Cholesterol is an essential nutrient for the function of diverse biological processes and for steroid biosynthesis across metazoans. However, the role of cholesterol in immune function remains understudied. Using the nematode Caenorhabditis elegans, which depends on the external environment for cholesterol, we studied the relationship between cholesterol and innate immunity. We found that the transporter CHUP-1 is required for the effect of cholesterol in the development of innate immunity and that the cholesterol-mediated immune response requires the nuclear hormone receptor NHR-8. Cholesterol acts through NHR-8 to transcriptionally regulate immune genes that are controlled by conserved immune pathways, including a p38/PMK-1 MAPK pathway, a DAF-2/DAF-16 insulin pathway, and an Nrf/SKN-1 pathway. Our results indicate that cholesterol plays a key role in the activation of conserved microbicidal pathways that are essential for survival against bacterial infections.

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The control of Staphylococcus aureus infection is being hampered by methicillin and other resistant strains. The identification of the unique antibiotic resistant genes from the genomes of various strains of S. aureus is of interest. We analyzed 11 S. aureus genomes sequences for Antibiotics Resistance Genes (ARGs) using CARD 2017 platform. We identified 32 ARGs across 11 S. aureus strains. Tet(38), norB, lmrB, mepA and mepR were present across genomes except for S. aureus strain UTSW MRSA 55. The mepA and mepR were found across 11 different genomes. However, FosB3, vgaALC, mphC and SAT-4 were found in UTSW MRSA 55, S.a. strain ISU935 and S.a. strain FDAARGOS_159. The prevalent mode of mechanism of antibiotics resistant was efflux pump complex or subunit conferring antibiotic resistance as well as protein(s). Analysis of norB, ImrB, norA, ImrB, tet (38), sav1866 and mecA have 12 to 14 TMHs. The results help in the understanding of Staphylococcus aureus pathogenesis in the context of antibiotic resistance.

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Biomphalaria pfeifferi, Bulinus globosus and Lymnaea natalensis act as obligatory vectors of schistosomiasis and fascioliasis in Sub-Saharan Africa. Although, they are known to be widely distributed throughout Nigeria, there is the need for precise species identification to help vector control initiatives. Snail shell morphometry has previously proved useful in taxonomic studies. We thus employed seven morphological parameters of snail shells in identifying three snail vectors from five water bodies in SouthWestern Nigeria. Snails were sampled for 14 months and total of 718 snails were collected, which include 204 B. pfeifferi, 316 B. globosus and 198 L. natalensis. Eleyele Lake had 278 snails which was the highest number followed by Osun River with 64 snails. Our finding revealed B. globosus as the dominant snail in all the five sites, while B. pfeifferi and L. natalensis were present in only three sites. The presence of the snails in otherwise uninfected water bodies may have implications for transmission and disease control in these areas. Our findings should prove useful for improved snail identification, information, which will be invaluable for vector control in affected communities.

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A body of evidence indicates that metazoan immune and aging pathways are largely interconnected, but the mechanisms involved in their homeostatic control remain unclear. In this study, we find that the PITX (pairedlike homeodomain) transcription factor UNC-30 controls the tradeoff between immunity and longevity from the nervous system in Caenorhabditis elegans. PITX/UNC-30 functional loss enhances immunity in a GATA/ELT-2-and p38 MAPK/PMK-1-dependent manner and reduced longevity by activating MXD/MDL-1 and the C2H2-type zinc finger transcription factor PQM-1. The immune inhibitory and longevity stimulatory functions of PITX/UNC-30 require the sensory neuron ASG and a signaling pathway controlled by NPR-1, which is a G protein-coupled receptor related to mammalian neuropeptide Y receptors. Our findings uncover a suppressive role of GABAergic signaling in the neural control of a biological tradeoff where energy is allocated toward immunity at the expense of longevity.

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