Neuroendocrine cells derived chemokine vasoactive intestinal polypeptide (VIP) in allergic diseases

Abstract

Worldwide increase incidences of allergic diseases have heightened the interest of clinicians and researchers to understand the role of neuroendocrine cells in the recruitment and activation of inflammatory cells. Several pieces of evidence revealed the association of neuropeptides in the pathogenesis of allergic diseases. Importantly, one such peptide that is secreted by neuronal cells and immune cells exerts a wide spectrum of immunological functions as cytokine/chemokine is termed as Vasoactive Intestinal Peptide (VIP). VIP mediates immunological function through interaction with specific receptors namely VPAC-1, VPAC-2, CRTH2 and PAC1 that are expressed on several immune cells such as eosinophils, mast cells, neutrophils, and lymphocytes; therefore, provide the basis for the action of VIP on the immune system. Additionally, VIP mediated action varies according to target organ depending upon the presence of specific VIP associated receptor, involved immune cells and the microenvironment of the organ. Herein, we present an integrative review of the current understanding on the role of VIP and associated receptors in allergic diseases, the presence of VIP receptors on various immune cells with particular emphasis on the role of VIP in the pathogenesis of allergic diseases such as asthma, allergic rhinitis, and atopic dermatitis. Being crucial signal molecule of the neuroendocrine-immune network, the development of stable VIP analogue and/or antagonist may provide the future therapeutic drug alternative for the better treatment of these allergic diseases. Taken together, our current review summarizes the current understandings of VIP biology and further explore the significance of neuroendocrine cells derived VIP in the recruitment of inflammatory cells in allergic diseases that may be helpful to the investigators for planning the experiments and accordingly predicting new therapeutic strategies for combating allergic diseases. Summarized graphical abstract will help the readers to understand the significance of VIP in allergic diseases.

Intestinal overexpression of IL‐18 promotes eosinophils‐mediated allergic disorders

“…Eosinophils were quantified by counting the anti‐MBP‐positive cells in the epithelial mucosa and lamina propria of the jejunum. Eosinophil numbers and area of jejunal tissue section were measured and calculated with the assistance of digital morphometric analysis (Luminera Corporation, Infinity Analyze 6·1·0), and expressed as eosinophils/mm 2 as described previously . The intestinal sections were taken from the same position in each set of mice, and at least four–five random sections/mouse were analysed for eosinophil levels and are expressed as eosinophils/mm 2 as described earlier …”

“…Eosinophil numbers and area of jejunal tissue section were measured and calculated with the assistance of digital morphometric analysis (Luminera Corporation, Infinity Analyze 6Á1Á0), and expressed as eosinophils/mm 2 as described previously. 18,19 The intestinal sections were taken from the same position in each set of mice, and at least four-five random sections/mouse were analysed for eosinophil levels and are expressed as eosinophils/mm 2 as described earlier. 9,20 Blood eosinophil analysis Peripheral blood samples were collected in heparinized tubes (Becton Dickinson, Franklin Lakes, NJ, USA) from the inguinal artery of anaesthetized mice.…”

All along the watchtower: group 2 innate lymphoid cells in allergic responses

“…Conversely, multiple neuropeptides have been shown to stimulate cytokine secretion by ILC2. These include VIP [10] and CGRP, which is produced by pulmonary neuroendocrine cells and can amplify allergic asthma [30,46]. Recently, three groups demonstrated that ILC2s express high levels of the receptor for the neuropeptide neuromedin U (NMU) [27–29], and that peripheral cholinergic neurons producing NMU rapidly amplify allergic inflammation in an ILC2 dependent manner in the gut and lung [28].…”

The role of regulatory neuropeptides and neurotrophic factors in asthma pathophysiology

“…There are a small number of review articles devoted to the role of regulatory neuropeptides in asthma pathogenesis [27,28,29]. The information on the expression of certain neuropeptides (substance P, vasoactive intestinal peptide, calcitonin generegulated peptide, tachykinins, neuropeptide Y (NPY), bombesins, granins), which can influence on the pathogenesis of a number of bronchopulmonary diseases, in particular asthma, is provided in the review authored by K.R.…”