Species do not live in a world separate from each other. Organisms interact with other organisms everyday, and over time adapt to each other accordingly. Often, the evolution of two species can become strongly linked to each other, for better or worse. Heliobacter pylori is a bacteria that thrives in the acidic conditions of the human stomach. It causes stomach ulcers and is strongly correlated with gastric cancer. As recently as the 1980’s, the idea of a bacteria being able to survive in the stomach’s harsh conditions and being responsible for this disease was so controversial that it took one doctor intentionally infecting himself to prove its role in stomach ulcers. That doctor later won the Nobel prize in medicine for his work.
H. pylori did not first start infecting humans in the 80’s though. H. pylori and humans have been living (and battling) together for millennia. The earliest humans also played host to H. pylori. One way this can be shown is a creative use of a phylogenetic tree. Scientists sampled many different strains of H. pylori, and used them to create an ancestral tree of the different strains. They then compared the tree they made to geographic locations of their samples. What they found was that lineages of H. pylori matched perfectly with the migration patterns of ancient humans as they moved out of Africa. Newer strains of H. pylori are found where humans migrated to most recently. The strains were carried and dispersed based on how early humans moved around the globe.
This intimate relation between H. pylori and humans provides a great opportunity to explore coevolution. Humans and H. pylori have been locked in an arms race for thousands of years. H. pylori colonization poses serious health consequences to the host, which creates a selective pressure for humans that can prevent H. pylori infection. Likewise, the human body is an incredibly hostile environment towards foreign invaders like H. pylori, which creates a strong selective environment for H. pylori cells that can overcome human defenses. There is evidence this selective pressure is so strong that H. pylori begins adapting specifically to the host after initial colonization. Although not an innate aspect of human biology, antibiotics are another human defense against H. pylori. Antibiotic use creates a selective pressure for H. pylori that is so strong that resistant strains can develop remarkably quickly after attempted treatment.
Please watch the below video to learn more!
For further information see:
Linz, B., Ballouxm, F., Moodley, Y., Manica, A., Liu, H., Roumagnac, P., Falush, D., Stamer, C., Prugnolle, F., van der Mer, S.W., Yamaoka, Y., Graham, D.Y., Perez-Trallero, E., Wadstrom, T., Suerbaum, S., Achtman, M. 2007. An African origin for the intimate association between humans and Helicobacter pylori. Nature 445: 915-918
Gao, W., Cheng, H., Hu, F., Li, J., Wang, L., Yang, G., Xu, L., Zheng, X. 2010. The Evolution of Helicobacter pylori Antibiotics Resistance Over 10 Years in Beijing, China. Helicobacter. 15: 460-466.
Oh, J.D., Kling-Bäckhed, H., Giannakis, M., Xu, J., Fulton, R.S., Fulton, L.A., Cordum, H.S., Wang, C., Elliott, Glendoria., Edwards, J., Mardis, E.R., Engstrand, L.G., Gordon, J.I. 2006. The complete genome sequence of a chronic atrophic gastritis Helicobacter pylori strain: Evolution during disease progression. PNAS. 103: 9999-10004.
Blecker, U., Landers, S., Keppens, E., Vandenplas, Y. 1994. Evolution of Helicobacter pylori Positivity in Infants Born From Positive Mothers. Journal of Pediatric Gastroenterology and Nutrition. 19: 87-90
Kennemann, L., Didelot, X., Aebischer, T., Khun, S., Drescher, B., Droge, M., Reinhardt, R., Correa, P., Meyer, T.F., Josenhan, C., Falush, D., Suerbaum S. 2011. Helicobacter pylori genome evolution during human infection. PNAS. 108: 5033-5038.
Marshall, B.J., Warren, J.R. 1984. Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulcers. The Lancet. 323: 1311-131.
Avasthi, T.S., Devi, S.H., Taylor, T.D., Kumar, N., Baddam, R., Kondo, S., Suzuki, Y., Lamouliatte, H., Mégraud, F., Ahmed, N. 2011. Genomes of Two Chronological Isolates (Helicobacter pylori 2017 and 2018) of the West African Helicobacter pylori Strain 908 Obtained from a Single Patient. Journal of Bacteriology. 193: 3385-3386.
Contributed by Jimmy Shah, Sanjana Rao, and Laura Galarza
FOOD ALLERGY 101
Did you know that over 15 million Americans suffer from food allergies today? Consider this. Every 3 minutes, a food allergy reaction sends someone to the ER. Given these severe, potentially life-threatening medical conditions that have no known cure, we think studying the origins of food allergies can have significant clinical implications. So what exactly is a food allergy?
