ArticleInfection and immunity2001
Malnutrition alters the innate immune response and increases early visceralization following Leishmania donovani infection.
Article in Infection and immunity, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 2 of them syntheses that pooled it.
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Who cites it
73 citing papers in PubMed, 2 syntheses or guidelines pooled it, 169 citations in OpenAlex.
- Nutritional supplements for patients being treated for active visceral leishmaniasis.The Cochrane database of systematic reviews · 2018Pooled it
- Of cattle, sand flies and men: a systematic review of risk factor analyses for South Asian visceral leishmaniasis and implications for elimination.PLoS neglected tropical diseases · 2010Pooled it
- Undernutrition-related diabetes in mice is linked to early undernutrition.American journal of physiology. Endocrinology and metabolism · 2026Article
- Dietary fish oil improves intestinal barrier function and intestinal microbiota composition and reduces systemic inflammation in a mouse model of moderate acute malnutrition.Journal of nutritional science · 2026Article
- Leishmaniasis.Nature reviews. Disease primers · 2025Review
- Malnutrition exacerbates pathogenesis of Lutzomyia longipalpis sand fly-transmitted Leishmania donovani.Communications biology · 2025Article
- Impact of Marasmic Malnutrition on Visceral Leishmaniasis: Progression and Treatment Efficacy in a Murine Model.Nutrients · 2025Article
- Protein undernutrition alters the colonic bacteriome, disrupts intestinal immune homeostasis, and impairs control ofFrontiers in nutrition · 2025Article
- Malnutrition disrupts adaptive immunity during visceral leishmaniasis by enhancing IL-10 production.PLoS pathogens · 2024Article
- The Interaction of Zinc as an Essential Trace Element withAdvanced biomedical research · 2024Review
- The Possible Role of Selected Vitamins and Minerals in the Therapeutic Outcomes of Leishmaniasis.Biological trace element research · 2023Review
- Hierarchical spatiotemporal modeling of human visceral leishmaniasis in Rio Grande do Norte, Brazil.PLoS neglected tropical diseases · 2023Article
- Gene Signatures of Symptomatic and Asymptomatic Clinical-Immunological Profiles of Human Infection byMicroorganisms · 2023Article
- Hematological and Clinical Features Associated with Initial Poor Treatment Outcomes in Visceral Leishmaniasis Patients with and without HIV Coinfection in Gondar, Northwest Ethiopia.Tropical medicine and infectious disease · 2023Article
- Malnutrition-related parasite dissemination from the skin in visceral leishmaniasis is driven by PGE2-mediated amplification of CCR7-related trafficking of infected inflammatory monocytes.PLoS neglected tropical diseases · 2023Article
- The effect of the sugar metabolism on Leishmania infantum promastigotes inside the gut of Lutzomyia longipalpis: A sweet relationship?PLoS neglected tropical diseases · 2022Article
- Pathologic Inflammation in Malnutrition Is Driven by Proinflammatory Intestinal Microbiota, Large Intestine Barrier Dysfunction, and Translocation of Bacterial Lipopolysaccharide.Frontiers in immunology · 2022Article
- Inflammatory stimuli alter bone marrow composition and compromise bone health in the malnourished host.Frontiers in immunology · 2022Article
- Thymus, undernutrition, and infection: Approaching cellular and molecular interactions.Frontiers in nutrition · 2022Review
- Malnutrition Aggravates Alterations Observed in the Gut Structure and Immune Response of Mice Infected withMicroorganisms · 2021Article
13 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Malnutrition is a risk factor for the development of visceral leishmaniasis. However, the immunological basis for this susceptibility is unknown. We have developed a mouse model to study the effect of malnutrition on innate immunity and early visceralization following Leishmania donovani infection. Three deficient diets were studied, including 6, 3, or 1% protein; these diets were also deficient in iron, zinc, and calories. The control diet contained 17% protein, was zinc and iron sufficient, and was provided ab libitum. Three days after infection with L. donovani promastigotes, the total extradermal (lymph nodes, liver, and spleen) and skin parasite burdens were equivalent in the malnourished (3% protein) and control mice, but in the malnourished group, a greater percentage (39.8 and 4.0%, respectively; P = 0.009) of the extradermal parasite burden was contained in the spleen and liver. The comparable levels of parasites in the footpads in the two diet groups and the higher lymph node parasite burdens in the well-nourished mice indicated that the higher visceral parasite burdens in the malnourished mice were not due to a deficit in local parasite killing but to a failure of lymph node barrier function. Lymph node cells from the malnourished, infected mice produced increased levels of prostaglandin E(2) (PGE(2)) and decreased levels of interleukin-10. Inducible nitric oxide synthase activity was significantly lower in the spleen and liver of the malnourished mice. Thus, malnutrition causes a failure of lymph node barrier function after L. donovani infection, which may be related to excessive production of PGE(2) and decreased levels of IL-10 and nitric oxide.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.