Catalytic Hydrolysis of VIP in Pregnant Women with Asthma

Olopade, Christopher O.; Yu, John; Abubaker, Jawed; Mensah, Edward; Paul, Sudhir

doi:10.1080/02770900600710730

Cited by 10 publications

(5 citation statements)

References 29 publications

(30 reference statements)

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“…In the above study, autoantibodies against alphaenolase protein induced an apoptotic cell death of retinal cells without an addition of complement. Autoantibodies to vasoactive intestinal peptide purified from asthmatic patients showed a catalytic enzyme-like activity [32]. We suppose that IgG autoantibodies against airway epithelial cell autoantigens (cytokeratin 18 and alpha-enolase) from patients with nonallergic asthma could directly induce cytotoxic damage to airway epithelial cells.…”

Section: Discussionmentioning

confidence: 99%

Increased IgG Antibody-Induced Cytotoxicity Against Airway Epithelial Cells in Patients with Nonallergic Asthma

et al. 2009

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Background IgG autoantibodies to airway epithelial cell proteins have been detected in patients with nonallergic asthma. Objective and Methods To evaluate the functional significance of these autoantibodies, we examined the presence of IgG antibody-induced cytotoxicity against airway epithelial cells (A549) by the microcytotoxicity assay using IgG antibodies purified from patients with nonallergic asthma. Results IgG antibody-induced cytotoxicity (expressed as percent cell lysis) was significantly increased in nine patients with nonallergic asthma (mean ± standard deviation; 30.6±7.3%) as compared with eight healthy controls (13.9±5.1%) and nine patients with allergic asthma (20.3± 10.4%; p<0.05). In addition, IgG antibody-induced cytotoxicity was significantly inhibited when IgG antibodies from patients with nonallergic asthma were pre-incubated with recombinant human airway epithelial cell autoantigens (cytokeratin 18 or alpha-enolase proteins; p<0.05). Conclusion These results suggest a possible involvement of IgG autoantibody-induced cytotoxicity against airway epithelial cells in the pathogenesis of nonallergic asthma.

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Section: Discussionmentioning

confidence: 99%

Increased IgG Antibody-Induced Cytotoxicity Against Airway Epithelial Cells in Patients with Nonallergic Asthma

et al. 2009

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“…Our hypothesis is in agreement with previous reports in murine models which demonstrated modulatory effects of thyroid hormone on VIP mRNA levels in different adult brain areas 23 and an upregulation of VIP content in the anterior pituitary gland under hypothyroid conditions 24 – 26 . Besides, our results link GD to other inflammatory/autoimmune diseases where VIP serum levels are decreased, such as juvenile idiopathic arthritis (JIA) 27 , early arthritis 15 , SpA 17 , osteoarthritis 28 and asthma 29 . Moreover, the fact that only the hyperthyroid subgroup with recent onset GD showed reduced VIP levels, suggests an association between low VIP levels and disease activity, as it has also been previously demonstrated in patients with early arthritis 15 , 16 , SpA 17 , Chagas cardiomyopathy 30 and JIA 27 .…”

Section: Discussionmentioning

confidence: 64%

Vasoactive intestinal peptide axis is dysfunctional in patients with Graves’ disease

