No abstract

The inflammatory response is modulated through interactions among the nervous, endocrine, and immune systems. Intercommunication between immune cells and the autonomic nervous system is a growing area of interest. Spatial and temporal information about inflammatory processes is relayed to the central nervous system (CNS) where neuroimmune modulation serves to control the extent and intensity of the inflammation. Over the past few decades, research has revealed various routes by which the nervous system and the immune system communicate. The CNS regulates the immune system via hormonal and neuronal pathways, including the sympathetic and parasympathetic nerves. The immune system signals the CNS through cytokines that act both centrally and peripherally. This review aims to introduce the concept of neuroimmune interaction and discuss its potential clinical application, in an attempt to broaden the awareness of this rapidly evolving area and open up new avenues that may aid in the treatment of inflammatory diseases.

Infl ammation is the body's response to insults, which include infection, trauma, and hypersensitivity. The inflammatory response is complex and involves a variety of mechanisms to defend against pathogens and repair tissue. In the lung, infl ammation is usually caused by pathogens or by exposure to toxins, pollutants, irritants, and allergens. During infl ammation, numerous types of infl ammatory cells are activated. Each releases cytokines and mediators to modify activities of other infl ammatory cells. Orchestration of these cells and molecules leads to progression of infl ammation. Clinically, acute infl ammation is seen in pneumonia and acute respiratory distress syndrome (ARDS), whereas chronic infl ammation is represented by asthma and chronic obstructive pulmonary disease (COPD). Because the lung is a vital organ for gas exchange, excessive infl ammation can be life threatening. Because the lung is constantly exposed to harmful pathogens, an immediate and intense defense action (mainly infl ammation) is required to eliminate the invaders as early as possible. A delicate balance between infl ammation and anti-infl ammation is essential for lung homeostasis. A full understanding of the underlying mechanisms is vital in the treatment of patients with lung infl ammation. This review focuses on cellular and molecular aspects of lung infl ammation during acute and chronic infl ammatory states.

We attempted to determine whether intrapulmonary sensory receptors are nourished by the pulmonary or the systemic circulation. Single-unit activity from the cervical vagus nerve was recorded in anesthetized, open chest, mechanically ventilated rabbits, comparing responses to right or left ventricular injection of 2% lidocaine (at 4 mg/kg). Airway mechanosensors [slowly adapting receptor (SARs) and rapidly adapting receptors] were inhibited by lidocaine, whereas chemosensors (C-fiber receptors and high-threshold A delta-receptors) were stimulated. Furthermore, all types of airway sensors were perfused preferentially by the pulmonary circulation. For example, 14 of the 15 tested SARs ceased discharge at 4.1 +/- 0.6 s after lidocaine injection into the right ventricle. The blocking effect lasted 35 +/- 6.2 s. In contrast, none of the 15 SARs ceased their activity after lidocaine injection into the left ventricle. Our data show that intrapulmonary sensors are mainly nourished by the pulmonary circulation. Their very short latency indicates that these sensors receive ample blood supply. Thus, intrapulmonary sensors rely on the pulmonary circulation to detect bioactive agents in the blood.