Microbial symbiosis and immunity: Difference between revisions
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[[Microbial symbiosis]] can occur through interactions between hosts and [[microbial organisms]] that are beneficial to both parties.<ref name=":2">Walter, Jens, Robert A. Britton, and Stefan Roos. "Host-microbial symbiosis in the [[vertebrate]] [[gastrointestinal tract]] and the Lactobacillus reuteri paradigm." Proceedings of the National Academy of Sciences 108, no. Supplement 1 (2011): 4645-4652.</ref> This symbiotic relationship, called [[mutualism (biology)|mutualism]], is constantly taking place throughout a host human or animal's body.<ref name=":3">Kitano, Hiroaki, and Kanae Oda. "Robustness trade‐offs and host–microbial symbiosis in the immune system." Molecular systems biology 2, no. 1 (2006).</ref> [[Microflora]] takes such a large part in supporting the host’s immunity to harmful pathogens, that it becomes vital to the host's health.<ref name=":1">Gallo, Richard L., and Teruaki Nakatsuji. "Microbial symbiosis with the innate immune defense system of the skin." Journal of Investigative Dermatology 131, no. 10 (2011): 1974-1980.</ref> |
[[Microbial symbiosis]] can occur through interactions between hosts and [[microbial organisms]] that are beneficial to both parties.<ref name=":2">Walter, Jens, Robert A. Britton, and Stefan Roos. "Host-microbial symbiosis in the [[vertebrate]] [[gastrointestinal tract]] and the Lactobacillus reuteri paradigm." Proceedings of the National Academy of Sciences 108, no. Supplement 1 (2011): 4645-4652.</ref> This symbiotic relationship, called [[mutualism (biology)|mutualism]], is constantly taking place throughout a host human or animal's body.<ref name=":3">Kitano, Hiroaki, and Kanae Oda. "Robustness trade‐offs and host–microbial symbiosis in the immune system." Molecular systems biology 2, no. 1 (2006).</ref> [[Microflora]] takes such a large part in supporting the host’s immunity to harmful pathogens, that it becomes vital to the host's health.<ref name=":1">Gallo, Richard L., and Teruaki Nakatsuji. "Microbial symbiosis with the innate immune defense system of the skin." Journal of Investigative Dermatology 131, no. 10 (2011): 1974-1980.</ref> |
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== Microbial Symbiosis in the Gastrointestinal Tract == |
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Symbiotic microorganisms, both beneficial and potentially pathogenic, reside in the [[gastrointestinal tract]] of humans. Imbalances in the bacterial composition, known as [[dysbiosis]], are thought to be a major determinant in [[inflammatory bowel diseases]] such as [[Crohn's disease]] in humans. It has long been known that intestinal microorganisms are important for the development of intestinal tissues. A recent study has demonstrated that a human symbiotic microorganism called [[Bacteroides|Bacteroides fragilis]] protects animals from experimental [[colitis]] induced by Helicobacter hepaticus. [[Polysaccharide A]] (PSA) from this bacteria singlehandedly protects humans from the inflammatory bowel diseases.<ref>[http://www.nature.com/nature/journal/v453/n7195/abs/nature07008.html A microbial symbiosis factor prevents intestinal inflammatory disease]</ref> |
Symbiotic microorganisms, both beneficial and potentially pathogenic, reside in the [[gastrointestinal tract]] of humans. Imbalances in the bacterial composition, known as [[dysbiosis]], are thought to be a major determinant in [[inflammatory bowel diseases]] such as [[Crohn's disease]] in humans. It has long been known that intestinal microorganisms are important for the development of intestinal tissues. A recent study has demonstrated that a human symbiotic microorganism called [[Bacteroides|Bacteroides fragilis]] protects animals from experimental [[colitis]] induced by Helicobacter hepaticus. [[Polysaccharide A]] (PSA) from this bacteria singlehandedly protects humans from the inflammatory bowel diseases.<ref>[http://www.nature.com/nature/journal/v453/n7195/abs/nature07008.html A microbial symbiosis factor prevents intestinal inflammatory disease]</ref> |
