Przy Boreliozie nasz organizm ma bardzo obnizona naturalna odpornosc

Przy Boreliozie nasz organizm ma bardzo obnizona naturalna odpornosc organizmu.

Czyli organizm nie ma szans aby uklad odpornosciowy sam zwalczyl bakterie.

Tutaj podano chorym na Borelioze antybiotyk.Po leczeniu wzrosla odpornosc organizmu.Warto zapoznac sie z plikiem PDF jest dokladnie wyjasnione.
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WNIOSKI
1. We krwi obwodowej chorych z boreliozą z Lyme stwierdzono istotny spadek odsetka PMN wykazujących ekspresję recepto...rów FcR i CR, mogący mieć wpływ na upośledzenie przebiegu reakcji odporności komórkowej w tej jednostce chorobowej.
 
2. W surowicy tych chorych równocześnie stwierdzono istotny wzrost poziomu krążących kompleksów immunlogicznych.
 
3. Zastosowana antybiotykoterapia wpłynęła na normalizację badanych parametrów,,
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Przedstawione wyniki badań własnych przeprowadzonych u chorych z boreliozą z Lyme wykazały obniżenie odsetka PMN z receptorami Fc dla fragmentu IgG i składnika C3 dopełniacza.

Jednocześnie w okresie ostrym choroby obserwowano wzrost poziomu KKI w surowicy chorych. W dostępnym piśmiennictwie jest stosunkowo niewiele danych dotyczących zachowania się granulocytarnych receptorów
FcR CR oraz KKI u chorych z boreliozą z Lyme (1).
 
Obserwowany w badaniach własnych wzrost poziomu KKI w ostrej fazie choroby przed leczeniem w porównaniu z grupą kontrolną można tłumaczyć wzmożoną produkcją przeciwciał przeciw B.b. wchodzących w skład KKI. Pancewicz i wsp. oraz Flisiak i wsp. obserwowali podwyższony poziom przeciwciał klasy IgM u chorych z boreliozą, który wraz z poprawą kliniczną ulegał obniżeniu (5, 14).

Na podstawie :

http://www.przeglepidemiol.pzh.gov.pl/zachowanie-sie-receptorow-granulocytow-fcr-igg-i-cr-oraz-krazacych-kompleksow-immunologicznych-u-chorych-z-borelioza-z-lyme?lang=pl


 http://www.przeglepidemiol.pzh.gov.pl/pobierz-artykul?id=196.
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tłumienie odporności wywołane infekcją Borrelia. Łącznie dane ujawniają nowy mechanizm, dzięki któremu B. burgdorferi niszczy adaptacyjną odpowiedź immunologiczną.
Co więcej, immunizacja grypy podana w czasie infekcji Borrelia również nie wywołała silnych odpowiedzi przeciwciał, dramatycznie zmniejszając ochronną zdolność przeciwwirusową odpowiedzi humoralnej.

Elsner RA, Hastey CJ, Olsen KJ, Baumgarth N.

https://www.ncbi.nlm.nih.gov/pubmed/26136236
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Borrelia burgdorferi Manipulates Innate and Adaptive Immunity to Establish Persistence in Rodent Reservoir Hosts

Borrelia burgdorferi sensu lato species complex is capable of establishing persistent infections in a wide variety of species, particularly rodents. Infection is asymptomatic or mild in most reservoir host species, indicating successful co-evolution of the pathogen with its natural hosts. However, infected humans and other incidental hosts can develop Lyme disease, a serious inflammatory syndrome characterized by tissue inflammation of joints, heart, muscles, skin, and CNS. Although B. burgdorferi infection induces both innate and adaptive immune responses, they are ultimately ineffective in clearing the infection from reservoir hosts, leading to bacterial persistence. Here, we review some mechanisms by which B. burgdorferi evades the immune system of the rodent host, focusing in particular on the effects of innate immune mechanisms and recent findings suggesting that T-dependent B cell responses are subverted during infection. A better understanding of the mechanisms causing persistence in rodents may help to increase our understanding of the pathogenesis of Lyme disease and ultimately aid in the development of therapies that support effective clearance of the bacterial infection by the host’s immune system
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Conclusion

