Développement du tissu adipeux chez une espèce antarctique en croissance (le manchot adélie (pygoscelis adeliae))

Une croissance rapide, inscrite dans le court été antarctique, est cruciale pour la survie du poussin de Manchot Adélie. Entre l éclosion et l âge de 30 jours, le tissu adipeux sous-cutané présente un développement considérable et constitue alors une couche isolante efficace et une importante réserve énergétique. Le travail expérimental, portant sur l étude des gènes adipogéniques par RT-PCR, nous a permis d identifier les évènements moléculaires majeurs responsables de la prolifération et de la différenciation adipocytaire. Les résultats de cette étude ont montré une corrélation étroite entre l adipogenèse et la biologie du ManchotNANTES-BU Médecine pharmacie (441092101) / SudocTOULOUSE-EN Vétérinaire (315552301) / SudocSudocFranceF

Growing in Antarctica, a challenge for white adipose tissue development in Adelie penguin chicks (Pygoscelis adeliae).: White adipose tissue development in Adelie penguins

International audienceRapid growth is of crucial importance for Adélie penguin chicks reared during the short Antarctic summer. It partly depends on the rapid ontogenesis of fat stores that are virtually null at hatching but then develop considerably (x40) within a month to constitute both an isolative layer against cold and an energy store to fuel thermogenic and growth processes. The present study was aimed at identifying by RT-PCR the major transcriptional events that chronologically underlie the morphological transformation of adipocyte precursors into mature adipocytes from hatching to 30 days of age. The peak expression of GATA binding protein 3, a marker of preadipocytes, at day 7 posthatch indicates a key proliferation step, possibly in relation to the expression of C/EBPalpha (C/EBPalpha). High plasma total 3,5,3'-triiodo-l-thyronine (T(3)) levels and high levels of growth hormone receptor transcripts at hatching suggested that growth hormone and T(3) play early activating roles to favor proliferation of preadipocyte precursors. Differentiation and growth of preadipocytes may occur around day 15 in connection with increased abundance of transcripts encoding IGF-1, proliferator-activated receptor-gamma, and C/EBPbeta, gradually leading to functional maturation of metabolic features of adipocytes including lipid uptake and storage (lipoprotein lipase, fatty-acid synthase) and late endocrine functions (adiponectin) by day 30. Present results show a close correlation between adipose tissue development and chick biology and a difference in the scheduled expression of regulatory factors controlling adipogenesis compared with in vitro studies using cell lines emphasizing the importance of in vivo approaches

<i>B</i>. <i>melitensis</i> oral infection results in an increase of CLN CD11b^high cells expressing either F4/80, Ly6c or both.

<p>CLN from mice orally infected with 10⁹<i>B</i>. <i>melitensis</i> per mouse for 15 days were prepared for flow cytometry. Total CLN cell numbers were analyzed for the respective percentages <b>(A)</b> or absolute numbers <b>(B)</b> of dendritic cells (F4/80^-CD11c^highMHCII^int and F4/80^-CD11c^intMHCII^high), CD11b^high macrophages/monocytes (F4/80^-Ly6c⁺, F4/80⁺Ly6c⁺ and F4/80⁺Ly6c^-) and neutrophils (CD11b^highLy6G⁺). <b>(C)</b> shows a representative contour plot of respective populations from a mock-infected or <i>Brucella</i>-infected mouse on CD19^-Ly6G^-CD11b^high (F4/80 vs. Ly6c) or CD19^-CD11b^low/intF4/80^-NK1.1^- cells (CD11c vs. MHCII). Populations shown in (A) were analyzed for their median fluorescence of <b>(D)</b> CD11b, <b>(E)</b> CD11c and <b>(F)</b> MHCII. Data represent mean and SEM of pooled results from two independent experiments with a total of 8 (mock-infected) and 9 (infected) mice per group. * p ≤ 0.05 as compared to respective mock infected control.</p

Infection by the oral route leads to preferential bacterial colonization of the CLN.

