c*********r
发帖数: 1312 | 1 上次在某个帖子里提到一个观点：
“还是听那个PI说，有人把免疫系统分为两大分支，一支负责监视寄生虫病原体什么的
，另一支和过敏啥的相关；这两分支相互平衡。最近有报道有人在过敏还是哮喘患者体
内注射寄生虫（其中包括他/她自己，这让我想起了Marshall和Morris），来加强前一
个分支抑制后一个分支，结果治好了过敏还是哮喘。。。下一步他/她要做大规模的试
验。。。这个只是听说而已，等他回来了，还需要查证查证。”
那个PI回来了，问他要消息来源，他说只是听到新闻，不知道是不是正式的文章发表。
于是自己查了一查，他说的那个目前还没找到，但找到几个有意思的报道。
先贴个这个：What Do Worms Have to Do With Asthma?
http://news.sciencemag.org/sciencenow/2011/02/what-do-worms-hav
WASHINGTON, D.C.—Parasites get a bad rap for a good reason. They cause a
litany of diseases with a terrifying host of symptoms. But mounting evidence
suggests that they can also prevent disease. And now there’s genetic
evidence to suggest that’s true. New research presented here yesterday at
the annual meeting of the American Association for the Advancement of
Science (which publishes ScienceNOW) finds that a gene associated with
increased risk of asthma is also linked to resistance against a parasitic
worm.
Scientists have long suspected that allergies and asthma—common in the
developed world and relatively rare in poor countries—are the result of
lack of exposure to microbes. This 2-decade-old idea, called the hygiene
hypothesis, suggests that lack of exposure to dangerous parasites in
childhood makes the adaptive arm of the immune system more likely to
overreact when it comes into contact with benign allergens.
Kathleen Barnes, an anthropologist and genetics expert at Johns Hopkins
University in Baltimore, Maryland, and her colleagues have been studying the
relationship between asthma and one particular parasitic worm, Schistosoma
mansoni, in Conde, a cluster of rural fishing villages on the coast of
Brazil. The worm is common in the region, and up to 85% of residents are
exposed to it.
Previous studies have shown that, in areas like Conde, where parasitic worms
are endemic, individuals who produce the most worm-specific antibodies—in
particular, an antibody called IgE, which triggers inflammation—tend to be
the most resistant to worm infection. According to Barnes’s research, that
resistance appears to be about 30% heritable.
The researchers noted that after they administered medication to rid Conde’
s residents of worms, the incidence of asthma and allergy symptoms increased
. So Barnes hypothesized that the mutations that help individuals fend off
parasitic worms might be the same mutations that make them susceptible to
asthma and allergies. If an individual produces a lot of IgE in response to
a worm, he or she might also produce a lot of IgE in response to an allergen.
The team collected blood and stool samples from 850 people in Conde. They
tested their blood for antibodies to the worm to gauge their immune response
and searched their stool for worm eggs to determine how heavily they were
infected. The researchers decided to focus on genes that have been linked to
asthma risk. They were particularly interested in IL-33, a gene linked to
inflammation that is overexpressed in the lung tissue of asthmatics compared
with people without the disease. “IL-33 stands as one of the strongest
candidate genes for asthma to date,” Barnes says.
Barnes and colleagues selected 23 genetic markers throughout the gene and
tested whether any of them were associated with worm resistance in the
residents of Conde. Five of them did show a strong association, and those
happened to be the exact same markers that are associated with asthma. “And
what we’re most excited about is that the relationship is inverse,”
Barnes says. “So a [gene variant] that conferred risk to asthma confers
protection against [worm infection].”
The researchers posit that natural selection might favor mutations that
protect against worm infection and that those same mutations might
inadvertently increase the risk of other diseases, such as asthma. The
researchers haven’t yet found the exact mutation responsible for the worm
resistance and asthma susceptibility. To find that, they’ll have to “drill
down deeper,” Barnes says. She speculates that the culprit may be a
mutation located in a genome region that regulates activity of the IL-33
gene.
Jennifer Ingram, a cell biologist who studies asthma at Duke University in
Durham, North Carolina, says the finding that deworming medication increased
the incidence of asthma symptoms is “striking.” She adds that Barnes’s
work is important because it points the field toward molecular mechanisms
that might contribute to asthma.
David Van Sickle, a medical anthropologist at the University of Wisconsin,
Madison, who presented during the same session as Barnes, points out that
the global prevalence estimates for asthma are based largely on asking
people whether a physician has ever told them they have asthma. But
diagnoses vary from culture to culture. Van Sickle found, for example, that
physicians in India are much less likely than doctors in Wisconsin to
diagnose a person who has clear symptoms of asthma with the disease. So the
true prevalence of asthma in India or other countries could be higher or
lower than current estimates. Changes in the prevalence of asthma wouldn’t
necessarily nullify the hygiene hypothesis, he says, but they could
complicate the picture. Still, he says Barnes's work is “elegant.”