The phenomena described earlier represent potential novel mechanism(s) for manipulation of the adaptive immune system by a pathogen that establishes persistent infections in its reservoir host. Elucidation of these mechanisms has important translational and clinical applications. A better understanding of how B. burgdorferi persists long term in rodents would be useful for understanding public health risks and devising appropriate preventative measures in endemic areas. Given the extensive similarities in the immune system of rodents and humans, it seems likely that the mechanisms of immune evasion and suppression outlined here may also be active in at least some infected humans. The induction of diseases such as carditis, arthritis, acrodermatitis chronica atrophicans, and neuroborreliosis seen in some patients with Lyme disease and infected companion animals, but rarely in mice, suggest maladaptation of B. burgdorferi to these hosts. Humans developing these inflammatory diseases to B. burgdorferi infection may have an immune system that is ineffectively suppressed by B. burgdorferi. There is good experimental evidence that a block of pro-inflammatory T cell responses, such as facilitated through blockade of IL-12, will cause reductions in arthritis development in C3H mice, but it also causes increases in Borrelia tissue loads (121, 122). Development of therapeutics that can shift the balance toward immune activation and bacterial clearance without causing inflammation-induced diseases might provide superior tools to the current antibiotic therapies.

Much remains to be elucidated about the mechanisms by which Borrelia evades the host response. This area of research provides a particularly rich ground for collaboration among evolutionary biologists, ecologists, microbiologists, and immunologists

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5316537/
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Tłumienie długotrwałej odporności humoralnej po zakażeniu Borrelia burgdorferi

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4489802/
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Antigens of Lyme disease of spirochaete Borrelia burgdorferi inhibits antigen or mitogen-induced lymphocyte proliferation.
https://www.ncbi.nlm.nih.gov/pubmed/8173554?dopt=Abstract
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CD4+ T cells promote antibody production but not sustained affinity maturation during Borrelia burgdorferi infection.
https://www.ncbi.nlm.nih.gov/pubmed/25312948?dopt=Abstract
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Borrelia burgdorferi elicited-IL-10 suppresses the production of inflammatory mediators, phagocytosis, and expression of co-stimulatory receptors by murine macrophages and/or dendritic cells.
https://www.ncbi.nlm.nih.gov/pubmed/24367705?dopt=Abstract
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Decreased up-regulation of the interleukin-12Rbeta2-chain and interferon-gamma secretion and increased number of forkhead box P3-expressing cells in patients with a history of chronic Lyme borreliosis compared with asymptomatic Borrelia-exposed individuals.
https://www.ncbi.nlm.nih.gov/pubmed/17177959?dopt=Abstract
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We demonstrated that an animal infected with Borrelia burgdorferi, the corkscrew-shaped bacteria that cause Lyme disease, launches only a short-lived immune response, and that protective immunity against repeat infections quickly wanes,” said Nicole Baumgarth, a professor in the School of Veterinary Medicine and an authority on immune response to infectious diseases at the UC Davis Center for Comparative Medicine. 

 “This study also suggests a possible mechanism responsible for the disappearance of antibodies following infection and subsequent treatment with antibiotics,” she said.
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The bacteria initially trigger a strong immune response in an infected animal, but findings from this study indicate that the bacteria soon cause structural abnormalities in “germinal centers” — sites in lymph nodes and other lymph tissues that are key to producing a long-term protective immune response.

For months after infection, those germinal centers fail to produce the specific cells — memory B cells and antibody-producing plasma cells — that are crucial for producing lasting immunity. In effect, the bacteria prevent the animal’s immune system from forming a “memory” of the invading bacteria ... 

http://www.researchfraud.com/lyme-immune-suppression/#pmid26136236

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