Herbalzym

Miracle natural treatment for multi-drug resistant TB

Tuberculosis (TB) is one of the most deadly infectious diseases. Last year, 10 million fell ill from TB and 1.6 million died worldwide. Regular TB takes about 6~9 months to cure, with four antibiotics daily. Up to half of patients with TB do not complete treatment, which contributes to prolonged infectiousness, drug resistance, relapse, and death.

Tuberculosis (TB) is one of the most deadly infectious diseases. Last year, 10 million fell ill from TB and 1.6 million died worldwide. Regular TB takes about 6~9 months to cure, with four antibiotics daily. Up to half of patients with TB do not complete treatment, which contributes to prolonged infectiousness, drug resistance, relapse, and death.

Drug-resistant (DR) TB can be acquired or directly transmitted. DR-TB takes about 2 years to cure, and the treatment is much rougher. The drugs are more toxic, and only about 50 % of people recover. DR-TB is going to increase to about 30 % of cases.

The standard treatment for DR-TB is arduous, with patients facing painful daily injections, as well as taking a cocktail of powerful drugs for two years with a lot of horrible side effects including nausea, vomiting, permanent deafness, psychosis and kidney problems.

Forms of DR-TB

• MDR (multidrug-resistant) TB that is resistant to rifampicin and isoniazid. Death rates are 30 %.

• XDR (extensively drug resistant) TB that is resistant to isoniazid, rifampicin, any Fluoroquinolne and at least one SLID (Kanamycin, Amikacin, Capreomycin). Death rates are 80 %.

• TDR (totally drug resistant) TB. Some new strains do not respond to any available antibiotics. Death rates are 100 %.

DR-TB is now the top infectious killer. The good news is we now have a powerful new natural-immunotherapy that can clear DR-TB bacteria without toxic drugs in a world first.

The body’s immune system is designed to identify and destroy pathogens by producing protective cells and compounds. . However, TB bacteria have evolved several tricks to evade eradication by the innate and adaptive immune system. Macrophages play a decisive role in immune recognition of TB bacteria. But They are able to disable the macrophage defenses. Further, TB bacteria trick the immune system to allow them to spread.

In theory, modulating your own immune responses could be used instead of using antibiotics to kill off DR-TB bacteria. Immune modulation is more than just boosting the body’s immune system. It involves bringing the immune function back into a balanced steady-state. It was always thought that we could not voluntarily influence the immune system.

However, multidimensional immune modulation and enhancement can be achieved by using certain natural products that contain natural and organic ingredients. TB Herbalzym™ is a natural immunomodulator of the potentiator type, which has demonstrated an amazing effects in clinical trials for treatment of DR-TB.

Almost 100% of patients (Korean men and women with DR-TB) were successfully cured in subsequent trials within 30 days. It gives hope for the people with DR-TB, removing the need for toxic drugs. It’s  miraculous and unbelievable news, but true. TB Herbalzym™ was developed in research on TB pathogenesis and mechanistic insights into bacterial immune evasion.

TB Herbalzym™ utilizes cell-to-cell signaling to optimally orchestrate the complex elements of the immune mechanism. TB Herbalzym™ contains the latest research based formula of enzymatically fermented 35 naturally-occurring bioactive compounds with therapeutic potential for the optimal immune responses.

If you are suffering from DR-TB (MDR, XDR, TDR-TB), you can additionally use TB Bacterzym™ and TB Teanzym™ with TB Herbalzym™. The combination of three natural products showed a powerful synergistic effect in clinical trials. DR-TB can be cured in a very short period of time without any side effects at all.

Innate Immune Responses to Tuberculosis.

Tuberculosis and the art of macrophage manipulation.

Molecular basis of mycobacterial survival in macrophages.

A Rab20-Dependent Membrane Trafficking Pathway Controls M. tuberculosis Replication by Regulating Phagosome Spaciousness and Integrity.

IFN-β: A Contentious Player in Host-Pathogen Interaction in Tuberculosis.

Exosomal RNA from Mycobacterium tuberculosis-Infected Cells Is Functional in Recipient Macrophages.

Mycobacterium tuberculosis: Manipulator of Protective Immunity.

Exosomes released from M. tuberculosis infected cells can suppress IFN-γ mediated activation of naïve macrophages.

Host sirtuin 1 regulates mycobacterial immunopathogenesis and represents a therapeutic target against tuberculosis.

Microbial co-infection alters macrophage polarization, phagosomal escape, and microbial killing.

Innate immunity in tuberculosis: host defense vs pathogen evasion.

Toll-like receptor 2 in host defense against Mycobacterium tuberculosis: to be or not to be-that is the question.

PPE38 Protein of Mycobacterium tuberculosis Inhibits Macrophage MHC Class I Expression and Dampens CD8+ T Cell Responses.

Mycobacterium tuberculosis Prolyl Oligopeptidase Induces In vitro Secretion of Proinflammatory Cytokines by Peritoneal Macrophages.

Mycobacterium tuberculosis PE25/PPE41 protein complex induces activation and maturation of dendritic cells and drives Th2-biased immune responses.

Expression of inhibitory regulators of innate immunity in patients with active tuberculosis.

Mathematical model of mycobacterium-host interaction describes physiology of persistence.

Distinct Strategies Employed by Dendritic Cells and Macrophages in Restricting Mycobacterium tuberculosis Infection: Different Philosophies but Same Desire.

Immunoevasion and immunosuppression of the macrophage by Mycobacterium tuberculosis.

Playing hide-and-seek with host macrophages through the use of mycobacterial cell envelope phthiocerol dimycocerosates and phenolic glycolipids.

Understanding and overcoming the barriers to T cell-mediated immunity against tuberculosis.

Perspectives on host adaptation in response to Mycobacterium tuberculosis: modulation of inflammation.

Cell death and autophagy in tuberculosis.

Multimodal nanoparticles that provide immunomodulation and intracellular drug delivery for infectious diseases.

Dormant Mycobacterium tuberculosis fails to block phagosome maturation and shows unexpected capacity to stimulate specific human T lymphocytes.

The Tim3-galectin 9 pathway induces antibacterial activity in human macrophages infected with Mycobacterium tuberculosis.

Identification of a novel role of ESAT-6-dependent miR-155 induction during infection of macrophages with Mycobacterium tuberculosis.

Cellular and humoral mechanisms involved in the control of tuberculosis.

The innate immune response in human tuberculosis.

Understanding delayed T-cell priming, lung recruitment, and airway luminal T-cell responses in host defense against pulmonary tuberculosis.

Modulation of cell death by M. tuberculosis as a strategy for pathogen survival.

TB: screening for responses to a vile visitor.

DC-SIGN and mannosylated surface structures of Mycobacterium tuberculosis: a deceptive liaison.

Patients with multidrug-resistant tuberculosis display impaired Th1 responses and enhanced regulatory T-cell levels in response to an outbreak of multidrug-resistant Mycobacterium tuberculosis M and Ra strains.

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