再贴个这个：Eat Your Worms: The Upside Of Parasites
http://www.npr.org/2010/12/02/131753267/eat-your-worms-the-upsi
For years evidence has been mounting that intestinal parasites can actually
be a good thing for people with inflammatory bowel disease because certain
parasitic worms seem to help the intestine heal.
Now scientists think they've found at least one reason why this is so,
thanks to a man who has spent years treating his own bowel disease with
worms. Years ago, that man placed a call to P'ng Loke, a parasitologist who
was then working at the University of California, San Francisco.
"He had moved into the Bay Area and basically was looking for someone who
works on worms, and so he called me and convinced me to have lunch with him,
" Loke recalls.
Over lunch, the man told Loke a remarkable story about how he'd recovered
from ulcerative colitis, a bowel disease in which the immune system appears
to attack the lining of the colon, causing devastating ulcers. And for this
man, Loke says, the usual treatments, including steroids, hadn't helped.
"So he was being faced with the options of really severe immune suppressants
or a colectomy," the removal of his colon, Loke says.
But this man was a young entrepreneur with his own ideas. He'd run across
the work of scientist Joel Weinstock who is now at Tufts Medical Center in
Boston. Weinstock had done something that seemed bizarre: He had started
using parasitic worms to treat people with ulcerative colitis.
Radiolab
Could parasites be the shadowy hands that pull the strings of life? Radiolab
uncovers a world full of parasites and explores nature's moochers, with
tales of lethargic farmers, zombie cockroaches and even mind-controlled
humans (kinda, maybe). And we examine claims that some parasites may
actually be good for you.
Listen To Radiolab's "Parasites"
"So people would swallow microscopic eggs, and the eggs then hatch within
the GI tract, and that living agent that comes out is capable to interact
with the host's immune system," Weinstock says.
Weinstock thought these parasites might help because in places where they
are common, inflammatory bowel disease is rare. His hunch turned out to be
correct: The people in his study got better.
Worms A Key Factor In Healing
Loke says that was good enough for the entrepreneur in San Francisco, who
started looking for his own source of parasitic worm eggs.
"He managed to find a parasitologist in Thailand who was willing to help him
obtain these eggs, and then he infected himself," Loke says.
And he too got better and was feeling fine by the time he had lunch with
Loke. But he wanted scientists to figure out why the cure had worked. So he
offered to let researchers study his intestine over the next few years.
During that time, the worms began to die off and the man's disease came back
. So he took another dose of worm eggs and got better again. Through it all,
Loke and his colleagues were collecting blood and tissue samples from the
man.
An illustration of the life cycle of Trichuris trichiura
Enlarge Public Health Image Libarary/CDC
A diagram of the life cycle of the Trichuris trichiura parasite. Enlarge the
image for a more detailed description.
An illustration of the life cycle of Trichuris trichiura
Public Health Image Libarary/CDC
Infections of Trichuris trichiura, commonly called human whipworm, are more
frequent in areas with poor sanitation and tropical weather. This
illustration, from the CDC's Division of Parasitic Diseases and Malaria,
explains the life cycle of the parasite. (1) Eggs are passed with the stool.
(2) In soil, the eggs divide into two cells, then further divide (3) until
they become embryonated (4) and are capable of infecting. Eggs are infective
between two weeks and a month and can be ingested via soil-contaminated
hands or food. They hatch in the small intestine (5), and adult worms attach
themselves to the walls of the colon (6), where they can live for about a
year. Female worms shed 3,000 to 20,000 eggs per day.
"What we found was that after worm infection, the regions of the colon that
were previously not making mucus, were now making mucus again," he says.
That's a key factor in healing, and it looked like the mucus came back
because the worms were causing the body to produce a substance called IL-22.
Weinstock says that makes sense.
"This is a molecule that promotes epithelial growth and healing and perhaps
does other things to the immune system that would be potentially beneficial,
" he says. Weinstock says other studies suggest parasites can regulate the
immune system in ways that prevent it from going wild and attacking healthy
tissue, and he says it's likely that human evolution took that into account.
"Humans have had parasites ever since we evolved from living in caves or
swinging from trees or however it used to be, and disrupting these
relationships probably had consequences," he says.
Weinstock says drug companies are now trying to create parasites that would
actually be approved by the FDA for treating inflammatory bowel disease. The
research appears in the journal Science Translational Medicine.