Carrión

Ramos-Leví

Seoane

et al. 2020

Sci Rep

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Vasoactive intestinal peptide (VIP) is a neuropeptide with potent immunoregulatory properties. Reduced serum VIP levels and alterations in VIP receptors/signaling on immune cells have been associated with different inflammatory/autoimmune diseases. However, its role in autoimmune thyroid diseases (AITD) remains unknown. This study examined the interrelationship between VIP system, autoimmune background and thyroid hormones in peripheral immune cells in patients with AITD. Only Graves' disease (GD) patients showed significantly lower serum VIP levels when compared to healthy subjects and to Hashimoto's thyroiditis patients. Serum VIP levels were lower at the onset of GD, showing a significant negative correlation with thyroid hormone levels. The expression of VIP receptors, VPAC1 and VPAC2, was significantly upregulated in peripheral blood mononuclear cells (PBMC) from GD patients. There was an impairment of VIP signalling in these patients, probably attributable to a dysfunction of VPAC1 with preservation of VPAC2. The correlation between VPAC1 and thyroid hormone receptor expression in PBMC from healthy subjects was lost in GD patients. In summary, the VIP system is altered in peripheral immune cells of GD patients and this finding is associated with different thyroid hormone receptor patterns, showing a dynamic inter-regulation and a prominent role of VIP in this setting. Experimental data and clinical observations in animal models and humans point to an important role of interactions between neuroendocrine and immune systems for the maintenance of the overall homeostasis 1,2. This bidirectional network is functionally supported by the presence of shared signalling molecules, including hormones, neuropeptides, cytokines, and their respective receptors. Thus, neuropeptides and hormones are able to modulate immune functions, and immune mediators are capable of affecting the endocrine system. Therefore, although the immune system itself has mechanisms of self-regulation, the neuroendocrine system is also involved in its control. Accordingly, impairment of mechanisms mediating such regulatory relationships has been linked with the development of autoimmune diseases 3. Thyroid hormones, triiodothyronine (T3) and thyroxine (T4), are implicated in key physiological processes, including development, differentiation, and regulation of metabolism 4. Besides, accumulating evidence proves the impact of thyroid status on immune responses and inflammation, by directly affecting the functional activity of monocytes, macrophages, lymphocytes and natural killer 3. Biological actions of thyroid hormones are mediated by classical signalling mechanisms initiated through binding to their corresponding nuclear receptors, TRα and TRβ, that directly modulate gene transcription 5. In addition, recent investigations have described that they also act at the plasma membrane via integrin αvβ3, triggering signalling cascades that indirectly contribute to the regulation of gene expression 4. Thyroid autoimmune diseases (AITD) include a broad...

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“…The VIP serum levels also correlated with the response to bronchodilator therapy, showing a better response in patients with higher VIP serum levels [28]. Catalytic auto-antibodies against VIP may play a role in serum from asthmatics with acute exacerbations [29,30]. Taken together, VIP seems to be effective in dilating pre-contracted bronchi, but shows no significant effect in bronchi with normal tonus.…”

Section: Asthmamentioning

confidence: 72%

Clinical Potential of VIP by Modified Pharmaco-kinetics and Delivery Mechanisms

Burian¹,

Ortner²,

Ruth³

et al. 2012

EMIDDT

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Vasoactive intestinal peptide (VIP) conveys various physiological effects in the digestive tract, nervous and cardiovascular system, airways, reproductive system, endocrine system, and more. A family of specific membrane bound receptors, termed VPAC1, VPAC2, and PAC1, bind VIP and trigger the effects. Many of them are of clinical interest. To date more than two thousand publications suggest the use of VIP in diseases like asthma, erectile dysfunction, blood pressure regulation, inflammation, endocrinology, tumours, etc. Despite this considerable potential, the peptide is not regularly used in clinical settings. A key problem is the short half life of inhaled or systemically administered VIP due to rapid enzymatic degradation. This shortcomings could be overcome with stable derivates or improved pharmacokinetics. A promising strategy is to use biocompatible and degradable depots, to protect the peptide from early degradation and allow for controlled release. This review focuses on aspects of clinical applications of VIP and the idea to use formulations based on biodegradable particles, to constitute a dispersible VIP-depot. Smart particle systems protect the peptide from early degradation, and assist the sustainable cell targeting with VIP for therapeutic or imaging purposes.

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Catalytic Hydrolysis of VIP in Pregnant Women with Asthma

Abstract: An increase in the VIP hydrolyzing activity of IgG is independently associated with asthma and pregnancy. The autoantibodies hold the potential of affecting the pathophysiology of the airways in pregnant asthmatics.

Cited by 10 publications

References 29 publications

Increased IgG Antibody-Induced Cytotoxicity Against Airway Epithelial Cells in Patients with Nonallergic Asthma

Increased IgG Antibody-Induced Cytotoxicity Against Airway Epithelial Cells in Patients with Nonallergic Asthma

Vasoactive intestinal peptide axis is dysfunctional in patients with Graves’ disease

Clinical Potential of VIP by Modified Pharmaco-kinetics and Delivery Mechanisms

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