Leishmaniases are endemic neglected tropical diseases caused by the intracellular parasitic protozoa of the genus Leishmania, transmitted by the bite of sandflies. The broad spectrum of clinical manifestations depends on the complex interactions between the parasite and the immune system of the host. These interactions may result in different clinical manifestations of the disease (cutaneous, mucocutaneous or visceral diseases).
Cutaneous leishmaniasis (CL) has affected about one million people worldwide. Leishmaniasis treatment is based on Glucantime or amphotericin B, but these are associated with severe adverse effects, potential toxicity, and therapeutic failure, including therapy dropout or even ineffectiveness. Another therapeutic option is through stimulation of the immune system, using antimonials and other anti-leishmanial drugs to resolve the infection. Gaining traction prior to the emergence of treatment failure with existing therapies, these newer approaches to anti-leishmanial drugs aim to capitalise on immunomodulatory activities with a lower toxicity.
These therapeutic approaches centre on the host-parasite interactions that lead to clinical manifestation. Leishmaniases are clinically manifested through the upregulation of cellular immune responses, involving macrophage and lymphocyte activation and modulation of cytokines. Macrophages phagocytose parasites, thereby activating trigger mechanisms for their microbicidal response. In CL, the immune mechanisms associated with parasite particularities and drug therapy define the progression or healing of the lesion, underlining the importance for developing immunomodulatory therapies.
In this Research Topic, we aim to investigate how drugs act on the host immune response, how the pathogenic protozoa and host organism are interconnected, and which mechanisms of control are active. We welcome studies that explore highly sensitive methods such as bioanalytics (i.e., evaluation of patient-specific biomarkers; proteins, nucleic acids, metabolites), and recent developments in high throughput screening. We aim to gain an overview of host immunity and Leishmania behaviour during infection.
Specific area of interest include, but are not limited to:
• Parasite modulation of host signalling pathways;
• Virulence factors;
• Parasite acquisition of nutrients from their host;
• Invasion of and egress from host cells.
We welcome the following article types: Original Research, Review, Mini Review, and Methods.
Leishmaniases are endemic neglected tropical diseases caused by the intracellular parasitic protozoa of the genus Leishmania, transmitted by the bite of sandflies. The broad spectrum of clinical manifestations depends on the complex interactions between the parasite and the immune system of the host. These interactions may result in different clinical manifestations of the disease (cutaneous, mucocutaneous or visceral diseases).
Cutaneous leishmaniasis (CL) has affected about one million people worldwide. Leishmaniasis treatment is based on Glucantime or amphotericin B, but these are associated with severe adverse effects, potential toxicity, and therapeutic failure, including therapy dropout or even ineffectiveness. Another therapeutic option is through stimulation of the immune system, using antimonials and other anti-leishmanial drugs to resolve the infection. Gaining traction prior to the emergence of treatment failure with existing therapies, these newer approaches to anti-leishmanial drugs aim to capitalise on immunomodulatory activities with a lower toxicity.
These therapeutic approaches centre on the host-parasite interactions that lead to clinical manifestation. Leishmaniases are clinically manifested through the upregulation of cellular immune responses, involving macrophage and lymphocyte activation and modulation of cytokines. Macrophages phagocytose parasites, thereby activating trigger mechanisms for their microbicidal response. In CL, the immune mechanisms associated with parasite particularities and drug therapy define the progression or healing of the lesion, underlining the importance for developing immunomodulatory therapies.
In this Research Topic, we aim to investigate how drugs act on the host immune response, how the pathogenic protozoa and host organism are interconnected, and which mechanisms of control are active. We welcome studies that explore highly sensitive methods such as bioanalytics (i.e., evaluation of patient-specific biomarkers; proteins, nucleic acids, metabolites), and recent developments in high throughput screening. We aim to gain an overview of host immunity and Leishmania behaviour during infection.
Specific area of interest include, but are not limited to:
• Parasite modulation of host signalling pathways;
• Virulence factors;
• Parasite acquisition of nutrients from their host;
• Invasion of and egress from host cells.
We welcome the following article types: Original Research, Review, Mini Review, and Methods.