<p>C57BL/6 mice were infected by intraperitoneal injection (10⁶ bacteria/mouse), intragastric by gavage or by the oral route (both at 10⁹ bacteria/mouse). At 8 days post-infection, mice were sacrificed and organs weighed and analyzed for their bacterial loads by plating homogenates on nutrient agar. Data represent mean organ weight or colony forming units (CFU) per organ and SEM of the pooled results from two independent experiments with 5 mice per group. Non-infected organs are not shown due to logarithmic scale. * p ≤ 0.05. CLN—cervical lymph nodes; MLN—mesenteric lymph nodes.</p

<i>Brucella</i> specifically targets and multiplies in cervical lymph nodes during oral infection and causes long-term lymphadenopathy.

<p>C57BL/6 mice were infected by gavage or by the oral route with 10⁹<i>B</i>. <i>melitensis</i> per mouse. At 2, 8, 29 or 50 days post-infection, mice were sacrificed and organs weighed and analyzed for their bacterial loads by plating homogenates on nutrient agar. Data represent mean organ weight or CFU per organ and SEM of the pooled results from two independent experiments with 4 mice per group.</p

Incidence of cervical lymphadenopathy with cervical lymph nodes being the only ones affected (CL) and general lymphadenopathy with lymph nodes other than CLN affected (GL) in children infected with <i>Brucella</i> by ingestion or by contact with animals.

<p>Analysis for significance of differences using Chi-square test yielded Χ² = 5.504 and p = 0.019.</p><p>Incidence of cervical lymphadenopathy with cervical lymph nodes being the only ones affected (CL) and general lymphadenopathy with lymph nodes other than CLN affected (GL) in children infected with <i>Brucella</i> by ingestion or by contact with animals.</p

Incidence of lymphadenopathy in 307 children (up to 14 years) diagnosed for brucellosis and with known routes of infection.

<p>Analysis for significance of differences using Chi-square test yielded Χ² = 5.752 and p = 0.016.</p><p>Incidence of lymphadenopathy in 307 children (up to 14 years) diagnosed for brucellosis and with known routes of infection.</p

Oral infection with <i>B</i>. <i>melitensis</i> induces pro-inflammatory gene expression in the CLN.

<p>C57BL/6 mice were infected with 10⁹<i>B</i>. <i>melitensis</i> per mouse or mock infected by the oral route. At 5 h, 2, 8, 15 or 29 days post-infection, mice were sacrificed, total RNA of the CLN was extracted and analyzed for expression of genes involved in inflammatory responses by reverse transcription real-time PCR. Results are given as fold expression compared to the signal obtained for mock-infected mice. Data represent means and standard deviations of two independent experiments with 3 or 4 mice per group. * p ≤ 0.05 as compared to mock infected expression levels.</p

Oral infection with <i>B</i>. <i>melitensis</i> results in CLN granuloma formation.

<p>Thin sections of cervical lymph nodes from mice orally infected with 10⁹<i>B</i>. <i>melitensis</i> per mouse for (A) 2, (B) 8, (C) 15, or (D) 29 days were stained with eosin-hematoxylin. (E) and (F) show higher magnifications from day 15 and 29, respectively. White arrowheads mark granulomatous structures that (E) develop as multifocal loose cell arrangements that (F) gradually solidify into compact granulomas composed of epithelioid cells with occasional multinucleated giant cells and few neutrophils.</p

During gavage infection with <i>S</i>. Typhimurium, bacteria colonize CLN, spleen and thymus at early time points.

<p>C57BL/6 mice were infected with 10⁵<i>S</i>. Typhimurium by gavage. After 2 or 3 days post-infection, mice were sacrificed and organs analyzed for their bacterial loads by plating homogenates on nutrient agar. Data represent mean CFU/organ and SEM of the pooled results from three (day 2) or two (day 3) independent experiments with 4 mice per group. ILN—inguinal lymph nodes; RLN—retropharyngeal lymph nodes; ALN—axillary lymph nodes.</p