Chawla, Ajay, Khoa Nguyen, and Y.P. Sharon Goh. "Macrophage-mediated inflammation in metabolic disease." Nature Reviews: Immunology. 11. (2011): n. page. Print. <www.nature.com/reviews/immunol>.
Okay so reading the article cited above, a couple of ideas struck me as interesting that were aside from the original objective of the paper...I wanted to elaborate on one specific one and will momentarily. Throughout the paper they address the world-wide dilemma (and especially in the United States) of obesity. They offer new evidence to support the idea that there is indeed a connection between our immune system responses and various metabolic diseases, such as obesity and diabetes. They tell us in explicit detail that macrophages take on the role of a liasion for cross-talk between the metabolic and immune systems in metazoans.
Obesity-induced insulin resistance was a major point in the paper that was found to be caused by classically activated macrophages in adipose tissue that contain the receptors TLR2 and TLR4. When obesity occurs, saturated fatty acids are more prevalent and bind to these receptors, activating the macrophages to produce pro-inflammatory cytokines such as TNF (tumor necrosis factor) and IL-1beta. These leads to various inflammation in adipose tissue by multiple cascade pathways involving inflammasomes, pro-inflammatory genes, alternative activation genes, etc. Figure 1 in the paper does an exceptional job in explaining this cross-talk.
On to the point of this post...the authors mentioned in the second half of the paper that although it is evident macrophages aid in the pathogenesis of metabolic disease such as obesity, the cross-talk found between the immune and metabolic systems most likely evolved to a mechanism to aid immunity. This is interesting because the macrophages in the adipose tissue are most likely required to be alternatively activated macrophages rather than the classically activated ones described above. An example they give in which the cross-talk between the two systems may be beneficial is an acute bacterial infection. This bacterial infection promototes glycogenolysis in muscle tissue, gluconeogenesis in liver tissue, and lipolysis in adipose tissue. As a result glucose and free fatty acid levels are increased and said to support the metabollic demands of macrophages and non-immune cells. As the authors claim that this cross-talk "probably evolved to modulate insulin action and nutrient availability during times of infection." This made me wonder then if the alternatively activated macrophages aided the immune system when bacterial infection is present, will the benefits of taking anti-biotics during bacterial infection nullify or decrease the positive effects of the macrophages when a bacterial infection is present? I understand that antibiotics potentially kill the bacterial infection before it can produce nutrients for immune system cells such as macrophages, but I was wondering if there are any indirect side effects when this occurs? I went through the attached paper, but still am a little unclear on the situation. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2896384/
I found an article that somewhat addresses your question with parasites. Here is the link: http://naldc.nal.usda.gov/download/3673/PDF
ReplyDeleteIt seems that immune complexes and apoptotic cells elicited during these infections induce alternative activation states of macrophages, affecting disease outcome by, promoting parasite survival and proliferation and, on the other hand, limiting collateral tissue damage because of excessive type 1 inflammation. So it seems that modulation of macrophage activation may be allowing parasite persistence and long-term host survival. Though the paper said that addition research maybe needed, a possible reason for this response is due to these parasites causing extensive damage as they pass through tissues, releasing proteolytic enzymes that damage cells and tissue. The alternatively activated macrophages could play an important role in the repair of tissue damage, which is essential to remedy tissue lesions caused by these parasites.
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