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The gut is home to an extremely complex [[microbiome]] of healthy and unhealthy [[bacteria]]. The immune system’s primary home is in the gut; so gastrointestinal [[microbiota]] has a direct effect on the body’s immune responses.<ref name=":0">Round, June L., and Sarkis K. Mazmanian. "The gut microbiota shapes intestinal [[immune system]] responses during health and disease." Nature Reviews Immunology 9, no. 5 (2009): 313-323.</ref> Without a regular microbiota, the body is more susceptible to infectious and non-infectious [[diseases]].<ref name=":0" /> A great diversity of symbiotic bacteria is necessary for animals to have fundamental [[nutrients]], digest certain compounds, protect against outside [[pathogens]], and create a healthy intestinal structure.<ref name=":0" /> An equilibrium of [[symbionts]] and [[pathobionts]] is critical to fight off outside pathogens and avoid [[inflammatory bowel disease]]. As we understand more about the roles of [[microbes]] in the gut, researchers will be able to discover more treatments like [[probiotics]] that can fill in niches of good bacteria to increase intestinal health and improve the [[immune system]].<ref>Hooper, Lora V., Lynn Bry, Per G. Falk, and Jeffrey I. Gordon. "Host–microbial symbiosis in the mammalian intestine: exploring an internal ecosystem." Bioessays 20, no. 4 (1998): 336-343.</ref> Heightening the robustness and diversity of bacteria flora in the gut aids in averting [[allergies]], [[autoimmune disease]], and [[cancer]].<ref name=":3" />There is still much to learn about the details of interactions between microbes and hosts in the [[gastrointestinal tract]], but research on symbionts like [[Lactobacillus reuteri]] help us understand how changes in the gastrointestinal [[microbiome]] can promote health.<ref name=":2" /> |
The gut is home to an extremely complex [[microbiome]] of healthy and unhealthy [[bacteria]]. The immune system’s primary home is in the gut; so gastrointestinal [[microbiota]] has a direct effect on the body’s immune responses.<ref name=":0">Round, June L., and Sarkis K. Mazmanian. "The gut microbiota shapes intestinal [[immune system]] responses during health and disease." Nature Reviews Immunology 9, no. 5 (2009): 313-323.</ref> Without a regular microbiota, the body is more susceptible to infectious and non-infectious [[diseases]].<ref name=":0" /> A great diversity of symbiotic bacteria is necessary for animals to have fundamental [[nutrients]], digest certain compounds, protect against outside [[pathogens]], and create a healthy intestinal structure.<ref name=":0" /> An equilibrium of [[symbionts]] and [[pathobionts]] is critical to fight off outside pathogens and avoid [[inflammatory bowel disease]]. As we understand more about the roles of [[microbes]] in the gut, researchers will be able to discover more treatments like [[probiotics]] that can fill in niches of good bacteria to increase intestinal health and improve the [[immune system]].<ref>Hooper, Lora V., Lynn Bry, Per G. Falk, and Jeffrey I. Gordon. "Host–microbial symbiosis in the mammalian intestine: exploring an internal ecosystem." Bioessays 20, no. 4 (1998): 336-343.</ref> Heightening the robustness and diversity of bacteria flora in the gut aids in averting [[allergies]], [[autoimmune disease]], and [[cancer]].<ref name=":3" />There is still much to learn about the details of interactions between microbes and hosts in the [[gastrointestinal tract]], but research on symbionts like [[Lactobacillus reuteri]] help us understand how changes in the gastrointestinal [[microbiome]] can promote health.<ref name=":2" /> |
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'''Microbial Symbiosis on the Epidermis''' |
== '''Microbial Symbiosis on the Epidermis''' == |