今天比较无聊，发个帖子抛砖引玉。^_^ | b****r
发帖数: 17995 | 2 哮喘抑制肺部寄生虫
这个假说我3年前就听到一个seminar讲了
这个人是打得活虫子吗 | p*****m
发帖数: 7030 | 3 是消化道的巴 radio lab podcast有一期说这个的，GA前一段有一集 里面一个大学教
授拿自己做实验 也是吃了好多hook worm治疗哮喘
【在 b****r 的大作中提到】
: 哮喘抑制肺部寄生虫
: 这个假说我3年前就听到一个seminar讲了
: 这个人是打得活虫子吗
| c*********r
发帖数: 1312 | 4 这个对学生物的和学医的可能比较好理解，但是对于其他的人，可能比较难接受。呵呵 | b****r
发帖数: 17995 | 5 挺好理解啊，很多虫子 生命周期要经过肺脏，比如蛔虫，吃下卵后，卵变成幼虫进入
肠壁，从血
液循环进入肺脏，然后从喉咙被咳嗽咳出来再进入肠道，变成成体，产卵从大便排出
哮喘的话终末细支气管收缩，很显然会造成虫子无法从肺脏活着排出也就不能完成生命
周期
虫子也会进化出抑制哮喘的分子来平衡宿主的这种抵抗机制，不然会绝种
【在 c*********r 的大作中提到】
: 这个对学生物的和学医的可能比较好理解，但是对于其他的人，可能比较难接受。呵呵
| p****n
发帖数: 9263 | 6 一直想不明白虫子为啥这么执着非得一生游遍人体各个器官才罢休，费那劲干嘛
【在 b****r 的大作中提到】
: 挺好理解啊，很多虫子 生命周期要经过肺脏，比如蛔虫，吃下卵后，卵变成幼虫进入
: 肠壁，从血
: 液循环进入肺脏，然后从喉咙被咳嗽咳出来再进入肠道，变成成体，产卵从大便排出
: 哮喘的话终末细支气管收缩，很显然会造成虫子无法从肺脏活着排出也就不能完成生命
: 周期
: 虫子也会进化出抑制哮喘的分子来平衡宿主的这种抵抗机制，不然会绝种
| c*********r
发帖数: 1312 | 7 你的分析还挺有意思。但我打赌我们的讨论要是转到其它版比如说我爱宝宝(
NextGeneration)版，大多数妈妈们宁可让宝宝生活在过度干净的环境而得了哮喘过敏
也不会愿意让宝宝适时的暴露在病原体中。呵呵，猜想而已。
曾经我给一个学文科的女生讲有关细菌方面的一些知识，她的吃惊的面孔我至今都记着
。。。不是在嘲笑文科生，只是我觉得不同的training和教育背景会造成对于一些科学
事实的理解、接受有天差地别的区别。^_^
【在 b****r 的大作中提到】
: 挺好理解啊，很多虫子 生命周期要经过肺脏，比如蛔虫，吃下卵后，卵变成幼虫进入
: 肠壁，从血
: 液循环进入肺脏，然后从喉咙被咳嗽咳出来再进入肠道，变成成体，产卵从大便排出
: 哮喘的话终末细支气管收缩，很显然会造成虫子无法从肺脏活着排出也就不能完成生命
: 周期
: 虫子也会进化出抑制哮喘的分子来平衡宿主的这种抵抗机制，不然会绝种
| p*****m
发帖数: 7030 | 8 你这个是自己想当然出来的吧。。。现在一般认为parasite能抑制autoimmune respons
e（比如哮喘）是通过改变Th1/Th2的平衡实现的，也有说和T-reg有关系的。怎么可能和
parasite物理上是不是通过呼吸道有关系啊。。。
打个比方 hookworm有n多的报道能治哮喘和一系列消化道的autoimmune disease (IBD,
Crohn's disease, etc)，如果哮喘是因为hookworm要通过呼吸道进入消化系统，那ho
okworm也能治消化道疾病又是什么原理呢？hookworm甚至还有报道能治multiphle scle
rosis这个脑袋里的autoimmune disease，难道是因为hookworm还要过血脑屏障？
【在 b****r 的大作中提到】
: 挺好理解啊，很多虫子 生命周期要经过肺脏，比如蛔虫，吃下卵后，卵变成幼虫进入
: 肠壁，从血
: 液循环进入肺脏，然后从喉咙被咳嗽咳出来再进入肠道，变成成体，产卵从大便排出
: 哮喘的话终末细支气管收缩，很显然会造成虫子无法从肺脏活着排出也就不能完成生命
: 周期
: 虫子也会进化出抑制哮喘的分子来平衡宿主的这种抵抗机制，不然会绝种
| b****r
发帖数: 17995 | 9 我是听seminar听来的
为什么不可能和parasite通过呼吸道有关？难道寄生虫没有资格或者没有机会和T细胞