Food allergies manifest as adverse immune system reactions to harmless food substances. Once the allergen enters the body, it will be recognized by and bind to serum immunoglobulin E (IgE) – antibodies found in the lungs, skin, and mucosal membranes. IgE is attached by FcɛRI surface receptors on mast cells, an immune cell that helps the body create inflammatory responses. Interestingly, studies have shown that the high-affinity IgE-FcɛRI receptor binding is involved in responding to not only allergen exposure, but also parasite invasion.
Symptom severity is correlated with IgE antibody concentration
After the binding occurs, the allergen will cause antibody cross-linking on the mast cell surface and lead to something called mast cell degranulation, which means the mast cell will release its internal pro-inflammatory molecules, like histamines, leukotrienes, and prostaglandins, into the bloodstream. This will cause the onset of the allergy symptoms many of us may know well (especially in the pollen-rich spring) – sneezing, itching, coughing, hives, GI discomfort, etc. The most severe of these is anaphylaxis, a rapid and potentially life-threatening body state where blood pressure is lowered and emergency symptoms arise as a result. This brings us to our central question: why would evolution naturally select for us to be allergic to food that sustains us? The anomaly of food allergies and their past, present, and future benefits remain largely poorly-defined. However, research shows us that IgE antibody recognition of the allergen and shared defense mechanisms play a significant role in evolving allergic responses over time.
EVOLUTION IN FOOD ALLERGY
Although not fully understood, allergic responses are thought to have evolved from an immune defense mechanism against parasite invasion and other harmful toxin colonization. For years, scientists saw allergies as genetic accidents where aberrant IgE antibody production was just a mishap. But given the conservative nature of evolution, the IgE antibody class couldn’t have just arisen to be destructive only in the case of genetic disorders. Even if they did, evolution wouldn’t keep them around if they were solely harmful. In 1991, Margie Profet created the toxin hypothesis – the idea that responding to toxins and allergic reactions occur in very similar ways, that allergies are inherently toxic or affiliated with toxic substances, and that allergic responses mostly involve symptoms by which toxins are expelled (sneezing, vomiting, coughing, etc.) Last month, scientists at Stanford published evidence supporting the sustained positive evolutionary pressure to keep these IgE antibodies around. First, they found that in normal mice, previous exposure to venom allowed for greater survivability following a lethal venom injection, as compared to mice who were only treated with control solution. Then, they tested the role of the allergic pathway. Specifically, they studied three different types of mice responding to bee venom injections – mice without IgE, mice without IgE receptors on mast cells, and mice without mast cells at all. Unlike the normal mice, the three mutants did not benefit from previous venom exposure, since they did not have the key immunological players coordinating allergic response (Tsai, 2015). Although allergies have become less threatening in our daily lives, this allergic-type, IgE-associated immune response provides support for the idea that allergic responses are closely linked to the ways in which our bodies fight off toxins, long ago and today.
In another study published in October 2015, researchers at the London School of Hygiene & Tropical Medicine hypothesized that there must be some molecular similarity between parasites and allergen proteins, as the same branch of the immune system is found to kick in in both circumstances. After extensive data analysis, the team found that 2,445 known parasite proteins were structurally and sequentially (think base pairs A, C, T, G) similar to those found in the portion of the allergen that is prone to immune system attack. Further, measuring human cell immune response to a protein from a parasitic worm that was similar to a protein from a prevalent pollen allergen family revealed that blood serum reacted against both worm infection and the allergen via the same antibody mechanism (Tyagi, 2015).
Overall, the precise origin of food allergies has yet to be defined. However, we can infer that thousands of years ago, our ancestors may have consumed foods that contained harmful proteins or mimicked harmful substances, so allergies may have very well evolved to protect us. For example, someone could have ingested a raw plant that looked like a poisonous plant in the same family, so his body was on high alert. The IgE response naturally kicked in and perhaps was sustained throughout several generations as a heritable characteristic because it gave certain individuals an advantage over others in surviving and reproducing. As a result, those advantaged individuals likely passed on these beneficial traits, so eventually the proportion of individuals with these advantageous characteristics increased because those who didn’t, would lesser survivability.
This beneficial defense mechanism is not a novel idea – if unwanted substances enter the body, whether it just appears to be harmful or actually is, the organism’s ability to survive is potentially at stake. Thus, evolution would select for mechanisms by which these substances can be fought internally and expelled from the body. It therefore makes perfect sense that evolution would select for allergic responses as a means to protect one against destructive parasites and toxins.
Ultimately, food allergies account for $25 billion dollars in health costs each year, and cause 30,000 cases of anaphylaxis, 2,000 hospitalizations, and approximately 150 deaths annually. This significant burden on our population’s health warrants study of how allergic responses occur and the reasoning behind why they do. In doing so, perhaps we can find a cure! But for now, keep in mind that food allergies aren’t necessarily all bad and that they might actually be shielding you from something far worse.
