ls would suggest they do,” he says.
His research is showing the impact of even a small infection in the face of chronic inflammation. Using an animal model of sickle cell disease, a disease marked by systemic inflammation, he’s studying the host’s defense to microbial products such as lipopolysaccharide.
He’s found a resulting transformation of macrophages, which typically work like garbage collectors for the immune system, into large, pro-inflammatory cytokine-spewing cells. “Macrophages residing in areas of sickle cell-induced tissue injury become large, express different receptors on their surface and, when exposed to a superimposed infectious stimulus like lipopolysaccharide, respond with an overwhelming release of pro-inflammatory cytokines that are harmful to the host.”
The mice die rapidly and these re-programmed macrophages may help explain why children with sickle cell disease are more prone to overwhelming and potentially deadly infections following surgery.
“We need more investigations, more data on humans,” says Dr. Meiler, noting that while short-term outcomes of inflammation in response to surgery are pretty well established, proof of longer-term outcomes will take more work.
In the meantime, patients can benefit from early, ongoing collaboration by all members of the health care team to ensure risk reduction through steps such as minimizing surgical incisions, avoiding transfusions whenever possible and, when indicated, pharmacological treatment before surgery to help reduce cardiovascular complications.
“The challenge will be to incorporate these measures consistently across the health care process so that all eligible patients benefit from these insights,” Dr. Miler says.
Source: Eurekalert
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