Neuropeptides and breathing in health and disease

Kaczyńska, Katarzyna; Zając, Dominika; Wojciechowski, Piotr; Kogut, Ewelina; Szereda-Przestaszewska, Małgorzata

doi:10.1016/j.pupt.2017.12.001

Cited by 27 publications

(25 citation statements)

References 175 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In our study, NT administration markedly reduced airway responsiveness to methacholine provocation and the effect was blocked by pretreatment with the NTR1 antagonist. In fact, widespread NT in components of the central and peripheral nervous systems has been postulated to regulate breathing in the physiological state and in the disease [33]. The neuropeptide and its receptors have been identified in the airway mucosa and lungs [34], and in the presynaptic cholinergic terminals and post-synaptic smooth muscles of the bronchi [35], indicating potential sites of NT action and the possibility of the modulation of airway hyperresponsiveness.…”

Section: Discussionmentioning

confidence: 99%

Beneficial Effects of Neurotensin in Murine Model of Hapten-Induced Asthma

Russjan

2019

IJMS

Self Cite

View full text Add to dashboard Cite

Neurotensin (NT) demonstrates ambiguous activity on inflammatory processes. The present study was undertaken to test the potential anti-inflammatory activity of NT in a murine model of non-atopic asthma and to establish the contribution of NTR1 receptors. Asthma was induced in BALB/c mice by skin sensitization with dinitrofluorobenzene followed by intratracheal hapten provocation. The mice were treated intraperitoneally with NT, SR 142948 (NTR1 receptor antagonist) + NT or NaCl. Twenty-four hours after the challenge, airway responsiveness to nebulized methacholine was measured. Bronchoalveolar lavage fluid (BALF) and lungs were collected for biochemical and immunohistological analysis. NT alleviated airway hyperreactivity and reduced the number of inflammatory cells in BALF. These beneficial effects were inhibited by pretreatment with the NTR1 antagonist. Additionally, NT reduced levels of IL-13 and TNF-α in BALF and IL-17A, IL12p40, RANTES, mouse mast cell protease and malondialdehyde in lung homogenates. SR 142948 reverted only a post-NT TNF-α decrease. NT exhibited anti-inflammatory activity in the hapten-induced asthma. Reduced leukocyte accumulation and airway hyperresponsiveness indicate that this beneficial NT action is mediated through NTR1 receptors. A lack of effect by the NTR1 blockade on mast cell activation, oxidative stress marker and pro-inflammatory cytokine production suggests that other pathways can be involved, which requires further research.

show abstract

Section: Discussionmentioning

confidence: 99%

Beneficial Effects of Neurotensin in Murine Model of Hapten-Induced Asthma

Russjan

2019

IJMS

Self Cite

View full text Add to dashboard Cite

show abstract

“…Endomorphins and opioid receptors have been localized within airway smooth muscles, nerves, epithelium, and mucus glands [20]. In the respiratory system, they have been described as potent inhibitors of tachykinergic and cholinergic constriction, neurogenic mucus secretion, and goblet cells secretion [20,73]. In the review by Stein and Kuchler [18], reduction of edema, plasma extravasation, cytokine release, and tissue damage evoked by opioid-receptor activation were described in various models of inflammation.…”

Section: Discussionmentioning

confidence: 99%

Endomorphin-2- and Neurotensin- Based Chimeric Peptide Attenuates Airway Inflammation in Mouse Model of Nonallergic Asthma

Russjan

Andrzejewski

Sulejczak

et al. 2019

IJMS

Self Cite

View full text Add to dashboard Cite

We examined anti-inflammatory potency of hybrid peptide-PK20, composed of neurotensin (NT) and endomorphin-2 (EM-2) pharmacophores in a murine model of non-atopic asthma induced by skin sensitization with 2,4-dinitrofluorobenzene and intratracheal challenge of cognate hapten. Mice received intraperitoneally PK20, equimolar mixture of its structural elements (MIX), dexamethasone (DEX), or NaCl. Twenty-four hours following hapten challenge, the measurements of airway responsiveness to methacholine were taken. Bronchoalveolar lavage (BALF) and lungs were collected for further analyses. Treatment with PK20, similarly to dexamethasone, reduced infiltration of inflammatory cells, concentration of mouse mast cell protease, IL-1β, IL-12p40, IL-17A, CXCL1, RANTES in lungs and IL-1α, IL-2, IL-13, and TNF-α in BALF. Simple mixture of NT and EM-2 moieties was less potent. PK20, DEX, and MIX significantly decreased malondialdehyde level and secretory phospholipase 2 activity in lungs. Intensity of NF-κB immunoreactivity was diminished only after PK20 and DEX treatments. Neither PK20 nor mixture of its pharmacophores were as effective as DEX in alleviating airway hyperresponsiveness. PK20 effectively inhibited hapten-induced inflammation and mediator and signaling pathways in a manner seen with dexamethasone. Improved anti-inflammatory potency of the hybrid over the mixture of its moieties shows its preponderance and might pose a promising tool in modulating inflammation in asthma.

show abstract

“…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.…”

Section: Asthmamentioning

confidence: 99%

“…The effect of neuropeptides on mucus secretion in this pathology has been also described. K. Kaczyńska et al provides a brief overview of the functions of a number of neuropeptides (leptin, substance P, neurotensin) in normal respiration and in chronic pulmonary pathology [28]. A.K.…”

Section: Asthmamentioning

confidence: 99%

The role of regulatory neuropeptides and neurotrophic factors in asthma pathophysiology

et al. 2019

View full text Add to dashboard Cite

In the last decade, the attention of scientists in the field of biomedicine is focused on studying the relationship between the immunological and neurogenic components of the inflammatory response and their contribution to the pathophysiology of allergic inflammation in asthma. The review is devoted to detailing the mechanism of neurogenic inflammation involving regulatory neuropeptides (substance P, vasoactive intestinal peptide, calcitonin gene-related peptide) in the pathogenesis of bronchial hyperreactivity in asthma. The role of neurotrophic growth factors (nerve growth factor, brain-derived neurotrophic factor) in the regulation of remodeling of bronchi in asthma has been analyzed. The study of neuroimmune mechanisms in the pathophysiology of asthma will it possible to find new therapeutic targets in this research area.

show abstract

Neuropeptides and breathing in health and disease

Cited by 27 publications

References 175 publications

Beneficial Effects of Neurotensin in Murine Model of Hapten-Induced Asthma

Beneficial Effects of Neurotensin in Murine Model of Hapten-Induced Asthma

Endomorphin-2- and Neurotensin- Based Chimeric Peptide Attenuates Airway Inflammation in Mouse Model of Nonallergic Asthma

The role of regulatory neuropeptides and neurotrophic factors in asthma pathophysiology

Contact Info

Product

Resources

About