pathogen

Centennial Shigella A strain of the dysentery-causing bacterium isolated in 1915 tells the story of a young soldier who died of the disease in the early days of World War I.

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Centennial Shigella

A strain of the dysentery-causing bacterium isolated in 1915 tells the story of a young soldier who died of the disease in the early days of World War I.

 

In early 1915, less than a year into the First World War, Private Ernest Cable, a 28-year-old British soldier serving in the 2nd Battalion of the East Surrey Regiment, stumbled into No. 14 Stationary Hospital in Wimereux, France. He was suffering from severe abdominal cramping and bloody diarrhea. Doctors diagnosed him with dysentery. Not long after, Cable was dead.

Nicholas Thomson, a genomicist at the Wellcome Trust Sanger Institute, first came to know of Cable’s lethal infection at a conference in October 2011. At the meeting, he met a woman named Philippa “Pippa” Bracegirdle, who worked in the archives of the UK National Collection of Type Cultures (NCTC), the oldest collection of bacterial cultures in the world. Over a drink, Bracegirdle mentioned that the collection contained an isolate of Shigella, the dysentery-causing kin of E. coli that had killed Cable. Later identified as Shigella flexneri serotype 2a, it was the first bacterial isolate deposited in NCTC’s now 5,000-sample-strong biobank.

With the 100-year anniversary of the start of “the war to end all wars” coming up in just a few years, Thomson was inspired to take a closer look at the isolate. Having studied the genetics of Shigella and other pathogens, he decided to sequence the bacterium. But as Thomson learned more from Bracegirdle about the isolate, he realized he had a rare opportunity to find out more about the patient who died from it a century ago.

 

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Protein Clumps Spread Inflammation ASC specks

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Protein Clumps Spread Inflammation ASC specks—protein aggregations that drive inflammation—are released from dying immune cells, expanding the reach of a defense response.

 

Research teams based in Germany and Spain have independently discovered that cells transmit inflammation by releasing ASC specks, bacteria-sized clumps of protein key for cytokines’ maturation, according to two papers appearing today (June 22) in Nature Immunology. The protein aggregations are a component of inflammasomes, which sense pathogens and cell damage and set off innate immune inflammation. Researchers previously thought inflammasomes acted only inside single cells, but this latest work has found that the ASC specks can effect extracellular inflammation. The teams also found that macrophages can take up released ASC specks, perpetuating the immune response.

ASC specks are prevalent in the tissues of people with some inflammatory diseases, and could be drug targets for reducing inflammation or diagnostic markers of these diseases, the researchers noted.

Their findings help explain the mystery of how relatively localized contact between a cell and a pathogen or product of cell damage can lead to widespread inflammation, explained George Dubyak, a cell physiologist at Case Western Reserve University in Cleveland, Ohio, who was not involved in the study. “The inflammasome specks can become carriers for intracellular signaling,” he said.

“I think this is much-needed information on how inflammation may actually spread after inflammasome activation and offers a whole host of activities for intervention now that have been unexplored,” saidRobert Keane, a professor of physiology and biophysics at the University of Miami Miller School of Medicine who was not involved in the study.

 

Full story at TheScientist