Download E SE HAHNEMANN NON AVESSE LETTO KANT

In-dept study
The Immune Antinfectious Reaction
in the Atherogenetic Process
Author: Angelo MICOZZI
E-mail: [email protected]
The assessment criteria of chronical diseases adopted by Hahnemann is requited by basic research in modern immunopathology. According to the original homeopathic model, chronical diseases are triggered by an infectious process determining a gradual and increasingly serious alteration of an individual’s vital force. This alteration is expressed through an evoluting symptomatology and can be easily compared to the immune reaction by which an individual interacts in
a specific way with the triggering pathogenic agent. Based on this model, the role of infectious
agents is not determinant to the pathogenetic consequences, but it is mediated by a specific immune reaction and provides a good example of pathologic model shared by homeopathic methodology.
Atherogenesis is an evoluting process that can be effectively studied and evaluated in the
light of modern immunopathological findings and provide an interesting reading for the chronical disease model called psoric by Hahnemann.
The atherogenetical mechanism shows a typical, slow evolution: a “clinical” silence [1] very
similar to what Hahnemann says on psoric latency [2] in its general aspects. In fact, this latency shows itself through a minimum, often not emphasised, symptomatology, to which the patient adjusts due to its slow and gradual course [3]. Its clinical expression can be chronical, as
in stress angina or claudicatio intermittens - as the atherosclerotic lesions increase their seriousness - but sometimes it expresses itself through a dramatic and acute event, such as myocardial infarction and ictus. Atherosclerosis is best known as an occlusive event due to stenotic
lesions limiting arterial blood circulation. However, vascular walls ectasias are not unlikely to
be found, and an aneurismatic disease is often developed especially in major arteries such as
aorta [4].
Atherosclerotic lesions are caused by a focal storage of lipoproteins in the arterial intima.
These lipoproteins carry molecules of lipids such as cholesterol and triglycerides, together with
proteins and phospholipids enabling their blood solubility. Lipoprotein storage is realised
through their link with some elements of arterious extracellular matrix, especially proteoglycans. This causes an increase in their permanence in the intima, which in turn generates a series of modifications needed for the gradual development of lesions. Lipoproteins, LDL (Low
Density Lipoproteins) in particular, oxidize very easily. The storage of oxidized LDL represents
the first and main phase in the atherosclerotic mechanism. In a subsequent phase, monocytes
and lymphocytes are recruited, which link to adhesion molecules (especially ICAM-1, also
called CD54) [5], present on the endothelium surface. This is a typically inflammatory event
that shows an increased number of cytokines in the lesion site, cytokines of the acute phase,
such as IL-1 and TNF. If the presence of lymphocytes is a signal of a specific immune reaction
to possible pathogenic agents involved, monocytes have a twofold role. Besides their phagocytizing function, they differentiate themselves into macrophages and tend to undergo a subsequent transformation into foam cells. This transformation depends on the insertion of oxidized
LDL into the cells, whose functional meaning can be seen as an attempt to rinse lipids in their
intimal storage. Contrary to expectations, LDL endocytosis within the macrophages is strictly
linked to a reduced expression of their receptors. The latter belong to a family of molecules
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whose most significant representative is CD36, present on the macrophagus membrane [6]. In
a subsequent phase to the LDL storage, macrophages stimulate the proliferation of smooth
muscular cells and addition of extracellular matrix in atherosclerotic plaques through the production of some growth factors such as PDGF (Platelet-Derivated Growth Factor) and FGF (Fibroblast Growth Factor).
If we carefully read the pathogenetic mechanism of atherosclerosis, we must consider LDL
receptors as the key molecules of the whole process. Two classes can be observed in the family
of these receptors, called “scavenger A and B” and showing different functions. Class “A” receptors enable the degradation of oxidized LDL in peritoneal macrophages, whereas class “B” receptors have an impact on the degradation at hepatic level, mainly helping the metabolism of
cholesterol esters from HDL (High Density Lipoprotein). A diet rich in cholesterol provokes an
80% reduction of B receptors in the liver [7]. The main representative of B receptors is a small
88kD glycoprotein, called CD36, that penetrates the membrane of macrophages. CD36-null
strains show a 76.5% increase in aortic atheromatosic lesions [8], in a highly variated diet (i.e.
a diet rich in fat). Moreover, recent studies have shown that a reduced CD36 expression is associated to a LDL increase also in human beings [9].
