neurokinin-a and Infections

Tachykinins represent a family of peptides which have significant effects on such diverse physiological responses as gut peristalsis, vascular permeability, and the transmission of pain. Traditionally, neurons have been identified as the major source of tachykinin peptides in peripheral tissues and in the central nervous system, resulting in their classification as neuropeptides or, more specifically, as neurokinins. The fact that a variety of cell types can express one or more members of the family of neurokinin receptors accounts for the remarkable ability of these tachykinin peptides to affect multiple organ systems and numerous biological responses. Perhaps one of the most surprising findings during the last 15 years has been the understanding that expression of neurokinin receptors on leukocyte populations can be constitutive or inducible. This fact establishes a receptor-mediated mechanism by which tachykinin peptides can affect both innate and specific immune responses. Due to the numerous cytokines, chemokines, and other soluble mediators that can modulate leukocyte responses, the importance of tachykinin-mediated modulation of the immune response has met with some skepticism. The following reviews make a strong case for neurokinin receptor expression by leukocytes as a significant participant in host response. From hematopoiesis to antigen-specific T lymphocyte responses, tachykinins are present and can dramatically modulate maturation and responsiveness of these immune cells. Studies which document this surprising role for neurokinin receptor expression by leukocytes are detailed in the following reviews.

Topics: Animals; Antiviral Agents; Bone Marrow; Hematopoietic Stem Cells; Humans; Immune System; Infections; Inflammation; Neurokinin A; Neurons; Receptors, Neurokinin-1; Substance P; T-Lymphocytes; Tachykinins

This study evaluated the effects and potential mechanisms of Qufeng Xuanfei decoction in animal model of post-infectious cough. Sixty SD rats were randomly divided into six groups (10 animals per group): control, disease model, low- (4.62 g kg(-1)), medium- (9.24 g kg(-1)), and high-dose (13.86 g kg(-1)) decoction, and positive treatment groups (dextromethorphan hydrobromide, 8 mL kg(-1)). To model post-infectious cough, all but control group animals were challenged with exposure to 50 g sawdust and 10 cigarette smokes for 30 min day(-1) for a total of 10 days, followed by subsequent exposures to lipopolysaccharide (20 µg) and capsaicin (10(-4) M) aerosols. The drugs were given by oral gavage for 15 days after which lung pathology, cell counts and cell differentials in bronchoalveolar lavage (BAL), and concentrations of neuropeptides [substance P (SP), neurokinins A (NKA) and B (NKB), and calcitonin gene-related peptide (CGRP)] in BAL (ELISA) were assessed. Compared with control group animals, significant inflammation and damage to bronchial epithelium were observed in the disease model group. A marked decrease in BAL percentages of all types of inflammatory cells was observed in the decoction-treated groups, with most changes in the medium-dose decoction group (p < 0.001 vs. disease model group). Further, airway inflammation and damage, as well as the levels of SP, NKA, NKB, and CGRP in BAL decreased the most in the medium-dose group (p < 0.001 vs. disease model group). In conclusion, medium-dose Qufeng Xuanfei decoction efficiently decreases the levels of neuropeptides, attenuates airway inflammation, and promotes recovery from disease.

Topics: Animals; Bronchoalveolar Lavage; Calcitonin Gene-Related Peptide; Cell Count; Cough; Disease Models, Animal; Drugs, Chinese Herbal; Infections; Lung; Male; Neurokinin A; Neurokinin B; Rats; Rats, Sprague-Dawley; Substance P