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Rheumatoid Arthritis

Bilateral X-ray of the hands and wrists of a 54 year old patient with rheumatoid
arthritis. On the right hand (left), there is arthritis in the wrist joints.
There is a loss of bone space and the bones are beginning to fuse. On the left
hand (right), there are bony growths in the left fi...Read MoreRead More
Image by ZEPHYR, Science Source
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 * Science
 * Coronavirus Coverage




THE END OF INFLAMMATION? NEW APPROACH COULD TREAT DOZENS OF DISEASES.

Cancer, aging, and severe COVID-19 have all been linked to damage from
inflammation. Now scientists are flipping their focus to find new drugs that may
revolutionize treatments.


ByConnie Chang
Published March 4, 2022
• 12 min read
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Growing up in Atlanta, Georgia, Lauren Finney Harden had always had allergies.
But after she moved to New York City for her first job in 2007, inflammation
“just exploded” throughout her body.

“I had insane full-body rashes and strange gastro issues. I’d get massive burps
that made me feel like I needed to throw up, but nothing would come up but air,”
she says. Eventually, she was diagnosed with lupus, a disease in which the
immune system attacks the body’s own tissues and organs. She was put on a drug
called prednisone, a corticosteroid that tamps down inflammation.

But the cure, at times, felt worse than the disease. “I looked four months
pregnant all the time,” Finney Harden says, “and I’d get cold sores every other
week; my body could not fight off anything.”

Finney Harden’s experience is unfortunately a common one with traditional
autoimmune treatments like prednisone. A broad immunosuppressant, prednisone
works by disabling the production of pro-inflammatory molecules that are crucial
for the body to mount an immune defense. So while prednisone—and drugs like
it—are adept at quickly snuffing out inflammation, they leave the body
vulnerable to any bug it encounters, and they can come with toxic side effects.

“Simply stopping inflammation is not enough to return tissue to its normal
state,” says Ruslan Medzhitov, a professor of immunobiology at Yale School of
Medicine. This approach ignores the other side of the inflammation coin:
resolution. Resolving inflammation is an active, highly choreographed process
for rebuilding tissue and removing the dead bacteria and cells. When that
process is disrupted, inflammatory diseases arise.

In the early 2000s researchers began to recognize the role of inflammation in
conditions as varied as Alzheimer’s, cancer, diabetes, and heart disease,
prompting them to recast inflammation as the unifying explanation for a myriad
of ailments, including those we develop as we age. Even aging itself, and its
associated pathologies, is driven by persistent inflammation.



“Until relatively recently, we believed that inflammation just stopped,” says
Molly Gilligan, an internal medicine resident at Columbia University who studies
how the immune system impacts cancer development. Immunologists thought that
products of inflammation—molecules that trigger it and dead cells and tissue—are
eventually metabolized, or spontaneously dissipate on their own.

The reality is more complicated, and recognizing that could have game-changing
effects on how we treat a wide swath of diseases.


WHY IS INFLAMMATION DANGEROUS? 

Inflammation evolved to serve an important function: It rids our bodies of stuff
that doesn’t belong, including foreign invaders like bacteria and viruses, tumor
cells, and irritants like splinters.

“A classic example of inflammatory onset is the bee sting—the site becomes hot,
red, swollen, and painful,” says Derek Gilroy, a professor of immunology at
University College London. This response comes from a series of biological
changes: blood vessels dilate to deliver white blood cells to the site of
injury, making tissues turn red. Fluid also floods the site, causing swelling.
The molecules that trigger these vascular transformations precipitate the
itching, pain, and fever associated with inflammation.

White blood cells, the body’s first responders, then swarm and kill the
invaders. Under normal circumstances, this carnage is contained, with the
initial inflammatory response subsiding within 24 to 48 hours.

When inflammation becomes chronic, though, the chemical weapons deployed by
front-line immune cells often damage healthy tissue, and our bodies become
collateral damage. The price exacted includes worn joints, damaged neurons,
scarred kidneys, and more. Autoimmune diseases like rheumatoid arthritis and
lupus, characterized by pain and worsening disability, have long been associated
with persistent inflammation.

