In general, most people understand the mechanism behind the sense of smell. Our noses pick up on an odour and our brains instruct us to react accordingly. If the aroma is pleasant, we tend to stay close. On the other hand, if what we pick up reeks, we head in another direction.
At the molecular level, the sense of smell is far more complex as it involves numerous part of the body known as the olfactory system. Inside our noses, olfactory bulbs detects molecules in the air, known as volatiles, and sends a signal to the brain. There, the information is processed and signals are sent out to invoke a variety of functions from memory to movement.
This mechanism of "smell" — biologically reacting to molecules in the air — may be best known to occur in the nose. Yet it is not the only organ that performs this function. Other parts of the body can also react to airborne chemicals, although the reactions are quite different.
The eyes offer a perfect example of this altered smelling process. They are continually coming into contact with volatiles and sending signals to the brain. The best studied of these chemicals is the lachrymatory factor, which is found in onions and gives them that distinct taste and smell. When the molecule hits ours eyes, a signal is sent to the brain much in the same way as a smell. The result is a directive to the lacrimal gland to start releasing tears to dilute out the chemical. The result is the all too common picture of someone crying while cutting up an onion.
Another recently identified type of smell occurs in the lungs. In this case, a molecule known as the olfactory receptor 78 can sense chemicals known to indicate a lack of oxygen, such as lactate. When this happens, the brain is told the body needs oxygen and we breathe as a result.
Our lungs may also be able to identify volatiles made by microbial invaders.
But this may not be the only way our lungs can sniff out trouble. Thanks to the work of a group of American researchers, our lungs may also be able to identify volatiles made by microbial invaders. But as their research shows, the target of the signal isn't the brain. Instead, it's the immune system.
The team focused on the role of volatiles in the lungs during infections in cystic fibrosis. Two well-known pathogens associated with this condition were chosen for the study, Pseudomonas aeruginosa and the fungus Aspergillus fumigatus. The team knew the lungs would react to these airborne chemicals upon contact. The question was whether a reaction would occur to the odours produced by these species.
The team used a complex yet fascinating model to mimic the lung in the lab. They constructed a miniature version of the typical human lung bronchiole. Inside this device, which measured only a few millimetres in length, the team placed all the right cells into a near-exact match of the three-dimensional matrix fund inside each of us.
At this point, it was time to determine whether the model lung could react to a standard infection. The team used the Aspergillusfungus as it causes a rapid and strong immune reaction. As expected, when the fungus was introduced into the system, the lung cells sensed the enemy through contact and produced a variety of defensive molecules such as cytokines, which act as homing beacons for immune cells.
Knowing they had successfully copied what happens in the lungs during infection, the team turned to the volatiles. Instead of putting the fungus directly into the environment, the team segregated the microbe from the cells. If any reaction was to occur, it only would be due to chemicals in the air.
The results of this study not surprisingly have implications for cystic fibrosis research.
When the results came back, the team was pleased to see a similar response from the miniature lung. The same defensive molecules were produced as were the cytokines when the Aspergillus volatiles were sensed. A similar response was seen when the Pseudomonas volatiles were introduced. Not surprisingly, when both the bacterium and the fungus were put into the system together, the response was significantly higher. The resulting immune response was highly inflammatory and paralleled what would be seen in cystic fibrosis patients.
The results of this study not surprisingly have implications for cystic fibrosis research. Having a sense of how the lungs can smell the invasion may help to better understand the progression of infection in these individuals. This may lead to options for treatment in the future.
This model may serve to better understand the link between volatiles and other lung diseases as well. With future testing, this model one day may be able to identify airborne triggers for a variety of problems such as asthma, chronic obstructive pulmonary disease, and the life-threatening condition acute respiratory distress syndrome. By learning how volatiles may influence lung health, we may gain get a better handle on these and other ailments and possibly find routes for meaningful therapies.
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