but it can provoke autoimmune symptoms, gliosis where the immune
system of the brain is activated from the infection in the body, and/or neural
functioning can be impaired from the impact of cytokines on the brain.
Een gezonde leefstijl kan je weerstand verhogen. Dit kan onder meer door het verminderen van laaggradige ontstekingen, chronische milde ontstekingen in het lichaam.
Henriëtte schreef:Hier nog info van de mooie site www.borreliose.nl m.b.t. het immuunsysteem;
De Borrelia burgdorferi heeft echter bijzondere genetische mechanismen om te overleven onder de aanvallen van het humorale en cellulaire immuunantwoord en een verandert milieu, zoals in een antibiotica omgeving.
Overlevingsstrategie
Details
Last Updated: 18 August 2017
De Borrelia burgdorferi is in staat om op verschillende wijzen te overleven en deze zijn o.a.:
het ontwijken van het immuunsysteem door het lokaliseren op plaatsen die niet toegankelijk zijn voor het immuunsysteem zoals intracellulair of in extracellulaire matrix.
het ontsnappen aan het immuunsysteem door een grote variatie in oppervlakte antigenen.
een verandering in T helper cellen respons als de oorzaak van de resistente vorm van Lyme Borreliose
een zichzelf voortplantende inductie van autoimmuniteit waardoor een infectie met Borrelia chronisch wordt. Dit wordt gesteund door het recente feit dat het Borrelia Osp A gelijk is aan het humane LFA-1 antigeen.
een andere haalbare hypothese is dat het immuunantwoord van de gastheer verandert of onderdrukt wordt om zodoende de bacterie te overleven.
de bacterie is in staat zich met een S-laag (glycoproteïnen) te bedekken waardoor de antigenen onzichtbaar worden voor het immuunsysteem
de bacterie kan granules afsplitsen, overgaan in L-vormen, blebs, mycoplasmen, cell wall deficient CWD, die geen antigenen bezitten omdat de celwand verdwenen. Dit gebeurt vooral in een bacteriostatisch of bacteriocid milieu door b.v. antibiotica concentraties
Sproetje schreef; Of is dat wanneer er geen lymeklachten meer zijn?
Ja, dat vraag ik me ook af....
Ik meen dat als het Igm niet meer aanwezig is dat de infectie al langere tijd actief is en aansluitend het Igg positief wordt.
Henriëtte
Yes, you can get Lyme disease twice – or more.
Those who have been treated for Lyme in the past can thus be newly infected in one of two ways:
By a tick carrying the same strain that infected them before
By a tick carrying a different species of B. burgdorferi
Evidence shows that this immunity probably only applies to the specific strain that infected you the first time.
In a 2014 study published in the New England Journal of Medicine, researchers studied 17 patients who had contracted Lyme disease at least two times. Out of all 17, only one patient had been infected with the same strain twice. After rigorous probability-based studies, the researchers concluded it would be nearly impossible to find such a sampling of patients completely by chance.
In other words, evidence strongly suggested a strain-specific immunity.
This means Lyme patients may be protected against one specific strain of Lyme disease bacteria for up to six to nine years, but they are as vulnerable as ever to all the other strains – not to mention other kinds of tick-borne diseases.
Dr. Pal has isolated a protein produced by the bacteria that disables one of the body’s first immune responses, giving insight into mechanisms that are largely not understood. He has also observed a never-before-seen phenomena demonstrating that even without this protein and with the immune system responding perfectly, the bacteria can spring back in the body weeks later.
Understanding this bacteria, which is among only a few pathogens that can actually persist in the body for long periods of time, has major implications for the treatment of tick-borne diseases like Lyme disease, which is an increasingly chronic and consistently prevalent public health issue.
Reinfection is defined here as the development of a new tick-transmitted infection with Lyme Borrelia occurring after successful antimicrobial treatment of a prior episode of Lyme disease. This is distinguished from relapse, which is defined here as the presence of objective clinical and/or microbiological evidence of persistent infection with Lyme Borrelia after a noncurative course of antimicrobial treatment [19]. Reinfection has been well-documented only after successfully treated early infection (nearly always erythema migrans) and not after late manifestations of Lyme disease.
Je kunt niet immuun worden tegen de ziekte van Lyme. Elke nieuwe tekenbeet vormt een nieuwe kans op besmetting.
Auto-immuun betekent dat het immuunsysteem zich tegen het lichaam zelf keert. Een auto-immuunziekte ontstaat als er bij het opruimen van lichaamseigen celresten iets verkeerd gaat
A growing number of studies indicate that Lyme disease may trigger an autoimmune response in some individuals or symptoms may mimic an autoimmune disease.
[.....]
immune evasion
Micro-organisms have developed sophisticated methods of facillitating survival in host.
Borrelia, a spirochete bacterium, has evolved many strategies to ensure survival including utilising arthropod salvary protiens [ sialostatin, Sal 15], to assist establishment of infection by inhibiting T and dendric cells [ 16,17]
Borrelia prefers micro-anaerobic environments where the immune surveillance is low, such as the CNS, joint, and skin.
To survive in the host, borrelia has adopted a communication mechanism, quorum sensing to communicate with other bacteria in the colony network [18]
Borrelia can inhabit biofilm with other symbiotic pathogens, and evade the immune system and antimicrobials [19]
It can create and release blebs, encapsulated bits of Borrelia DNA to distract the immune system [20]
Borrelia is a pleomorphic bacterium [ exists as spirocheatal, L-and cyst form] [9], with a very slow replication rate [12-24 h. in vitro] [21]
Borrelia can employ multiple methods of antigenic variation of its outer surface proteins to evade immune detection.
It has 21 or more plasmids which enable it to change antigenicity and adapt its survival in the tick and the host [22,23]
B. hermsii, relapsing fever Borrelia alters its variable outer membrane protein (VMP)regularly which elicits waves of spirocheatemia of different antigen type and as a result prolonged IgM response [25]
Whereas, B.burgdorferi sensu lato employs segmental recombinations which results in a large number of Borrelia strains each whith different VlsE ( variable membrane protein-like sequence expressed lipoprotein) [24]
These differences can be responsible for sympton variation between genospecies [25,3]
The L-vorm lacks a cell wall allowing intracellular location and evasion of the immune system cystic forms
(intra-or extracellular) that may represent persistent Borrelia infection [9]
The clinical relevance of pleomorphic forms is not well understood [26]
Brazilian Borrelia (Baggio-Uoshinari syndrome) is unusual in that only the L-form has been detected, not a spirochaete [27]
Borrelia has the capacity to move faster than a human neutrophil, the fastest moving immune cell [28] which represents another survival mechanism.
[.....]
Terug naar “Artikelen en Linkjes”
Gebruikers op dit forum: Geen geregistreerde gebruikers en 0 gasten