Enjeux et amélioration de la réduction de l'acidité dans les fruits mûrs du palmier à huile, Elaeis guineensis Jacq. (synthèse bibliographique)

Introduction. L'acidification de l'huile de palme détermine la qualité et la stabilité de cette importante denrée alimentaire. Cette synthèse analyse les causes de l'acidification de l'huile et son impact sur la qualité et la stabilité de l'huile. Les enjeux liés à la réduction de l'acidification de l'huile et les approches utilisées sont aussi analysés, en particulier la réduction par l'amélioration génétique. Littérature. L'acidification est principalement due à l'action de la lipase endogène du mésocarpe, mais peut aussi être causée par des lipases microbiennes ou une hydrolyse autocatalytique. Plusieurs facteurs, notamment le matériel végétal, les conditions de récolte et de traitement post-récolte des régimes, d'extraction et de conservation de l'huile impactent de manière significative l'acidification de l'huile. L'acidification réduit la qualité et la valeur marchande de l'huile et engendre une baisse de productivité. Des fonds génétiques à faible acidité ont été identifiés. La variabilité de ce caractère rend possible la sélection variétale. Un gène impliqué dans l'acidification de l'huile est identifié, mais l'action d'autres gènes ou facteurs génétiques est soupçonnée. Conclusions. Ces recherches ont permis la récente commercialisation des premiers palmiers avec une huile faiblement acide. Ceci améliorera la qualité de l'huile tout en augmentant le rendement et en facilitant la gestion des opérations de récolte et de post-récolte, en particulier pour les petits producteurs. Il est nécessaire de continuer la recherche de tous les facteurs génétiques impliqués au niveau du genre Elaeis. La validation des ressources génomiques permettrait la sélection assistée par marqueurs de variétés à faible acidité de l'huile

Data from: IL-33 mediated iLC2 activation and neutrophil IL-5 production in the lung response after severe trauma: a reverse translation study from a human cohort to a mouse trauma model

Background: The immunosuppression and immune dysregulation that follows severe injury includes type 2 immune responses manifested by elevations in interleukin (IL) 4, IL5, and IL13 early after injury. We hypothesized that IL33, an alarmin released early after tissue injury and a known regulator of type 2 immunity, contributes to the early type 2 immune responses after systemic injury. Methods and findings: Blunt trauma patients admitted to the trauma intensive care unit of a level I trauma center were enrolled in an observational study that included frequent blood sampling. Dynamic changes in IL33 and soluble suppression of tumorigenicity 2 (sST2) levels were measured in the plasma and correlated with levels of the type 2 cytokines and nosocomial infection. Based on the observations in humans, mechanistic experiments were designed in a mouse model of resuscitated hemorrhagic shock and tissue trauma (HS/T). These experiments utilized wild-type C57BL/6 mice, IL33-/- mice, B6.C3(Cg)-Rorasg/sg mice deficient in group 2 innate lymphoid cells (ILC2), and C57BL/6 wild-type mice treated with anti-IL5 antibody. Severely injured human blunt trauma patients (n = 472, average injury severity score [ISS] = 20.2) exhibited elevations in plasma IL33 levels upon admission and over time that correlated positively with increases in IL4, IL5, and IL13 (P < 0.0001). sST2 levels also increased after injury but in a delayed manner compared with IL33. The increases in IL33 and sST2 were significantly greater in patients that developed nosocomial infection and organ dysfunction than similarly injured patients that did not (P < 0.05). Mechanistic studies were carried out in a mouse model of HS/T that recapitulated the early increase in IL33 and delayed increase in sST2 in the plasma (P < 0.005). These studies identified a pathway where IL33 induces ILC2 activation in the lung within hours of HS/T. ILC2 IL5 up-regulation induces further IL5 expression by CXCR2+ lung neutrophils, culminating in early lung injury. The major limitations of this study are the descriptive nature of the human study component and the impact of the potential differences between human and mouse immune responses to polytrauma. Also, the studies performed did not permit us to make conclusions about the impact of IL33 on pulmonary function. Conclusions: These results suggest that IL33 may initiate early detrimental type 2 immune responses after trauma through ILC2 regulation of neutrophil IL5 production. This IL33–ILC2–IL5–neutrophil axis defines a novel regulatory role for ILC2 in acute lung injury that could be targeted in trauma patients prone to early lung dysfunction

Cyclic stretch induced IL-33 production through HMGB1/TLR-4 signaling pathway in murine respiratory epithelial cells.