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Natural [[cutaneous microbiota]] on human skin is vital for the epidermis to fulfill its role as a line of defense against infection. Important microflora that live on the skin, such as [[Staphylococcus epidermidis]] produce [[antimicrobial peptides]] (AMPs). These AMPs signal immune responses and maintain an inflammatory [[homeostasis]] by reducing the release of extra [[cytokine]]. [[Staphylococcus epidermidis]] and other important microflora work similarly to support [[homeostasis]] and general health in areas all over the human body such as the [[oral cavity]], [[vagina]], [[gastrointestinal tract]], and [[oropharynx]]. <ref name=":1" /> |
Natural [[cutaneous microbiota]] on human skin is vital for the epidermis to fulfill its role as a line of defense against infection. Important microflora that live on the skin, such as [[Staphylococcus epidermidis]] produce [[antimicrobial peptides]] (AMPs). These AMPs signal immune responses and maintain an inflammatory [[homeostasis]] by reducing the release of extra [[cytokine]]. [[Staphylococcus epidermidis]] and other important microflora work similarly to support [[homeostasis]] and general health in areas all over the human body such as the [[oral cavity]], [[vagina]], [[gastrointestinal tract]], and [[oropharynx]]. <ref name=":1" /> |
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== Bacteriocins == |
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Various commensals (primarily Gram-positive bacteria), secrete bacteriocins, peptides which bind to receptors on closely-related target cells, forming ion-permeable channels and large pores.<ref name=":4">{{Cite journal|last=Hammami|first=Riadh|last2=Fernandez|first2=Benoit|last3=Lacroix|first3=Christophe|last4=Fliss|first4=Ismail|date=2012-10-30|title=Anti-infective properties of bacteriocins: an update|url=http://link.springer.com/article/10.1007/s00018-012-1202-3|journal=Cellular and Molecular Life Sciences|language=en|volume=70|issue=16|pages=2947–2967|doi=10.1007/s00018-012-1202-3|issn=1420-682X}}</ref> The resulting efflux of metabolites and cell contents and dissipation of ion gradients causes bacterial cell death. <ref name=":4" /> However, bacteriocins can also induce death by translocating into the periplasmic space and cleaving DNA non-specifically (colicin E2), inactivating the ribosome (colicin E3), inhibiting synthesis of peptidoglycan, a major component of the bacterial cell wall (colicin M). <ref name=":4" /> Bacteriocins are classified according to their biochemical properties, genetics, and bioactivity. <ref name=":4" /> |
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Bacteriocins have immense potential to treat human disease. For example, diarrhea can be caused by a variety of factors, but is often caused by bacteria such as ''C. difficile.'' <ref name=":4" /> ''Microbispora ATCC PTA-5024'' secretes the bacteriocin Microbisporicin, which kills clostridia by targeting prostaglandin synthesis.<ref>{{Cite journal|last=Castiglione|first=Franca|last2=Lazzarini|first2=Ameriga|last3=Carrano|first3=Lucia|last4=Corti|first4=Emiliana|last5=Ciciliato|first5=Ismaela|last6=Gastaldo|first6=Luciano|last7=Candiani|first7=Paolo|last8=Losi|first8=Daniele|last9=Marinelli|first9=Flavia|date=2008-01-25|title=Determining the Structure and Mode of Action of Microbisporicin, a Potent Lantibiotic Active Against Multiresistant Pathogens|url=http://www.sciencedirect.com/science/article/pii/S1074552107004061|journal=Chemistry & Biology|volume=15|issue=1|pages=22–31|doi=10.1016/j.chembiol.2007.11.009}}</ref> Additionally, bacteriocins are particularly promising because they kill bacteria differently than antibiotics do. As a result, many antibiotic-resistant bacteria succumb to death at the hands of bacteriocins. For example, ''in vitro'' growth of methicillin-resistant ''S. aureus'' was inhibited by the bacteriocin nisin A, produced by ''Lactococcus lactis.'' <ref name=":4" /><ref>{{Cite journal|last=Piper|first=C.|last2=Draper|first2=L. A.|last3=Cotter|first3=P. D.|last4=Ross|first4=R. P.|last5=Hill|first5=C.