相互作用一
下？一开始就说不可能可不是科学的态度。其他地方T细胞的反应也许只是无意中的副
作用
我这个说法当然只是一个假说。但是一套抵御系统在完全不同的情况下被不同角度的使
用，例子
不难找，好比巨噬细胞大家都知道是吞噬消灭很多细菌的必须免疫细胞，但是HIV病毒
不是也可以
利用巨噬细胞保护和复制自己？
respons
能和
IBD,
ho
scle
【在 p*****m 的大作中提到】
: 你这个是自己想当然出来的吧。。。现在一般认为parasite能抑制autoimmune respons
: e（比如哮喘）是通过改变Th1/Th2的平衡实现的，也有说和T-reg有关系的。怎么可能和
: parasite物理上是不是通过呼吸道有关系啊。。。
: 打个比方 hookworm有n多的报道能治哮喘和一系列消化道的autoimmune disease (IBD,
: Crohn's disease, etc)，如果哮喘是因为hookworm要通过呼吸道进入消化系统，那ho
: okworm也能治消化道疾病又是什么原理呢？hookworm甚至还有报道能治multiphle scle
: rosis这个脑袋里的autoimmune disease，难道是因为hookworm还要过血脑屏障？
| p*****m
发帖数: 7030 | 10 我觉得你没分清楚提出一个可验证的假说和提出一个解释的区别。。要说解释 圣经那
个要有光怎么不比大爆炸简单一点？
【在 b****r 的大作中提到】
: 我是听seminar听来的
: 为什么不可能和parasite通过呼吸道有关？难道寄生虫没有资格或者没有机会和T细胞
: 相互作用一
: 下？一开始就说不可能可不是科学的态度。其他地方T细胞的反应也许只是无意中的副
: 作用
: 我这个说法当然只是一个假说。但是一套抵御系统在完全不同的情况下被不同角度的使
: 用，例子
: 不难找，好比巨噬细胞大家都知道是吞噬消灭很多细菌的必须免疫细胞，但是HIV病毒
: 不是也可以
: 利用巨噬细胞保护和复制自己？
| b****r
发帖数: 17995 | 11 哮喘能卡虫子的假说还是可以验证的吧，比如拿死虫子能引起哮喘，抑制哮喘症状则人
更容易得
寄生虫病，不能引起哮喘的虫子毒力更强
【在 p*****m 的大作中提到】
: 我觉得你没分清楚提出一个可验证的假说和提出一个解释的区别。。要说解释 圣经那
: 个要有光怎么不比大爆炸简单一点？
| p*****m
发帖数: 7030 | 12 你再想想？这个结果照样符合一般的假说 比如说parasite抑制T helper的activity
而且，你这个假说没法解释 hookworm为什么不光治哮喘 还能治IBD和MS
其实我的主要意思是，这个东东已经有很多研究了 我们没有必要海阔天空的设计解释
是把 呵呵 至少我不会认为我闭着眼睛想出来的解释能超过领域内多年的研究。现在的
生物学已经没有多少eureka的空间了
【在 b****r 的大作中提到】
: 哮喘能卡虫子的假说还是可以验证的吧，比如拿死虫子能引起哮喘，抑制哮喘症状则人
: 更容易得
: 寄生虫病，不能引起哮喘的虫子毒力更强
| b****r
发帖数: 17995 | 13 你的假说 parasite抑制T helper的activity和我的一定是互斥的吗，寄生虫和机体的
作用必定是
通过某个分子通路的，也许你这个就是啊.而且如果我这个假说是正确的，有可能给进
一步阐明其
他的分子机制提供一些线索
而且我不明白用来解释在一个器官发生的现象的假说为啥要解释那么多别的器官发生的
症状？可
能肠炎也和肠道对寄生虫的炎症反应有关，但那并不证伪我现有的假说。也许你的T细
胞假说是个
适合范围更广的假说，但是我估计也不是可以解释所有已经发现的现象的。
【在 p*****m 的大作中提到】
: 你再想想？这个结果照样符合一般的假说 比如说parasite抑制T helper的activity
: 而且，你这个假说没法解释 hookworm为什么不光治哮喘 还能治IBD和MS
: 其实我的主要意思是，这个东东已经有很多研究了 我们没有必要海阔天空的设计解释
: 是把 呵呵 至少我不会认为我闭着眼睛想出来的解释能超过领域内多年的研究。现在的
: 生物学已经没有多少eureka的空间了
|
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