Interleukin 33 (IL-33), an inflammatory and mechanically responsive cytokine, is an important component of a TLR4-dependent innate immune process in mucosal epithelium. Although TLR4 also plays a role in sensing biomechanical stretch, a pathway of stretch-induced TLR4-dependent IL-33 biosynthesis has not been revealed. In the current study, we show that short term (6 h) cyclic stretch (CS) of cultured murine respiratory epithelial cells (MLE-12) increased intracellular IL-33 expression in a TLR4 dependent fashion. There was no detectable IL-33 in conditioned media in this interval. CS, however, increased release of the notable alarmin, HMGB1, and a neutralizing antibody (2G7) to HMGB1 completely abolished the CS mediated increase in IL-33. rHMGB1 increased IL-33 synthesis and this was partially abrogated by silencing TLR4 suggesting additional receptors for HMGB1 are involved in its regulation of IL-33. Collectively, these data reveal a HMGB1/TLR4/IL-33 pathway in the response of respiratory epithelium to mechanical stretch

IL33-mediated ILC2 activation and neutrophil IL5 production in the lung response after severe trauma: A reverse translation study from a human cohort to a mouse trauma model

<div><p>Background</p><p>The immunosuppression and immune dysregulation that follows severe injury includes type 2 immune responses manifested by elevations in interleukin (IL) 4, IL5, and IL13 early after injury. We hypothesized that IL33, an alarmin released early after tissue injury and a known regulator of type 2 immunity, contributes to the early type 2 immune responses after systemic injury.</p><p>Methods and findings</p><p>Blunt trauma patients admitted to the trauma intensive care unit of a level I trauma center were enrolled in an observational study that included frequent blood sampling. Dynamic changes in IL33 and soluble suppression of tumorigenicity 2 (sST2) levels were measured in the plasma and correlated with levels of the type 2 cytokines and nosocomial infection. Based on the observations in humans, mechanistic experiments were designed in a mouse model of resuscitated hemorrhagic shock and tissue trauma (HS/T). These experiments utilized wild-type C57BL/6 mice, IL33^-/- mice, B6.C3(Cg)-Rora^sg/sg mice deficient in group 2 innate lymphoid cells (ILC2), and C57BL/6 wild-type mice treated with anti-IL5 antibody.</p><p>Severely injured human blunt trauma patients (<i>n</i> = 472, average injury severity score [ISS] = 20.2) exhibited elevations in plasma IL33 levels upon admission and over time that correlated positively with increases in IL4, IL5, and IL13 (<i>P</i> < 0.0001). sST2 levels also increased after injury but in a delayed manner compared with IL33. The increases in IL33 and sST2 were significantly greater in patients that developed nosocomial infection and organ dysfunction than similarly injured patients that did not (<i>P</i> < 0.05). Mechanistic studies were carried out in a mouse model of HS/T that recapitulated the early increase in IL33 and delayed increase in sST2 in the plasma (<i>P</i> < 0.005). These studies identified a pathway where IL33 induces ILC2 activation in the lung within hours of HS/T. ILC2 IL5 up-regulation induces further IL5 expression by CXCR2⁺ lung neutrophils, culminating in early lung injury. The major limitations of this study are the descriptive nature of the human study component and the impact of the potential differences between human and mouse immune responses to polytrauma. Also, the studies performed did not permit us to make conclusions about the impact of IL33 on pulmonary function.</p><p>Conclusions</p><p>These results suggest that IL33 may initiate early detrimental type 2 immune responses after trauma through ILC2 regulation of neutrophil IL5 production. This IL33–ILC2–IL5–neutrophil axis defines a novel regulatory role for ILC2 in acute lung injury that could be targeted in trauma patients prone to early lung dysfunction.</p></div

Time course analysis of mean circulating levels of interleukin (IL) 33 and soluble suppression of tumorigenicity (sST2) in blunt trauma patients.

<p>The inflammatory mediators were assessed in serial plasma samples obtained at the indicated time points, starting with the first blood draw upon hospital admission and followed by 2 blood draws within the first 24 hours after injury and then daily thereafter up to day 7. A: Time course of IL33 in trauma patients (<i>n</i> = 472 survivors) versus healthy volunteers (HVs) (<i>n</i> = 12). B: Time course of sST2 in trauma patients (<i>n</i> = 472) versus HVs (<i>n</i> = 12). C: Time course analysis of mean circulating levels of IL33 in trauma patients diagnosed with nosocomial infection (NI) (<i>n</i> = 44) versus patients without NI (<i>n</i> = 44) matched for age, sex, and injury severity. D: Time course analysis of mean circulating levels of sST2 in trauma patients with NI (<i>n</i> = 44) versus patients without NI (<i>n</i> = 44). * <i>P</i> < 0.05.</p

The effects of exogenous recombinant interleukin (IL) 5 or IL5 neutralization on neutrophil IL5 expression in the lungs of C57BL/6 mice after resuscitated hemorrhagic shock and tissue trauma (HS/T).

