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1.
PLoS Negl Trop Dis ; 18(4): e0012048, 2024 Apr.
Article in English | MEDLINE | ID: mdl-38564496

ABSTRACT

BACKGROUND: Numerous studies indicate a potential protective role of helminths in diabetes mellitus (DM) progression. The complement system, vital for host defense, plays a crucial role in tissue homeostasis and immune surveillance. Dysregulated complement activation is implicated in diabetic complications. We aimed to investigate the influence of the helminth, Strongyloides stercoralis (Ss) on complement activation in individuals with type 2 DM (T2D). METHODOLOGY: We assessed circulating levels of complement proteins (C1q, C2, C3, C4, C4b, C5, C5a, and MBL (Lectin)) and their regulatory components (Factor B, Factor D, Factor H, and Factor I) in individuals with T2D with (n = 60) or without concomitant Ss infection (n = 58). Additionally, we evaluated the impact of anthelmintic therapy on these parameters after 6 months in Ss-infected individuals (n = 60). RESULTS: Ss+DM+ individuals demonstrated reduced levels of complement proteins (C1q, C4b, MBL (Lectin), C3, C5a, and C3b/iC3b) and complement regulatory proteins (Factor B and Factor D) compared to Ss-DM+ individuals. Following anthelmintic therapy, there was a partial reversal of these levels in Ss+DM+ individuals. CONCLUSION: Our findings indicate that Ss infection reduces complement activation, potentially mitigating inflammatory processes in individuals with T2D. The study underscores the complex interplay between helminth infections, complement regulation, and diabetes mellitus, offering insights into potential therapeutic avenues.


Subject(s)
Anthelmintics , Diabetes Mellitus, Type 2 , Helminths , Strongyloides stercoralis , Strongyloidiasis , Animals , Humans , Diabetes Mellitus, Type 2/complications , Diabetes Mellitus, Type 2/drug therapy , Complement Factor B , Complement Factor D/therapeutic use , Complement C1q , Strongyloidiasis/complications , Strongyloidiasis/drug therapy , Complement Activation , Anthelmintics/therapeutic use , Lectins
2.
IJID Reg ; 9: 18-24, 2023 Dec.
Article in English | MEDLINE | ID: mdl-37745942

ABSTRACT

Objectives: A number of epidemiological studies have demonstrated that there is an inverse relationship between helminth infections and diabetes mellitus, suggesting that helminth infection may have a positive effect on type 2 diabetes mellitus (T2DM). However, the association between hookworm infection and T2DM has barely been studied. Hence, we aimed to investigate and analyze the interaction and association between hookworm infection and T2DM. Methods: We examined the effect of hookworm infection on biochemical parameters, including plasma random blood glucose, glycated hemoglobin, and the plasma levels of pancreatic hormones, incretins, and adipokines in individuals with T2DM with (INF, n = 35) or without (UN, n = 35) hookworm infection. Moreover, we re-evaluated these analyte concentrations in a subset of INF individuals 6 months following anthelmintic therapy. Results: Compared to UN individuals, INF individuals had significantly lowered levels of random blood glucose and glycated hemoglobin. INF individuals also exhibited significantly diminished levels of adiponectin, adipsin, C-peptide, insulin, and glucagon compared to UN individuals. In contrast, INF individuals displayed substantially elevated levels of visfatin and incretins compared to UN individuals. Interestingly, this effect was not seen following anthelmintic treatment. Conclusion: Our study findings indicate that concomitant hookworm infection exerts a beneficial effect on glycometabolic parameters in T2DM.

3.
Front Nutr ; 10: 1194682, 2023.
Article in English | MEDLINE | ID: mdl-37324745

ABSTRACT

Introduction: Low body mass index (BMI) is a major risk factor for tuberculosis (PTB). Low BMI can impair the immune system and thus might affect TB incidence. Methods: We examined the plasma levels of Type 1, Type 17, pro-inflammatory, Type 2 and regulatory cytokines and CC and CXC chemokines in PTB and latent TB (LTB) individuals with low BMI (LBMI) or normal BMI (NBMI). Results: Our data show that PTB is associated with significantly lower levels of IFNγ, TNFα, IL-2, IL-17A, IL-6, IL-12, IL-4 and IL-5 cytokines but significantly higher levels of IL-10, TGFß and GM-CSF in LBMI compared to NBMI. Similarly, PTB is also associated with significantly lower levels of CCL2, CCL3, CCL11, CXCL1, CXCL9 and CXCL10 chemokines in LBMI compared to NBMI. Our data reveals that LTB is associated with significantly lower levels of IFNγ, TNFα, IL-2, IL1ß, IL-12, IL-13 cytokines but significantly higher levels of IL-10, TGFß, IL-4 and IL-22 in LBMI compared to NBMI. Similarly, LTB is also associated with significantly lower levels of CCL2, CXCL1, CXCL9 and CXCL10 and significantly higher levels of CCL1, CCL3, and CCL4 in LBMI compared to NBMI. Conclusion: Thus, LBMI has a major impact on the cytokine and chemokine milieu of both PTB and LTB and might predispose to the increased risk of tuberculosis by this immunomodulatory effect.

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