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A More Personal Post

Andover Rooksbury Mill 02
Rooksbury Mill located in Andover, Hampshire UK
As you may have noticed, my posts have become a bit irregular in the last few weeks. This is due to the fact that I am about to start a new position as a medical writer in England. As you can imagine, this turn of events has caused quite a stir in my life.

While I found blogging immensely rewarding, I also discovered that it is also a lonely career choice. It’s easy to underestimate the value of simple coffee pause chatter and general social interactions when that’s the status quo. However, when your life becomes completely devoid of these simple gestures, it becomes less vibrant. I found myself longing for day-to-day connections.

Blogging also lacks mentors. Even though I started to take online classes to fill in the gaps of my writing knowledge, it was hard to gauge my progress. As a result, I was never quite certain if my style was improving or if it was even understandable. Moreover, I had personal issues with calling myself a medical writer when I had never before worked in the industry.

Now, all of this is about to change, and I am extremely excited to start a new chapter in my life. Unfortunately, this does have consequences for my blogs. I will be unable to provide weekly overviews of current research as I have been doing for the last year. My goal, once I am settled in my new country, is to post monthly overviews instead.

Also, I am considering posting blogs about my transition from academia to medical writing. I believe this topic may be of considerable interest to those also considering taking the jump.

I see this period not as a discontinuation but more as a bumpy transition to more interesting content. I won’t be gone for long.

Sincerely,

M.E. Morgan

 

The Dark Side of Retinoic Acid and Interleukin-22

Salmonella species growing on XLD agar - Showing H2S production
IL-22 secretion during intestinal inflammation gives Salmonella a competitive advantage.
This week on TIBDI: Th1 cells can activate macrophages with innate signals alone, retinoic acid is no hero in Crohn’s disease, and interleukin-22 allows some pathogens to thrive.

TCRs Are Not Always Needed

Macrophages and T cells play are important in inflammatory bowel disease (IBD). Learning about how these cells interact could lead to more insight about how IBD progresses. Hope O’Donnell of the University of Minnesota has now gleaned new insights about their interactions. She looked into the mechanisms behind non-cognate stimulation of Th1 cells (non-TCR stimulation) and their ability to secrete macrophage-activating IFNγ. Using genetically manipulated mice and a Salmonella infection model, her results show that Th1 (and CD8+) cells produce plenty of IFNγ as long as they are exposed to Toll-like receptor ligands and products of activated inflammasomes like interleukin (IL)-18 and IL-33. This study underscores the flexibility and strength of the adaptive immune response.

The Pitfalls of Retinoic Acid

Retinoic acid is the current darling of those studying anti-inflammatory responses as it has been shown that retinoic acid can lead to regulatory T cell development. To determine if retinoic acid was actually lowered during Crohn’s disease (CD), Dr. Theodore J. Sanders of the Blizard Institute in London measured retinaldehyde dehydrogenase (RALDH) activity in cell samples collected from CD patients and controls. In all of the dendritic cells and macrophages tested, the RALDH activity (ability to produce retinoic acid) was increased in CD patients compared to controls. Surprisingly, blocking retinoic acid signaling actually decreased the ability of monocytes to differentiate into TNFα-producing macrophages in in vitro tests. This would suggest that retinoic acid is less helpful in CD than what one would expect.

Salmonella Exploits Interleukin-22

Interleukin-22 is a cytokine that is designed to boost immune defenses at the gut-lumen interface. It induces antimicrobial peptide release along with factors that sequester essential metal ions (like iron) that bacteria need to grow. Dr. Judith Behnsen of the University of California has now discovered that these processes can be exploited by certain pathogens, like Salmonella. She found that IL-22 deficient mice were much less susceptible to Salmonella overgrowth. The reason was that Salmonella has the ability to compensate for the loss of ambient metal ions, while this is not the situation for many commensals. This allows Salmonella to create for a rather large niche for itself, while IL-22-induced processes decimate the competition.

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