPIES. Food protein-induced enterocolitis syndrome. Non-IgE-mediated food allergy. Food allergy. Cow milk allergy. ResumenSEIOA es una alergia alimentaria con patofisiología y prevalencia desconocidas, que típicamente comienza en el primer año de vida, mientras que la producida por pescado suelo tener su comienzo en adultos. La forma aguda se manifiesta entre la hora y 4 horas tras la ingesta del alimento con emesis, palidez, letargia progresiva por deshidratación y shock hipovolémico en el 15% de los casos. La forma crónica se manifiesta con emesis intermitente, diarreas y crecimiento pobre con progresión hacia la deshidratación y shock hipovolémico en un periodo de días o semanas. La forma crónica se ha podido observar únicamente en niños menores de 3 años alimentados con leche de vaca o fórmula de soja. Los desencadenantes más frecuentes son la leche de vaca, la soja, el arroz y avena. El diagnóstico es clínico y puede ser difícil debido a la ausencia de síntomas alérgicos típicos (urticaria, asma…) y a la relación retardada con la ingesta. Es recomendable la provocación controlada si el diagnóstico clínico o el alimento implicado no son claros y tamb...

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Human neutrophils synthesize IL-8 in an IgE-mediated activation

Cited by 30 publications

References 69 publications

Induction of cyclooxygenase-2 expression by allergens in lymphocytes from allergic patients

Induction of cyclooxygenase-2 expression by allergens in lymphocytes from allergic patients

Expression of the transcription factor NFAT2 in human neutrophils: IgE-dependent, Ca2+- and calcineurin-mediated NFAT2 activation

Food Protein–Induced Enterocolitis Syndrome

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