Abstract
In respiratory diseases, there is an increased expression of multiple inflammatory proteins in the respiratory tract, including cytokines, chemokines, and adhesion molecules. Chemokines have been shown to regulate inflammation and immune cell differentiation. Moreover, many of the known inflammatory target proteins, such as matrix metalloproteinase-9 (MMP-9), intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), cyclooxygenase-2 (COX-2), and cytosolic phospholipase A2 (cPLA2), are associated with airway and lung inflammation in response to various stimuli. Injuriously environmental stimuli can access the lung through either the airways or the pulmonary and systemic circulations. The time course and intensity of responses by resident and circulating cells may be regulated by various inflammatory signalings, including Src family kinases (SFKs), protein kinase C (PKC), growth factor tyrosine kinase receptors, nicotinamide adenine dinucleotide phosphate (NADPH)/reactive oxygen species (ROS), PI3K/Akt, MAPKs, nuclear factor-kappa B (NF-κB), activator protein-1 (AP-1), and other signaling molecules. These signaling molecules regulate both key inflammatory signaling transduction pathways and target proteins involved in airway and lung inflammation. Here, we discuss the mechanisms involved in the expression of inflammatory target proteins associated with the respiratory diseases. Knowledge of the mechanisms of inflammation regulation could lead to the pharmacological manipulation of anti-inflammatory drugs in the respiratory diseases.
Highlights
Inflammation is a protective response to cellular and tissue damage/injury
Many of the known inflammatory target proteins, such as matrix metalloproteinase-9 (MMP9), intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), cyclooxygenase-2 (COX-2), and cytosolic phospholipase A2, are associated with inflammatory signaling pathways induced by various stimuli, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), adenosine-5-triphosphate (ATP), cigarette smoke extract (CSE), lipoteichoic acid (LTA), or lipopolysaccharide (LPS) [2,3,4,5,6]
We demonstrated that overexpression of HO-1 protects against TNF-α-mediated airway inflammation by downregulation of TNFR1-dependent oxidative stress and NF-κB activation [83]. These results show that NF-κB plays a key role in mediating the expression of inflammatory proteins in airway and lung inflammation and injury (Figure 2)
Summary
Inflammation is a protective response to cellular and tissue damage/injury The purpose of this process is to destroy and remove the injurious agents and injured tissues, thereby promoting tissue repair. When this beneficial response occurs in an uncontrolled manner, the result is excessive cellular/tissue damage that results in chronic inflammation and destruction of normal tissue [1]. This review will focus on some general aspects of inflammatory signaling regulation and summarize current knowledge regarding the presence and functional roles of these inflammatory signal molecules within the respiratory system, and their proposed involvement in the expression inflammatory target proteins in response to proinflammatory mediators during airway and lung inflammation. The pharmacological interventions protect against inflammationinduced airway and lung diseases will be discussed
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