MLMoussa Labsi

Moussa Labsi

*This is an algorithmically generated author record based on publicly available information.

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Moussa Labsi has a total of 27 co-authors. Here are the top co-authors by number of shared publications:


Latest Publications

  • Nitric Oxide, Neutrophil/Lymphocyte, and Platelet/Lymphocyte Ratios as Promising Inflammatory Biomarkers in Complicated Crohn’s Disease: Outcomes of Corticosteroids and Anti-TNF-α Therapies

    by Imene Soufli, Abdelkrim Hablal, Samia Bessaad, Manel Amri, Moussa Labsi, Rania Sihem Boussa, Fahima Ameur, Houda Belguendouz, Sonia Ait Younes, Nassim Sid Idris, et al.

    Crohn’s disease (CD) is a relapsing–remitting inflammatory bowel disease with a progressive course. The aim of our study was to evaluate the relationship between nitric oxide (NO), pro-inflammatory cytokines, and blood count-based ratios in patients with complicated Crohn’s disease as well as the outcome of corticosteroid or anti-TNF-α therapy. In this context, we evaluated the NLR as the ratio of neutrophils count to lymphocytes count, PLR as the ratio of platelets count to lymphocytes count, and MLR as the ratio of monocytes count to lymphocytes count in patients and controls. Furthermore, we assessed NO production by the Griess method in plasma along with iNOS and NF-κB expression by immunofluorescence method in intestinal tissues of patients and controls. In the same way, we evaluated plasma TNF-α, IL-17A, and IL-10 levels using ELISA. Our results indicate that blood count-based ratios NLR, PLR, and MLR were significantly higher in patients compared to controls. In addition, increased systemic levels of NO, TNF-α, and IL-17A and colonic expression of iNOS and NF-κB were observed in the same patients. Interestingly, the high ratio of NLR and MLR as well as NO production were significantly decreased in treated patients. Collectively, our findings suggest that nitric oxide as well as the blood count-based ratios (NLR, PLR, MLR) could constitute useful biomarkers in complicated Crohn’s disease, predicting the response to treatments.


  • Beneficial effect of dimethyl fumarate on experimental autoimmune uveitis is dependent of pro-inflammatory markers immunomodulation

    by Moussa Labsi, Imene Soufli, Houda Belguendouz, Sara Djebbara, Leila Hannachi, Zine-Charaf Amir, Chafia Touil-Boukoffa

    Autoimmune uveitis is an inflammatory disease of the eye and is one of the major causes of blindness worldwide. Experimental autoimmune uveoretinitis (EAU) constitutes an animal disease model of human endogenous uveitis. In our study, we investigated the immunomodulatory effect of dimethyl fumarate (DMF) using bovine retinal extract-induced uveitis in a Female Wistar rats. To evaluate the in vivo efficacy, Female Wistar rats were divided into seven experimental groups: control group (n = 5), consisting of non-immunized animals; Uveoretinitis (n = 5), and DMF/Uveoretinitis groups (n = 15), which received a subcutaneous injection of bovine retinal extract emulsified in complete Freund’s adjuvant; MC group (n = 5), treated by daily intragastric administration of methylcellulose 0.08% in tap water; DMF group, consisting of control positive group, rats received daily oral gavage administration of 500 μL of dimethyl fumarate at 100 mg/Kg dissolved in 0.08% methylcellulose in tap water (n = 5). On day 14 post immunization, the rats were then euthanized and associated indications were investigated to evaluate the therapeutic efficacy. Nitric oxide (NO) and TNF-α were assessed in plasma. Meanwhile, eyes were collected for histological and immunohistochemical studies. The retinal expression of iNOS, CD68, CD20, CD25, CD4, and CD8 was examined. Interestingly, DMF enhanced a significant reduction of NO and TNF-α production in the treated group. This effect was strongly related to the histological structure of eyes improvement. In the same context, a significant decrease of iNOS, CD68, and CD20 expression and CD25 increase expression were reported in retinal tissue of DMF/Uveoretinitis group in comparison to the immunized group. Collectively, our results indicate that DMF treatment has a beneficial effect in experimental autoimmune uveoretinitis and could constitute a good candidate for monitoring an ocular inflammatory diseases.