<p>A: Neutrophils in the lungs of C57BL/6 mice did not express suppression of tumorigenicity (ST2) but were positive for CD125 (IL5 receptor). The control cells for ST2 expression were gated from the CD45⁺Lin^-CD25⁺CD127⁺, and the control cells for CD125 expression were gated from the CD45⁺ cells. B: Exposure of lung neutrophils isolated from HS/T mice to exogenous recombinant mouse IL5 (10 ng/ml) increased IL5 mRNA levels (<i>n</i> = 5/group, detected by PCR). C: Exposure of neutrophils isolated from the bone marrow to 10 ng/ml exogenous recombinant mouse IL5 induced their expression of IL5 (<i>n</i> = 3–7/group, detected by flow cytometry). D: IL5 neutralization did not change the frequency of neutrophils in the lungs after HS/T (<i>n</i> = 3–6/group). E: IL5 neutralization did inhibit the increase in lung neutrophil expression of IL5 after HS/T (<i>n</i> = 3–6/group). * <i>P</i> < 0.05. FSC-H, forward scatter-height.</p

Correlations of circulating interleukin (IL) 33 and soluble suppression of tumorigenicity (sST2) with type 2 cytokines (IL4, IL5, and IL13) and IL6 in blunt trauma patients (<i>n</i> = 472, all survivors) upon admission, at 24 hours, and days 2 to 3 postinjury.

<p>Correlations of circulating interleukin (IL) 33 and soluble suppression of tumorigenicity (sST2) with type 2 cytokines (IL4, IL5, and IL13) and IL6 in blunt trauma patients (<i>n</i> = 472, all survivors) upon admission, at 24 hours, and days 2 to 3 postinjury.</p

Effects of interleukin (IL) 33 deletion on group 2 innate lymphoid cells (ILC2) and neutrophil responses in lungs after resuscitated hemorrhagic shock and tissue trauma (HS/T).

<p>The increase of ILC2 frequency (A) and the ILC2 IL5 expression (B) at 6 hours after HS/T was inhibited in IL33^-/- mice (<i>n</i> = 5–8/group). C: The increase in neutrophil (Ly6G⁺CD11b⁺ gated from CD45⁺ cells) frequency after HS/T was not changed by IL33 deletion (<i>n</i> = 6–7/group). D: The increase of neutrophil IL5 expression (IL5⁺ gated from CD45⁺Ly6G⁺CD11b⁺ cells) at 6 hours after HS/T was inhibited in IL33^-/- mice, compared with the C57BL/6 WT mice (<i>n</i> = 5–7/group). * <i>P</i> < 0.05. FSC-H, forward scatter-height.</p

Effects of group 2 innate lymphoid cells (ILC2) deletion on lung frequency and interleukin (IL5) expression after resuscitated hemorrhagic shock and tissue trauma (HS/T).

<p>A: ILC2 nearly absent in ILC2-deficient Rora^sg/sg mice compared with the C57BL/6 or the bone marrow transplantation (BMT) wild-type (WT) (Rora^+/+) mice, and no increase of ILC2 frequency was observed in ILC2-deficient mice after HS/T (<i>n</i> = 3–6/group). B: ILC2 deficiency had no impact on the increase in neutrophil frequency after HS/T (<i>n</i> = 5–8/group). C: The increase neutrophil IL5 expression after HS/T was inhibited in ILC2-deficient mice, compared with the C57BL/6 mice or the BMT WT mice (<i>n</i> = 5–6/group). * <i>P</i> < 0.05. FSC-H, forward scatter-height; KO, knockout.</p

Effects of interleukin (IL) 33 deletion, ILC2 deficiency, and IL5 neutralization on lung injury after resuscitated hemorrhagic shock and tissue trauma (HS/T).

<p>A: Lung tissue sections stained with hematoxylin and eosin (H&E). Representative histologic sections are shown along with the average lung injury scores from control mice and at 6 hours after HS/T. IL33^-/- mice, mice with ILC2 deletion, and C57BL/6 WT mice pretreated with neutralizing anti-IL5 antibody are shown. 200× magnification; scale bar 100 μm. B: Lung injury scores were calculated on lung H&E sections (<i>n</i> = 3–5/group). * <i>P</i> < 0.05.</p