Anesthetic drug comes to the rescue of blood-stage Plasmodium infection: Procaine (PCA) (trade name: Novocain), a local anesthetic drug,  decreases the expression of CTLA-4, PD-L1, and LAG-3, promotes CD4+ T-cell function, increases secretion of protective antibodies, promotes and clears blood-stage malaria, via up-regulation of its target gene, 18/September/2018, 7.35 am

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Mechanistic insights into how a known anesthetic drug functions as an analgesic agent: Levobupivacaine (brand name: Chirocaine),  a local anesthetic drug, increases the expression of PD-L1, attenuates acute and chronic pain, and suppresses mechanical and thermal hypersensitivity and inhibits nociceptive neuron excitability, via up-regulation of its target gene, 18/September/2018, 7.56 am
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Introduction: What they say

A study from the Department of Microbiology and Immunology, University of Iowa Carver College of Medicine, Iowa City, Iowa, USA shows thatRegulatory T cells impede acute and long-term immunity to blood-stage malaria through CTLA-4.” This research paper was published, in September 2017 issue of the journal “Nature Medicine” [One of the best research journals in General biology with an I.F of 28.710], by Prof. Harty J and his research team members.

In connection with the study presented above, Prof. Harty J’s research team members had earlier shown that “Therapeutic blockade of PD-L1 and LAG-3 rapidly clears established blood-stage Plasmodium infection.” This research paper was published in the December 2011 issue of the journal Nature Immunology” [One of the best research journals in General biology with an I.F of 28.710].


What we say:

On the foundation of these interesting findings, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that: Anesthetic drug comes to the rescue of blood-stage Plasmodium infection: Procaine (PCA) (trade name: Novocain), a local anesthetic drug,  decreases the expression of CTLA-4, PD-L1, and LAG-3, promotes CD4+ T-cell function, increases secretion of protective antibodies, promotes and clears blood-stage malaria, via up-regulation of its target gene


From significance of the study to Public health relevance:

Given that: (1) 214 million new cases of malaria had been reported in 2015; (2) nearly 438,000 people out of 214 million people who were infected with Malaria had died in 2015; (3) malaria has the potential to affect nearly half the global population; (4) molecular pathways involved and the mechanism of development of drug-resistant malaria are far from understood; (4) treating drug-resistant malaria is still a daunting task; (5) millions of deaths occur due to malaria every year; (6) out of the 125 million international travellers who visit countries, such as Ivory Coast, Angola, Burkina Faso, Burkina Faso, Mozambique and Mali, more than 30, 000 contract the disease; (7) most of the malaria cases are registered in developing countries, such as sub-Saharan Africa—that cannot afford high-cost required for the treatment of drug-resistant malaria—,compared to developed countries, such as US (10,000 malaria cases/ per year) and UK (1,500 malaria cases/year), (8) humans could not mount immunity against blood stage-malaria; and prevent re-infections; (9) billions of dollars are being spent each year globally for the treatment of Malaria, there is an urgent need to find: (i) a way to inhibit drug-resistant malaria; and (ii) a side-effect-free-Natural product-based drug that prevents relapse/recurrence of blood-stage/drug-resistant Malaria.


What is known?

Prof. Hardy’s research team has shown that blockade of CTLA-4, PD-1 ligand PD-L1 and the inhibitory receptor LAG-3: a) promote CD4+ T-cell function; b) increase the number of follicular helper T cells, germinal-center B cells etc.; c) enhance the levels of protective antibodies; d) augment parasite clearance; e) promote species-transcending immunity to blood-stage malaria; f) prevent reinfection through potentiation of adaptive immunity; and g) clear blood-stage malaria, suggesting that inhibiting the expression of immune evasion molecules, such as CTLA-4, PD-1, PD-L1, and LAG-3, may attenuate chronic malaria-driven T-cell dysfunction; and promote parasite clearance in blood-stage malaria.


From research findings to Therapeutic opportunity:

This study suggests, for the first time, that the local anesthetic drug Procaine (PCA) may aid in the treatment of blood-stage malariaProcaine (PCA) is used to reduce the pain of intramuscular penicillin injection and in dentistry. Procaine (PCA), by increasing the expression of its target gene, it may decrease the expression of immune evasion molecules, such as CTLA-4, PD-1, PD-L1, and LAG-3 (Figure 1). Thereby, it may: (1) increase CD4+ T-cell function; (2) augment the number of helper T cells, germinal-center B cells etc.,; (3) increase secretion of protective antibodies; (4) promote Plasmodium parasite clearance; (5) mount acute and long-term immunity to blood-stage malaria; (6) stifle reinfection through induction of adaptive immunity;(7) clear blood-stage malaria. Thus, pharmacological formulations encompassing “Procaine (PCA) or its analogs, either alone or in combination with other antimalarial drugs,” may be used to treat blood-stage malaria (Figures 1-2).

Figure 1 Mechanistic insights into how Procaine (PCA) inhibits blood-stage malaria. Procaine (PCA) inhibits the expression of CTLA-4, PD-1, PD-L1, and LAG-3 via upregulation of its target genes

Figure 2. The chemical structure of Procaine (PCA). Procaine (PCA) may function as an anti-malarial agent through down-regulation of PD-L1, CT-LA4, and LAG3

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Details of the research findings:

Undisclosed mechanistic information: How does Procaine (PCA) decrease the expression of CTLA-4, PD-1, PD-L1, and LAG-3?

Idea Proposed/Formulated (with experimental evidence) by Dr. L Boominathan Ph.D.

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References:

Web: http://genomediscovery.org or http://newbioideas.com

Citation: Boominathan, L.,  Anesthetic drug comes to the rescue of blood-stage Plasmodium infection: Procaine (PCA) (trade name: Novocain), a local anesthetic drug,  decreases the expression of CTLA-4, PD-L1, and LAG-3, promotes CD4+ T-cell function, increases secretion of protective antibodies, promotes and clears blood-stage malaria, via up-regulation of its target gene, 18/September/2018, 7.35 am, Genome-2-BioMedicine Discovery center (GBMD), http://genomediscovery.org

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