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Surprise: Scientists discover that inflammation helps to heal wounds

Date:
October 5, 2010
Source:
Federation of American Societies for Experimental Biology
Summary:
New research study may change how sports injuries involving muscle tissue are treated as well as how much patient monitoring is necessary when potent anti-inflammatory drugs are prescribed for a long time.

A new research study published in The FASEB Journal may change how sports injuries involving muscle tissue are treated, as well as how much patient monitoring is necessary when potent anti-inflammatory drugs are prescribed for a long time. That's because the study shows for the first time that inflammation actually helps to heal damaged muscle tissue, turning conventional wisdom on its head that inflammation must be largely controlled to encourage healing.

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These findings could lead to new therapies for acute muscle injuries caused by trauma, chemicals, infections, freeze damage, and exposure to medications which cause muscle damage as a side effect. In addition, these findings suggest that existing and future therapies used to combat inflammation should be closely examined to ensure that the benefits of inflammation are not eliminated.

"We hope that our findings stimulate further research to dissect different roles played by tissue inflammation in clinical settings, so we can utilize the positive effects and control the negative effects of tissue inflammation," said Lan Zhou, M.D., Ph.D., a researcher involved in the work from the Neuroinflammation Research Center/Department of Neurosciences/Lerner Research Institute at the Cleveland Clinic in Ohio.

Zhou and colleagues found that the presence of inflammatory cells (macrophages) in acute muscle injury produce a high level of a growth factor called insulin-like growth factor-1 (IGF-1) which significantly increases the rate of muscle regeneration. The research report shows that muscle inflammatory cells produce the highest levels of IGF-1, which improves muscle injury repair. To reach this conclusion, the researchers studied two groups of mice. The first group of mice was genetically altered so they could not mount inflammatory responses to acute injury. The second group of mice was normal. Each group experienced muscle injury induced by barium chloride. The muscle injury in the first group of mice did not heal, but in the second group, their bodies repaired the injury. Further analysis showed that macrophages within injured muscles in the second group of mice produced a high level of IGF-1, leading to significantly improved muscle repair.

"For wounds to heal we need controlled inflammation, not too much, and not too little," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal, "It's been known for a long time that excess anti-inflammatory medication, such as cortisone, slows wound healing. This study goes a long way to telling us why: insulin-like growth factor and other materials released by inflammatory cells helps wound to heal."


Story Source:

The above story is based on materials provided by Federation of American Societies for Experimental Biology. Note: Materials may be edited for content and length.


Journal Reference:

  1. H. Lu, D. Huang, N. Saederup, I. F. Charo, R. M. Ransohoff, L. Zhou. Macrophages recruited via CCR2 produce insulin-like growth factor-1 to repair acute skeletal muscle injury. The FASEB Journal, 2010; DOI: 10.1096/fj.10-171579

Cite This Page:

Federation of American Societies for Experimental Biology. "Surprise: Scientists discover that inflammation helps to heal wounds." ScienceDaily. ScienceDaily, 5 October 2010. <www.sciencedaily.com/releases/2010/10/101004130105.htm>.
Federation of American Societies for Experimental Biology. (2010, October 5). Surprise: Scientists discover that inflammation helps to heal wounds. ScienceDaily. Retrieved October 31, 2014 from www.sciencedaily.com/releases/2010/10/101004130105.htm
Federation of American Societies for Experimental Biology. "Surprise: Scientists discover that inflammation helps to heal wounds." ScienceDaily. www.sciencedaily.com/releases/2010/10/101004130105.htm (accessed October 31, 2014).

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