FOR FURTHER READING…
Brandtzaeg, Per. 2010. Food Allergy: Separating the Science from the Mythology. Nature Reviews Gastroenterology & Hepatology 7, no. 7: 380–400.
Fitzsimmons, Colin Matthew, Franco Harald Fakone, and David William Dunne. 2014. Helminth Allergens, Parasite-Specific IgE, and Its Protective Role in Human Immunity. Frontiers in Immunology 5: 61.
Gross, Michael. 2015. Why did evolution give us allergies? Current Biology, no. 2: 53-55.
Liu, Andrew H. 2015. Revisiting the Hygiene Hypothesis for Allergy and Asthma. Journal of Allergy and Clinical ImmMatricardi, P. M. 2014. Molecular Evolution of the Allergy. Allergologie 37, no. 10: 423–24.
Machado, D. C., Horton, D., Harrop, R., Peachell, P. T. and Helm, B. A. (1996), Potential allergens stimulate the release of mediators of the allergic response from cells of mast cell lineage in the absence of sensitization with antigen-specific IgE. Eur. J. Immunol., 26: 2972–2980. doi: 10.1002/eji.1830261224
Platts-Mills, Thomas A. E. 2012. Allergy in Evolution. New Trends in Allergy and Atopic Eczema, edited by J. Ring, U. Darsow, and H. Behrendt, 96:1–6.
Ratnaparkhe, Milind B., Tae-Ho Lee, Xu Tan, Xiyin Wang, Jingping Li, Changsoo Kim, Lisa K. Rainville, et al. 2014. Comparative and Evolutionary Analysis of Major Peanut Allergen Gene Families. Genome Biology and Evolution 6, no. 9: 2468–88.
Sicherer, Scott H., and Hugh A. Sampson. 2009. Food Allergy: Recent Advances in Pathophysiology and Treatment. Annual Review of Medicine 60, no. 1 (2009): 261–77.
Tsai, Mindy, Phillip Starkl, Thomas Marichal. 2015. Testing the “toxin hypothesis of allergy: mast cells, IgE, and innate and acquired immune responses to venoms. Elsevier. Vol. 36: 80-87.
Tyagi, Nidhi, Edward Franell, Colin Fitzsimmons, Stephanie Ryan. Comparisons of Allergic and Metazoan Parasite Proteins: Allergy of the Price of Immunity. PLOS Computational Biology.
Wang, Jing, Litao Yang, Xiaoxiang Zhao, Jing Li, and Dabing Zhang. 2014. Characterization and Phylogenetic Analysis of Allergenic Tryp_alpha_amyl Protein Family in Plants Journal of Agricultural and Food Chemistry 62, no. 1: 270–78.
Zusi, Karen. 2015. An Evolutionary Basis for Allergies. The Scientist. http://www.the-scientist.com
Contributed by Ziqi Wu, Tian Mi, Lei Huang, Zhuo Li.
Imagine myriad fishes, including creatures the size of school buses, swimming in the Earth’s seas. Yup. That’s how things used to be 360 million years ago. It was not until the appearance of Devonian-Mississippian vertebrates that the modern range of body sizes became readily visible in the marine system. What happened in between these times? What made the creatures’ sizes shrink and spoiled the fun of scuba diving nowadays?
The answer is that a massive extinction happened about 359 million years ago, at the end of the Devonian Period. The scientists named it the Lilliput Effect: a temporary size reduction following mass extinction, which is usually temporary, but sometimes becomes persistent in specialized groups, such as birds, plankton, or island faunas. But how can a smaller size increase an organism’s fitness? One popular misconception is that the fittest organisms in a population are those that are strongest and largest. However, the Lilliput Effect has proved this wrong.
A giant fish has the length of a school bus before the die-off. However, after the asteroid hit earth and a mass extinction took place, the surviving fishes, and their descendants, are smaller since smaller size gives them an advantage.
The mechanism underlying the effect is controversial. One hypothesized model points to the effect of weather. Researchers (Dahl et al.) tracked down redox history of the atmosphere and oceans and found out that the radiation of large predatory fish (animals with high oxygen demand) correlates with atmosphere oxygenation. Therefore, a lower level of oxygen in the atmosphere might have played a role in the overall shrinkage. A temperature model based on Bergmann’s rule proposes that size is negatively influenced by temperature (Bergmann 1847). Previous studies suggested that warm-blooded vertebrate species are larger in colder climates than their congeners inhabiting warmer climates (Harries and Knorr 2009).
However, a more recent study points to another advantage of smaller size: smaller individuals grow and reproduce faster, and they adapt to their environments more quickly because of their relatively short generation times (Sallan and Galimberti 2015). Using holocephalans and ray-finned fishes as examples, they demonstrated that smaller vertebrates tend to have high reproductive rates, short generation times, and large populations. These traits may increase survival while promoting diversification via higher variation and population fragmentation.
