# Structural Biochemistry/Mucus Membrane System
## Introduction

Due to many potentially-harmful particles that settle on our airway paths, our bodies have developed innate defense mechanisms that are continually working to protect us from various infections. With the use of the perfluorocarbon/osmium/transmission electron microscopy fixation techniques and with confocal microscopy, the transport of mucus can now be visualized under high resolutions. The airway surface liquid, also identified as ASL, acts as the first line of defense and is lined along the epithelia lining. It is made up of two layers, the perciliary liquid layer, also known as PCL, and the mucus layer. The mucin rich mucus layer lies on top of the PCL, the very watery layer that surrounds the cilia (Matsui). The mucus layer is made up of heavily glycosylated macromolecules, genes MUC5AC and MUC5B. These macromolecules act as a spider web for trapping inhaled particles. Because of the large carbohydrate sequences which comprise these macromolecules, mucins bind to nearly almost every particle so that it can be cleared before it reaches the lungs. The viscoelastic properties of the mucus allows for the conversion of energy from beating cilia into mucus unidirectional transport along the airway surface. The frictional interaction of the PCL and mucus lining also acts as a secondary form of transport. If all else fails, the lungs also have another line of defense, cough clearance. Cough clearance is completely independent of cilia. Just to go over briefly, the efficiency of the cough is related to the height and volume of liquid on the airway surface. the PCL and mucus lining encounter vast amounts of various foreign particles. This can range anything from the fart that the person in front of you let out and the dust you may inhale when playing football to inhaling toxic fumes that may have accidentally slipped out from the lab. To go over some specific irritants, agents such as ammonia, organic vapors, and cigarette smoke induce mucus secretion from both the epithelial secretory cells and the submucosal glands. These cells are stimulated by direct and reflex stimulation, respectively. Prolonged inhalation of SO2 and cigarette smoke can cause goblet cell hyperplasia and enlargement of the submucosal glands. Also, various drugs induce mucus secretion. For example, prostaglandin (PG) stimulates mucus secretion among cats. But when prostaglandin is inhaled by humans, PG stimulates cough receptors.

## Mechanism

The mechanism of mucus clearanceis triggered by the effects of pollution or from stress from the body. Now when the mammalian body is stressed from the constant intake of foreign particles, extracellular nucleotides and nucleosides stimulate Cl- transport and inhibit Na+ absorption. This allows for the correct height and volume of the ASL. Under normal circumstances, the epithelial lining along the airways adjust Na+ and Cl− transport so that the PCL liquid levels stay intact. ATP is also released onto the airways, where it is metabolized into adenosine to activate the Cl- secretory channels. All of this is done to balance absorption and secretion for efficient mucus homeostasis. “Mechanotransduction is the process by which physical forces are translated to physiologic responses and is widely important in tissue homeostasis.”Pollution, in this case cigarette smoke, is a direct factor to the disruption of homeostasis among the ASL. When cigarette smoke is inhaled, an obvious effect is lung damage. What most people don’t realize is that it also causes your body to take longer and larger breaths to allow for optimal oxygen inhalation. Recent studies show that when normal human airway epithelial cells were subject to tidal breathing, the height of the ASL doubled, along with an increase of ATP in response to the shear stress.

## Reference

* http://www.jci.org/articles/view/15217
* http://www.ncbi.nlm.nih.gov/pmc/articles/PMC509095/pdf/1021125.pdf
* http://www.aapsj.org/articles/aapsj0801/aapsj080112/aapsj080112.pdf
* http://www.annualreviews.org/doi/pdf/10.1146/annurev.ph.41.030179.002101