|date=2009-09-01|title=A comparison of the activities of lacticin 3147 and nisin against drug-resistant Staphylococcus aureus and Enterococcus species|url=https://academic.oup.com/jac/article/64/3/546/774205/A-comparison-of-the-activities-of-lacticin-3147#13535179|journal=Journal of Antimicrobial Chemotherapy|language=en|volume=64|issue=3|pages=546–551|doi=10.1093/jac/dkp221|issn=0305-7453}}</ref> Nisin A binds to [[lipid II]], the precursor to bacterial cell wall synthesis, resulting in increased membrane permeability. <ref>{{Cite journal|last=Hsu|first=Shang-Te D.|last2=Breukink|first2=Eefjan|last3=Tischenko|first3=Eugene|last4=Lutters|first4=Mandy A. G.|last5=de Kruijff|first5=Ben|last6=Kaptein|first6=Robert|last7=Bonvin|first7=Alexandre M. J. J.|last8=van Nuland|first8=Nico A. J.|date=2004-10-01|title=The nisin–lipid II complex reveals a pyrophosphate cage that provides a blueprint for novel antibiotics|url=http://www.nature.com/nsmb/journal/v11/n10/abs/nsmb830.html|journal=Nature Structural & Molecular Biology|language=en|volume=11|issue=10|pages=963–967|doi=10.1038/nsmb830|issn=1545-9993}}</ref> |
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== References == |
== References == |
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{{reflist}} |
{{reflist}} |
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Revision as of 03:02, 16 February 2017
Microbial symbiosis can occur through interactions between hosts and microbial organisms that are beneficial to both parties.[1] This symbiotic relationship, called mutualism, is constantly taking place throughout a host human or animal's body.[2] Microflora takes such a large part in supporting the host’s immunity to harmful pathogens, that it becomes vital to the host's health.[3]
Microbial Symbiosis in the Gastrointestinal Tract
Symbiotic microorganisms, both beneficial and potentially pathogenic, reside in the gastrointestinal tract of humans. Imbalances in the bacterial composition, known as dysbiosis, are thought to be a major determinant in inflammatory bowel diseases such as Crohn's disease in humans. It has long been known that intestinal microorganisms are important for the development of intestinal tissues. A recent study has demonstrated that a human symbiotic microorganism called Bacteroides fragilis protects animals from experimental colitis induced by Helicobacter hepaticus. Polysaccharide A (PSA) from this bacteria singlehandedly protects humans from the inflammatory bowel diseases.[4]
The gut is home to an extremely complex microbiome of healthy and unhealthy bacteria. The immune system’s primary home is in the gut; so gastrointestinal microbiota has a direct effect on the body’s immune responses.[5] Without a regular microbiota, the body is more susceptible to infectious and non-infectious diseases.[5] A great diversity of symbiotic bacteria is necessary for animals to have fundamental nutrients, digest certain compounds, protect against outside pathogens, and create a healthy intestinal structure.[5] An equilibrium of symbionts and pathobionts is critical to fight off outside pathogens and avoid inflammatory bowel disease. As we understand more about the roles of microbes in the gut, researchers will be able to discover more treatments like probiotics that can fill in niches of good bacteria to increase intestinal health and improve the immune system.[6] Heightening the robustness and diversity of bacteria flora in the gut aids in averting allergies, autoimmune disease, and cancer.[2]There is still much to learn about the details of interactions between microbes and hosts in the gastrointestinal tract, but research on symbionts like Lactobacillus reuteri help us understand how changes in the gastrointestinal microbiome can promote health.[1]
Microbial Symbiosis on the Epidermis
Natural cutaneous microbiota on human skin is vital for the epidermis to fulfill its role as a line of defense against infection. Important microflora that live on the skin, such as Staphylococcus epidermidis produce antimicrobial peptides (AMPs). These AMPs signal immune responses and maintain an inflammatory homeostasis by reducing the release of extra cytokine. Staphylococcus epidermidis and other important microflora work similarly to support homeostasis and general health in areas all over the human body such as the oral cavity, vagina, gastrointestinal tract, and oropharynx. [3]
