Biology subjects

Karikari, A. A.

Publications and source records attributed to Karikari, A. A..

3 recordsLinked to original sources

bioRxiv2024

Trophic Interactions of Anopheles Gambiae Mosquito Larvae in Aquatic Ecosystem: A Metagenomics Approach

BackgroundUnderstanding the trophic interactions of Anopheles gambiae mosquito larvae in aquatic environments is essential for malaria prevention efforts such as in gene drive application. In this study, metagenomics method was employed to explore the feeding behavior and ecological associations of An. gambiae larvae within their aquatic ecosystems. MethodsAnopheles gambiae larvae and their co-existing fauna species were collected from December 2022 to June 2023. DNA from dissected midguts of the co-existing fauna was sequenced using Illumina NovaSeq for diet analysis through a shotgun sequencing approach. ResultsThe study revealed a complex network of trophic interactions in the freshwater habitat, with significant resource sharing between A. gambiae larvae and other filter-feeding species, including various Diptera and non-Dipteran feeders. Contrary to assumptions, predator species did not exhibit exclusive predation on Anopheles larvae, preferring other fauna instead. ConclusionThis study has demonstrated complex trophic interactions among Anopheles gambiae larvae and other organisms in freshwater ecosystems. It has offered essential insights for optimizing vector control strategies, such as in gene drive applications. Additionally, the study has provided valuable information on the aquatic fauna of the study area, which can serve as a baseline for developing a macroinvertebrate identification database for freshwater systems in Ghana. A complementary study that further explores the ecological role of An. gambiae larvae in these freshwater habitats is presented in a subsequent publication.

ecology↗

bioRxiv2024

Hemozoin induces Malaria via activation of DNA damage, p38 MAPK and Neurodegenerative Pathways in Human iPSC-derived Neuronal Model of Cerebral Malaria

Malaria caused by Plasmodium falciparum infection results in severe complications including cerebral malaria (CM), in which approximately 30% of patients end up with neurological sequelae. Sparse in vitro cell culture-based experimental models which recapitulate the molecular basis of CM in humans has impeded progress in our understanding of its etiology. This study employed healthy human induced pluripotent stem cells (iPSCs) derived neuronal cultures stimulated with hemozoin (HMZ)-the malarial toxin as a model for CM. Secretome, qRT-PCR, Metascape, and KEGG pathway analyses were conducted to assess elevated proteins, genes, and pathways. Neuronal cultures treated with HMZ showed enhanced secretion of interferon-gamma (IFN-{gamma}), interleukin (IL)1-beta (IL-1{beta}), IL-8 and IL-16. Enrichment analysis revealed malaria, positive regulation of cytokine production and positive regulation of mitogen-activated protein kinase (MAPK) cascade which confirm inflammatory response to HMZ exposure. KEGG assessment revealed up-regulation of malaria, MAPK and neurodegenerative diseases-associated pathways which corroborates findings from previous studies. Additionally, HMZ induced DNA damage in neurons. This study has unveiled that exposure of neuronal cultures to HMZ, activates molecules and pathways similar to that observed in CM and neurodegenerative diseases. Furthermore, our model is an alternative to rodent experimental models of CM.

neuroscience↗

bioRxiv2021

Inflammation and Cellular Stress Induced Neurological Sequelae of Plasmodium falciparum Malaria

BackgroundMalaria caused by Plasmodium falciparum results in severe complications including cerebral malaria (CM) especially in children. While the majority of falciparum malaria survivors make a full recovery, there are reports of some patients ending up with neurological sequelae. MethodsWe performed an analysis of pooled transcriptome data of whole blood samples derived from two studies involving various Plasmodium falciparum infections, comprising mild malaria (MM), non-cerebral severe malaria (NCM) and CM. Pathways and gene ontologies (GOs) elevated in the distinct falciparum infections were identified. ResultsContrary to other research findings, our analysis showed MM share similar biological processes with cancer and neurodegenerative diseases, NCM is associated with drug resistance and glutathione metabolism and CM is correlated with endocannabinoid signaling and non-alcoholic fatty liver disease (NAFLD). GO revealed the terms biogenesis, DNA damage response and IL-10 production in MM, down-regulation of cytoskeletal organization and amyloid-beta clearance in NCM and aberrant signaling, neutrophil degranulation and gene repression in CM. Differential gene expression analysis between CM and NCM showed the up-regulation of neutrophil activation and response to herbicides while regulation of axon diameter was down-regulated in CM. ConclusionsThe results of this study have demonstrated that the deleterious effect of falciparum malaria on the brain may not be limited to CM and NCM alone but also MM. However, the severity of neurological deficit in CM might be due to the down-regulation of various genes involved in cellular function through transcriptional repression, axonal dysfunction, dysregulation of signaling pathways and neurodegeneration as a result of inflammation and cellular stress. We anticipate that our data might form the basis for future hypothesis-driven malaria research.

molecular biology↗