Pregnancy-associated malaria (PAM) constitutes one of the most severe forms of malaria infection leading to fetal growth restriction and high risk of infant death. The severity of the pathology is largely attributed to the recruitment of monocytes and macrophages in the placenta which is evidenced by dysregulated inflammation found in placental blood. Importantly, CD36+ monocytes/macrophages are also thought to participate in the tight control of the pro- and anti-inflammatory responses following Plasmodium detection through elimination of apoptotic cells and malaria-infected erythrocytes, internalization and recycling of oxidized forms of low-density lipoprotein and collaboration with TLR2 in pro-inflammatory response. Interestingly, previous work demonstrated that CD36 expression was upregulated on inflammatory macrophages following stimulation of the Nrf2 transcription factor, whilst the PPARγ pathway was inhibited and non-functional in the same inflammatory conditions. This current study examined the possible role of Nrf2-driven gene expression, CD36 and Haem-Oxygenase-1 (HO-1), in PAM clinical outcomes. Clinical data and biological samples including peripheral blood mononuclear cells were collected from 27 women presenting PAM. Polychromatic flow cytometry was used to characterize innate immune cell subpopulations and quantify CD36 protein expression level on monocytes. mRNA levels of CD36, PPARγ, Nrf2 and HO-1 were determined by qPCR and related to clinical outcomes. Finally, the capacity of monocytes to modulate CD36 expression upon rosiglitazone or sulforaphane treatment, two respective PPARγ or Nrf2 activators, was also investigated. The CD36 receptor, mostly expressed by CD14+ circulating monocytes, statistically correlated with increased infant birth weights. Interestingly, mRNA levels of the transcription factor Nrf2 and the enzyme HO-1 also correlated with lower parasitaemia and increased infant birth weight, while PPARγ mRNA levels did not. Finally, monocytes isolated from low infant birth weight pregnant women were capable of up-regulating CD36 via the Nrf2 pathway ex vivo. Altogether these results suggest that Nrf2-driven CD36 and HO-1 expression on innate immune cells could contribute to a protective and detoxifying mechanism during PAM. More powered and mechanistical studies are however needed to strengthen the conclusions of this study.

The capacity of marine sponges to cope with environmental changes is often attributed to the specific composition of their bacterial communities. In this study, we assessed the bacterial microbiome of two dominant sponges, Rhabdastrella globostellata (Rg) and Hyrtios erectus (He), living in the Bouraké lagoon (New Caledonia), where abiotic conditions daily fluctuate according to the tide. Sponge specimens, sediment and seawater samples were collected at 2–3 m depth. The bacterial communities were assessed using 16S rRNA metabarcoding, and variations between the two sponges were compared using PCA biplots. Chloroflexi was the dominant phyla in both He and Rg with an average relative abundance of 41.2% and 53.2%, respectively, while it was absent in sediment and seawater. Among the phylum Chloroflexi, SAR202 clade was dominant in both sponges, reaching an average relative abundance of 53.2% (He) and 78.7% (Rg). Principal component analysis (PCA) was used to identify the main variables driving the bacterial community structure in both sponges. The results indicated that the bacterial community structure in both sponges was strongly associated with Chloroflexi (70.9% of the phyla variance) and SAR202 clade (86.6% of the clade variance). The high relative abundance of the phylum Chloroflexi and the SAR202 clade observed in this study is the highest reported so far in the literature in marine sponges. Such a high relative abundance of these bacteria could suggest their involvement in the well‐being of sponges in the extreme environmental conditions of Bouraké.

The Anthropocene epoch is associated with the spreading of metals in the environment increasing oxidative and genotoxic stress on living organisms ^1,2 . Once regarded as a curiosity, plants hyperaccumulating metals are now envisioned as an opportunity to remediate metal contaminated soils. About 500 plant species adapted to metalliferous soils acquired the capacity to hyperaccumulate (>0.1% of dry weight) nickel in their shoot ³ . The phylogenetic distribution of these hyperaccumulators in 50 families suggest that this complex trait evolved multiple times independently from basic mechanisms involved in metal homeostasis. However, the exact nature of these mechanisms and whether they are shared between various lineages is not known. Here, using cross-species transcriptomic analyses in different plant families, we have identified convergent functions that may represent major nodes in the evolution of nickel hyperaccumulation. In particular, our data point out that constitutive high expression of IREG/Ferroportin transporters recurrently emerged as a mechanism involved in nickel hyperaccumulation.