In extreme cases, such as the cytokine storms associated with sepsis or severe
COVID-19, inflammation can destroy and disable multiple organs, leading to
catastrophic system failure and death.




WHAT HAPPENS AFTER INFLAMMATION?

Medzhitov likens an infection to a broken pipe that has flooded an office with
water. Fixing the pipe might stop water from streaming in, but it doesn’t
restore the office to its previous, functional state. Similarly, inflammation
has a clean-up phase known as resolution, and it proceeds in a series of highly
coordinated steps.

Like inflammation’s onset, its resolution is orchestrated by an army of
signaling molecules. Among the most intensely studied are the specialized
pro-resolving mediators, or SPMs, which were discovered in the 1990s by Charles
Serhan, a professor of anesthesia at Harvard Medical School. Serhan was inspired
by his postdoctoral mentor, Bengt Samuelsson, who uncovered how fatty molecules
called lipids trigger inflammation. Serhan was searching for similar molecules
when he identified lipoxin. But to his surprise, rather than inciting
inflammation, lipoxin seemed to hamper it.

Over the next several years, Serhan and his colleagues identified additional
SPMs. These molecules are derived from essential fatty acids such as those
omega-3s famously found in cold-water fish like salmon and sardines. But they
are difficult to study in the lab. “One of the main challenges is that they have
short half-lives, so the body metabolizes them very quickly,” Gilligan says.
Because of this, researchers who work on them often turn to synthetic versions
of the molecules, or mimetics, which are simpler, more stable, and cheaper to
produce.

Catherine Godson, a professor of molecular medicine at University College
Dublin, has long been interested in diabetes, given its impact on global public
health as the most common cause of kidney failure. When she learned of SPMs, she
was excited by the idea of encouraging resolution to treat diabetics, a
“population with a particularly high risk for infection.”

In mice with diabetic kidney disease, scarring from kidney inflammation
gradually destroys the organ. Her team is testing the therapeutic potential of a
lipoxin mimetic in these and other animal models. They’ve also looked at the
mimetic’s effect in human tissue in lab cell cultures taken from patients with
atherosclerosis, an inflammatory disease of the blood vessel wall. In both
cases, inflammatory factors plummeted when the mimetic was introduced; for the
mice, the kidneys recovered their function in a stunning reversal of established
disease.



Gilroy notes, however, that the story on SPMs is incomplete. “While lipoxins are
present at levels in the body that indicate that they’re important in
resolution, other SPMs such as resolvins require more evaluation,” he says.


MANIPULATING MACROPHAGES

Scientists speculate that one way lipoxins and other pro-resolution molecules
work is by interacting with immune cells called macrophages.

Because they’re so abundant during inflammation, macrophages have traditionally
been thought of as pro-inflammatory cells, says Gerhard Krönke, an immunologist
and rheumatologist at the University of Erlangen-Nürnberg. “But a paradigm shift
in the last decade or so suggests that macrophages are pivotal players in the
resolution of inflammation.”

Gilroy agrees, calling macrophages “linchpin cells at the juxtaposition of
inflammation and resolution: It can go one way if we’re healthy and the other
way if we’re not.”

Initially, when the danger posed by invaders is at its peak, the macrophages
drawn to the area are inflammatory—secreting pro-inflammatory cytokines and
amping up production of antimicrobial agents. But this balance shifts as the
tide of the confrontation turns. After the number of viruses declines, the
debris left behind—viral remnants, dead immune cells, and other waste—must be
collected and cleared away before it sparks another cycle of inflammation.
That’s when the macrophages switch gears.

Attracted by “eat me” signals expressed on the surface of dying cells,
macrophages readily engulf and clear cellular corpses from the environment. But
it’s not just about clearing the wreckage—this act also flips a genetic switch,
reprogramming macrophages to restore balance to the system and heal the tissues.

“Macrophages start to produce factors that tell the local tissue, Don’t recruit
any more inflammatory cells here, or, Let’s proliferate and start repairs
there,” says Kodi Ravichandran, an immunologist at Washington University in St.
Louis whose research focuses on how dead cells are cleared from the body.




