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    • Although HIV cannot target bacteria it is worth considering

    2018-10-23

    Although HIV cannot target bacteria, it is worth considering what effects that antiretroviral drugs used to treat the viral infection might have on the gut microbiota. One possibility is that immune recovery might induce alterations in microbiome profiles in the gut environment. Indeed, recent studies linked bacterial richness with immune function (Nowak et al., 2015). However, the results of this study reinforce also the hypothesis that favourable changes in the gut cycloastragenol may also be counted as additional contributors to the recovery of mucosal and systemic immunity. In this context, we found that the antiretroviral therapy most likely drastically decreased the abundance of pathogenic species involved in glycan and lipid (ceramide) modification, thereby most likely favouring the integrity of the colonic surface and the maintenance of its functions (Deeks et al., 2013; Masoodi et al., 2013). Other concrete examples that demonstrate the role of gut bacteria as being fundamental for aiding in inflammation and immune recovery involve the metabolism of pro- and anti-inflammatory mediators. Indeed, our data demonstrate that gut bacteria, most likely bacteria of the family Succinivibrionaceae, may play a role in controlling the accumulation of pro-inflammatory molecules that would otherwise promote inflammation in the gut environment (Serhan, 2014). This is the case for the leukotriene LTB4, which might be less likely to accumulate in the gastrointestinal tract when it is accumulated in the gut bacteria. Leukotrienes are potent pro-inflammatory lipid mediators (Bertin et al., 2012). Therefore, reducing their concentration in the large intestine may exert a positive effect that mitigates inflammation and the loss of mucosal epithelium. This may play a direct role in promoting immune recovery because the capacity of gut bacteria to accumulate LTB4 was only observed in ART responders. Similarly, gut bacterial members (e.g., bacteria of the family Succinivibrionaceae and possibly Erysipelotrichaceae as suggested by taxonomic assignments of transport proteins being expressed) may also contribute to the accumulation of additional molecules that have the ability to reduce viral infection (i.e., BV) and signalling molecules (i.e., oleamide) that help to reduce inflammation (Froldi et al., 1992; Genis et al., 1992; Bertin et al., 2012). Other bacteria such as the Bifidobacteria may also be implicated in additional health benefits. While gut bacteria help to control the accumulation of important molecules that are associated with inflammation, immune recovery and viral infectivity, we also demonstrated that human cells respond by increasing the biosynthesis of anti-inflammatory and pro-solving lipid mediators that circulate in the plasma and help diminishing inflammation (Isanaka et al., 2009), and controlling HIV replication (e.g. by non-enzymatic acetylation of histones). An orchestrated solution to inflammation is thus plausible between the host and the gut ecosystem that is aimed at helping to reduce inflammation and boost immune recovery (for a summary see Fig. 7). It is therefore plausible that the metabolic connection between the host and the gut ecosystem is stronger than previously thought and that they can work together to improve immune recovery. It will be important to identify the mechanisms by which such metabolic connections are established and to clearly identify whether an HIV-infected individual responds better to ART as a result of the additional contributions of the microbiota or whether the gut bacteria metabolism is altered as a consequence of the improvement in health of the host after ART. This last hypothesis may agree with the fact that human genetics and human health shape the gut microbiome (Goodrich et al., 2014). Although, we cannot rule out either of these two possibilities, this study supports the first hypothesis: a specialized subset of active microorganisms structured in a more even configuration than the total gut community (Vujkovic-Cvijin et al., 2013; Vázquez-Castellanos et al., 2015) is implicated in key inflammation and immune traits. Thus, we reasoned that the accumulation of pro-inflammatory molecules during HIV infection may be one of the most easily controlled factors that can modulate the composition of the active microbiota, which is shifted to reduce their concentration in the gut environment and to help immune and inflammation recovery.