The pathogenetic role of infectious and inflammatory processes in the deregulation of LDL
receptors was hypothesised long ago. An elegant experimental model with Syrian hamsters the inoculation of bacteric LPS (lipopolysaccharides) and zymosan, aiming respectively at reproducing infectious and inflammatory conditions - showed that oxidised LDL levels were 4-6
times higher than controls. Among the infectious agents who cause an increase in oxidised
LDL, Chlamydia pneumoniae has undoubtedly raised the attention of many researchers. Assumed for a long time as the cause of atypical pneumonia, this intracellular-forced bacterium
causes several chronical effects [10], among which atherosclerosis. One of the most important
phases of this process seems to be the interaction between chlamydia and monocytes/macrophages, whose final event is the creation of foam cells. In this matter, two pathogenetic mechanisms can be observed: the direct action of bacteric lipopolysaccharides, if LDL
are present, and the action of Hsp60 (heat shock proteins of chlamydia), the latter contributing to the oxidation of low density lipoproteins. Contrary to expectations, the entrance of LDL
in the macrophages is independent from their link with scavenger receptors [11]. This can be
explained by saying that receptors bind themselves only to non-oxidised lipomolecules and
prevent endocytosis. To this end, the interaction between chlamydia pneumoniae and the scavenger receptor could have a key role [12].
Also cytomegalovirus (CMV) was related to atherogenesis, especially in young patients. Many
epidemiological studies, animal models and molecular analysis confirm this assumption since
they show the presence of viral Dna in atherosclerotic lesions [13]. Serocholesterol concentrations appears to be strictly related to the IgG antibody positivity of CMV. This aspect offers an
interesting scenario on the role of the specific immune reaction in the pathenogenesis of many
diseases, including atherosclerosis.
All epidemiological studies underline the strict relation between the infectious memory, expressed in permanent IgG immunoglobulins, and the atherogenetic mechanism. According to
homeopathic methodology, the idea of persistent infectious agent has been known for a long
time [14], as the ensuing alteration of the vital force, which can be represented as the modification of the balance preexistent to infection, for many aspects similar to the immune reaction.
In particular, IgG seropositivity in Chlamydia pneumoniae is now considered as an important
risk factor in coronary artery diseases, because of its high association with the lipidic profile
and its procoagulant activity [15]. Elegant animal models suggest that the immunitary reaction to CMV has a role in the aetiopathogenesis of vascular damage, especially as concerns the
high endothelial sensitivity to infection [16], also when viral Dna is not present in the atherosomatic site. Similarly, other works show that the presence of specific IgG to Helicobacter pylori and HAV (hepatitis A virus) has a significant role in the formation of atherosomatic plaques
[17]. To stress how the immune reaction affects the pathologic process, intimal lesions have revealed to contain T specific lymphocytes able to react to Chlamydia pneumoniae antigens [18].
This specific reaction seems to occur also in thromboembolic venous disease [19]. Some Authors stressed also the possible antigenic similarity between Chlamydia and some lipoproteins,
with creation of immunocirculating complexes, containing specific IgG, that increase the risk
of atherogenesis [20]. Chlamydia pneumoniae can infect many cells, among which monocytes
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and macrophages, who play a fundamental role in the development of atherosclerosis. The infectious persistence inside the macrophages allows the maintenance of a local immune reaction, mediated by T specific lymphocytes [21].
The pathogenic model of atherosclerosis shows very interesting similarities with the methodology left by Hahnemann and used to study chronical diseases. According to this analogy,
whose characterising element is the infectious trigger, a drug offering a good similarity with the
patient’s general symptomatology and with aetiologic elements of atherosclerosis can be detected. We have seen that Chlamydia pneumoniae has a clear role in the specific activation of this
process, inducing an immune reaction that can be considered the real atherogenetic boost. Following Hahnemann’s anti-infectious “specific” remedy, the study of medical issues allows us to
detect a drug having an action on anti-chlamydia immune reaction. We have proposed for long
time the use of nitric acid, in LM potency, with the aim of seroconverting specific IgG and IgA
antibodies of both Chlamydia pneumoniae and thrachomatis [22]. This study aims at proposing
a clinical experimentation on the effects of nitric acid in reducing the quantity of LDL, in presence of IgG/IgA anti-chlamydia pneumoniae antibodies. Our initial data enable us to stress
the efficacious action of this drug not only on LDL reduction, but also on the seroconvertion of
antibodies.
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