Bacteriocins
Various commensals (primarily Gram-positive bacteria), secrete bacteriocins, peptides which bind to receptors on closely-related target cells, forming ion-permeable channels and large pores.[7] The resulting efflux of metabolites and cell contents and dissipation of ion gradients causes bacterial cell death. [7] However, bacteriocins can also induce death by translocating into the periplasmic space and cleaving DNA non-specifically (colicin E2), inactivating the ribosome (colicin E3), inhibiting synthesis of peptidoglycan, a major component of the bacterial cell wall (colicin M). [7] Bacteriocins are classified according to their biochemical properties, genetics, and bioactivity. [7]
Bacteriocins have immense potential to treat human disease. For example, diarrhea can be caused by a variety of factors, but is often caused by bacteria such as C. difficile. [7] Microbispora ATCC PTA-5024 secretes the bacteriocin Microbisporicin, which kills clostridia by targeting prostaglandin synthesis.[8] Additionally, bacteriocins are particularly promising because they kill bacteria differently than antibiotics do. As a result, many antibiotic-resistant bacteria succumb to death at the hands of bacteriocins. For example, in vitro growth of methicillin-resistant S. aureus was inhibited by the bacteriocin nisin A, produced by Lactococcus lactis. [7][9] Nisin A binds to lipid II, the precursor to bacterial cell wall synthesis, resulting in increased membrane permeability. [10]
References
- ^ a b Walter, Jens, Robert A. Britton, and Stefan Roos. "Host-microbial symbiosis in the vertebrate gastrointestinal tract and the Lactobacillus reuteri paradigm." Proceedings of the National Academy of Sciences 108, no. Supplement 1 (2011): 4645-4652.
- ^ a b Kitano, Hiroaki, and Kanae Oda. "Robustness trade‐offs and host–microbial symbiosis in the immune system." Molecular systems biology 2, no. 1 (2006).
- ^ a b Gallo, Richard L., and Teruaki Nakatsuji. "Microbial symbiosis with the innate immune defense system of the skin." Journal of Investigative Dermatology 131, no. 10 (2011): 1974-1980.
- ^ A microbial symbiosis factor prevents intestinal inflammatory disease
- ^ a b c Round, June L., and Sarkis K. Mazmanian. "The gut microbiota shapes intestinal immune system responses during health and disease." Nature Reviews Immunology 9, no. 5 (2009): 313-323.
- ^ Hooper, Lora V., Lynn Bry, Per G. Falk, and Jeffrey I. Gordon. "Host–microbial symbiosis in the mammalian intestine: exploring an internal ecosystem." Bioessays 20, no. 4 (1998): 336-343.
- ^ a b c d e f Hammami, Riadh; Fernandez, Benoit; Lacroix, Christophe; Fliss, Ismail (2012-10-30). "Anti-infective properties of bacteriocins: an update". Cellular and Molecular Life Sciences. 70 (16): 2947–2967. doi:10.1007/s00018-012-1202-3. ISSN 1420-682X.
- ^ Castiglione, Franca; Lazzarini, Ameriga; Carrano, Lucia; Corti, Emiliana; Ciciliato, Ismaela; Gastaldo, Luciano; Candiani, Paolo; Losi, Daniele; Marinelli, Flavia (2008-01-25). "Determining the Structure and Mode of Action of Microbisporicin, a Potent Lantibiotic Active Against Multiresistant Pathogens". Chemistry & Biology. 15 (1): 22–31. doi:10.1016/j.chembiol.2007.11.009.
- ^ Piper, C.; Draper, L. A.; Cotter, P. D.; Ross, R. P.; Hill, C. (2009-09-01). "A comparison of the activities of lacticin 3147 and nisin against drug-resistant Staphylococcus aureus and Enterococcus species". Journal of Antimicrobial Chemotherapy. 64 (3): 546–551. doi:10.1093/jac/dkp221. ISSN 0305-7453.
- ^ Hsu, Shang-Te D.; Breukink, Eefjan; Tischenko, Eugene; Lutters, Mandy A. G.; de Kruijff, Ben; Kaptein, Robert; Bonvin, Alexandre M. J. J.; van Nuland, Nico A. J. (2004-10-01). "The nisin–lipid II complex reveals a pyrophosphate cage that provides a blueprint for novel antibiotics". Nature Structural & Molecular Biology. 11 (10): 963–967. doi:10.1038/nsmb830. ISSN 1545-9993.