Altogether, although there is empirical evidence suggesting that Lilliput effect could be a general response to environmental stress following various mass extinction events, there remain many puzzles to be solved.
For further reading, see:
Adam K. Huttenlocker and Jennifer Botha-Brink. 2013. Body size and growth patterns in the therocephalian Moschorhinus kitchingi (Therapsida: Eutheriodontia) before and after the end-Permian extinction in South Africa. Paleobiology39(2), 353-277.
Bing Huang, David A.T. Harper, Renbin Zhan, Jiayu Rong. 2010. Can the Lilliput Effect be detected in the brachiopod faunas of South China following the terminal Ordovician mass extinction? Palaeogeography, Palaeoclimatology, Palaeoecology, Volume 285, Issues 3–4, Pages 277-286.
Keller, G., Abramovich,S. 2009. Lilliput effect in late Maastrichtian planktic foraminifera: Response to environmental stress. Palaeogeography, Palaeoclimatology, Palaeoecology 284: 47-62
Peter J. Harries, Paul O. Knorr. 2009. What does the ‘Lilliput Effect’ mean? Palaeogeography, Palaeoclimatology, Palaeoecology, Volume 284, Issues 1–2, Pages 4-10.
Richard J. Twitchett. 2007. The Lilliput effect in the aftermath of the end-Permian extinction event, Palaeogeography, Palaeoclimatology, Palaeoecology, Volume 252, Issues 1–2, Pages 132-144, ISSN 0031-0182.
Sallan L, Galimberti AK. 2015. Body-size reduction in vertebrates following the end-Devonian mass extinction.Science 350(6262):812-815.
“Now, here, you see, it takes all the running you can do, to keep in the same place.”
– Lewis Carroll, Through the Looking-Glass
In this quote from Through the Looking-Glass by Lewis Carroll, The Red Queen gives Alice this explanation for the peculiarities of the land she has just entered. Scientists have used this interpretation, where Alice must “run” in order to stay alive, in order to represent certain scenarios found in nature. In the wild, situations occur where the fates of two species are intertwined. The Red Queen Hypothesis is an instance of coevolution, when two species evolve over time in response to one another.
It is a common misconception that life evolves randomly or by chance. While it is true that randomness is a factor, evolution is also impacted by non-random events. In a situation where the fates of predator and prey are closely linked, the two species become engaged in a deadly arms race, and this is one of the factors that can impact evolution. Prey are constantly evolving novel mechanisms to avoid their predators. In response to this, predators will need to evolve their own mechanisms to identify prey. Many times, this cycle repeats itself, causing both predator and prey to evolve together.
Red Queen and Fruit Flies. A good model of the Red Queen Hypothesis can be seen in the way the fruit fly Drosophila melanogaster evolves when it is infected by a parasite. Recently, researchers found that a phenomenon occurred in the first generation of infected flies where the parents’ genes became shuffled in their offspring: a process known as recombination. Genetic changes like this make it more likely that the mother’s offspring will not be recognizable by the same type of pathogen that attacked her.
The relationship between Drosophila and parasites is a classic example of the Red Queen Hypothesis, where two species evolve together in order to reach some sort of balance. In this case, the host is trying to outpace the parasite by altering the genes of its offspring so that the parasite can’t detect it. Soon enough, the parasite in turn develops new mechanisms to detect the novel prey. These species are engaged in a constant arms race that will never find a perfect balance, and just like Alice in Through the Looking-Glass, must keep running in order to stay alive.
For more information, check out these papers:
Campos, J. L., Halligan, D. L., Haddrill, P. R., and B. Charlesworth. 2014. The relation between recombination rate and patterns of molecular evolution and variation in Drosophila melanogaster. Molecular Biology and Evolution. 31: 1010-1028.
Hunter, C. M., and N. D. Singh. 2014. Do Males Matter? Testing the effects of male genetic background on female meiotic crossover rates in Drosophila melanogaster. Evolution. 68: 2718-2726.
Meselson, M. S., and C. M. Radding. 1975. A General Model for Genetic Recombination. Proceedings of the National Academy of Sciences. 72: 358-61.
O’Shea, K. L., and N. D. Singh. 2015. Tetracycline-exposed Drosophila melanogaster males produce fewer offspring but a relative excess of sons. Ecology and Evolution. 5: 3130-3139.
Shinn, C., Blanchet, S., Loot, G., Lek, S., and G. Grenouillet. 2015. Phenotypic variation as an indicator of pesticide stress in gudgeon: Accounting for confounding factors in the wild. Science of the Total Environment. 538: 733-742
Singh, N. D., Criscoe, D. R., Skolfield, S., Kohl, K. P., Keebaugh, E. S., T. A. Schlenke. 2015. Fruit flies diversify their offspring in response to parasite infection. Evolution. 349: 747-750.