EPicks: Acute phase response to exertional heat stroke in mice

In this video, Orlando Laitano discusses his latest paper investigating the acute phase response to exertional heat stroke in mice.

Read more in Experimental Physiology:
Acute Phase Response to Exertional Heat Stroke in Mice

John Iwaniec, Gerard P. Robinson, Christian K. Garcia, Kevin O. Murray, Lucas de Carvalho, Thomas Clanton, Orlando Laitano.

https://physoc.onlinelibrary.wiley.co...

Transcript:

Hello, my name is Orlando Laitano, and I’m an Assistant Professor at Florida State University.

Today I will be presenting the work entitled ‘Acute phase response to exertional heat stroke in mice’.

Recovery from exertional heat stroke is characterised by a robust inflammatory response, but the time course of the major acute phase proteins associated with this inflammatory response remains unknown.

Also, skeletal muscles have been shown to contribute to inflammatory response after stressful situations.

However, whether skeletal muscles can produce and release acute phase proteins into the circulation after exertional heat stroke is also unknown.

It is very challenging to study exertional heat stroke in humans as it can be lethal.

Therefore, we relied on a pre-clinical model where mice exercised in the heat of an environmental chamber set at 37.5°C and 40% relative humidity.

Mice exercised until they displayed neurological dysfunction, which occurred at a core temperature of 42°C.

To make sure that our model was inducing an inflammatory response that was mediated by cytokines, we measured the abundance and phosphorylation of STAT3 in the liver.

We observed that both were transiently elevated 30 minutes after exertional heat stroke.

One of the acute phase proteins we measured was serum amyloid A1 (SAA1).

We observed again a transient increase in both plasma and liver SAA1. This is relevant because SAA1 helps the immune system to neutralise bacterial infection.

The other acute phase protein that we studied was fibrinogen, which is known to participate in the coagulation cascade.

Fibrinogen was decreased in the liver and in the plasma, which was presumably being consumed to produce clotting formation, but to our surprise we observed an increased fibrinogen production in the skeletal muscles after exertional heat stroke.

In conclusion, our work shows that a single episode of exertional heat stroke induces a transient, acute phase response, and that the skeletal muscles can produce fibrinogen and therefore provide a source of fibrinogen to support clotting formation during recovery during recovery from the severe manifestation of heat-related illnesses.