CLEARING AWAY CELLULAR DEBRIS 

Now consensus is building that many of the illnesses attributed to
inflammation—both chronic and acute—can be traced to a failure in resolution.
Often that translates into a failure to clear away dead cells.

“If you knock out receptors in the macrophages of mice that recognize dying
cells, for example, they become incapable of eating up these cells, resulting in
a lupus-like disease,” with symptoms such as arthritis and skin rash, says
Krönke. 

A similar mechanism is at work in older people, says Gilroy. As we age, the body
loses a protein that recognizes dying cells; this blocks macrophages’ ability to
find and eat debris. Locked in a pro-inflammatory state, these macrophages
continue to produce molecules that amplify the inflammatory response early on.

Perhaps COVID-19 has been more severe in older populations “because they’ve lost
some of the pro-resolution pathways with age,” suggests Luke O’Neill, an
immunologist at Trinity College Dublin. He notes that COVID-19 has also been
problematic for people with genetic differences that impact immune function,
resulting in overactive inflammatory responses or underactive pro-resolving
ones. His group and others have demonstrated that macrophages primed for
inflammatory action play a significant role in critical COVID-19 cases, and they
are currently testing pro-resolving strategies to combat this effect.

Cancer’s course, too, is affected when inflammation fails to resolve. The soup
of toxins, growth factors, and other inflammatory by-products that accompany
inflammation spurs cancer’s growth and spread. Many conventional treatments end
up exacerbating the problem, according to Dipak Panigrahy, an assistant
professor of pathology at Beth Israel Deaconess Medical Center in Boston.

“Chemotherapy and radiation are like sledgehammers,” Panigrahy says. “They may
kill the tumor, but the debris they create stimulates inflammation, which feeds
circulating tumor cells that survive the treatment.”



A decade ago, Panigrahy was puzzling over this conundrum when he met Serhan at a
conference on lipids in Cancún, Mexico. “I had just presented my research on
cell death in cancer and how there’s no way to clear the resulting debris when I
heard Serhan’s talk about how he discovered these lipids that eliminated
debris,” he says. The two Boston-based researchers have shared a close
collaboration ever since.

In proof-of-concept experiments conducted on mice, Panigrahy’s group was able to
prevent tumors from recurring after surgery by dosing the animals with mimetics
of resolvin, one of the pro-resolving mediators discovered in Serhan’s lab.
Phase one clinical trials for pancreatic, brain, and colon cancers will begin
this year, says Panigrahy.


LONG COVID AND INFLAMMATION

Although much work remains to decode its secrets, “long COVID likely results
from a catastrophic failure of appropriate immune response and resolution,”
Gilroy suggests.

Meg St. Esprit is part of a large cohort of COVID-19 survivors who continue to
suffer symptoms months after the virus has passed. She and her family contracted
the disease in November 2020, and for seven days the mother of four in
Pittsburgh, Pennsylvania, was beset by a high fever and severe headaches.
Debilitating fatigue, vertigo, and brain fog soon followed. But while her
husband and children recovered, St. Esprit’s symptoms lingered, and new ones
emerged.

Since her bout with COVID-19, she has developed blood clots and
myocarditis—dangerous consequences of inflammation. It’s also as if her entire
body has gone haywire. “Different parts of it regularly flare up now,” she says.
“My thumb joints swell to twice their normal size, my knee puffs out like a
grapefruit, and I’ve had hives more times than I can count.”

Drugs to tweak the natural inflammatory process would thus be a powerful tool in
our arsenal for long COVID as well. Even now the hunt is on. O’Neill and
colleagues, for example, are testing molecules in clinical trials that push
macrophages to be pro-resolving. SPMs are being tested extensively in animal
models of diseases like cancer and sepsis, and more modestly in small patient
trials studying eczema and periodontal disease.



But Gilroy cautions that the answer may be more nuanced than anti-inflammatory
versus pro-resolution, and that drugs targeting both approaches may be needed.

“It’s like driving a car at full speed,” he says. “In order to stop, you take
your foot off the accelerator, which would be like dampening inflammation’s
onset. And then you apply the brakes, or in other words, promote its
resolution.”

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