  • All-trans retinoic acid (ATRA) prevents lipopolysaccharide-induced neuroinflammation, amyloidogenesis and memory impairment in aged rats

    by Nassima Behairi, Mourad Belkhelfa, Hayet Rafa, Moussa Labsi, Nahla Deghbar, Nora Bouzid, Hamida Mesbah-Amroun, Chafia Touil-Boukoffa


  • Open Access

    Immuno-modulatory activities of Punica granatum peel aqueous extract on the development of secondary hydatid cysts

    by Labsi Moussa, Khelifi Lila, Mezioug Dalila, Bouaziz Samia, Touil-Boukoffa Chafia

    Introduction: In recent years, significant emphasis is being placed about the phytotherapy. In this regard, pomegranate has recently shown many biological activities, such as anti-inflammation, antioxidant, anti-microbial, and anti-parasitic activities. In our current study, we investigate the protective immunity induced by using therapy with Punica granatum peel aqueous extract against the infectivity of mice by the protoscoleces. Material and Methods: Protoscoleces (PSCs) were obtained by aseptic puncture of fertile human pulmonary hydatid cysts. Swiss mice were inoculated intraperitoneally (i.p) with 200 µl of a suspension containing 2000 viable protoscoleces to induce secondary experimental echinococcosis. An aqueous Punica granatum peel was daily administered orally starting two days. After the disease induction, we investigated the preventive effect of Punica granatum peel aqueous extract (PGE). Cysts development and hepatic damage were evaluated macroscopically and histologically. Results: Interestingly, our results showed an important inhibition of cysts development. The rate of hydatid cyst growth inhibition is concomitant with the improvement of the histological structure of liver. Conclusion: Our histological study suggest a potential immuno-modulatory effect of Punica granatum peel aqueous extract on the development of secondary hydatid cysts. Collectively, our results indicate that in vivo treatment with PGE is effective against Echinococcus granulosus.

  • Open Access

    Echinococcus granulosus experimental infection down-modulates Nitric Oxide production in DSS induced colitis in mice.

    by Khelifi Lila, Labsi Moussa, Soufli Imen, Touil-Boukoffa Chafia

    Background: Inflammatory bowel diseases (IBD) are immune-mediated diseases, which are common in western industrialized countries while they are uncommon in developing countries. The hygiene hypothesis suggests that the loss of exposure to helminthes such as Echinococcus granulosus engendered a development of IBD. This parasite causes cystic hydatid disease which is endemic in Algeria. Previous data reported that helminthes reduce inflammatory process in experimental colitis. The aim of our study is to investigate the immuno-modulatory effect of the secondary infection with Echinococcus granulosus on Nitric Oxide (NO) production in Dextran Sulfate Sodium (DSS) induced colitis model. Materials and Methods: A group of Swiss mice is infected intraperitoneally (i.p) with 200 µl of a suspension containing 2000 viable protoscoleces of Echinococcus granulosus. After 3 months of infection, experimental colitis is induced in infected and uninfected mice by dissolving DSS in their drinking water for 7 days and then were sacrificed. We estimated disease activity index (DAI) which took into account body weight, stool consistency and gross bleeding. Nitric oxide (NO), is determined to investigate the inflammatory response. Results: Our results show that the disease activity index (DAI) of colitis increased at slow pace in the infected mice which developed cysts in comparison to the uninfected mice. In addition, a significant decrease in nitric oxide production is observed in plasma of infected mice. Conclusion: Our experiments suggest a potential immuno-modulatory effect of Echinococcus granulosus on Dextran Sulfate Sodium (DSS) experimental colitis by nitric oxide (NO) down-modulation.