Trichinella spiralis -induced immunomodulation signatures on gut microbiota and metabolic pathways in mice.

The hygiene hypothesis proposes that decreased exposure to infectious agents in developed countries may contribute to the development of allergic and autoimmune diseases. Trichinella spiralis, a parasitic roundworm, causes trichinellosis, also known as trichinosis, in humans. T.

Pharmacokinetic and pharmacodynamic bioequivalence of Gan & Lee insulin analogues aspart (rapilin®), lispro (prandilin®) and glargine (basalin®) with EU- und US-sourced reference insulins.

Aim: For the successful approval and clinical prescription of insulin biosimilars, it is essential to show pharmacokinetic (PK) and pharmacodynamic (PD) bioequivalence to the respective reference products sourced from the European Union and the United States.

Methods: Three phase 1, randomized, double-blind, three-period crossover trials compared single doses of the proposed biosimilar insulin analogues aspart (GL-Asp, n = 36), lispro (GL-Lis, n = 38) and glargine (GL-Gla, n = 113), all manufactured by Gan & Lee pharmaceuticals, to the respective EU- and US-reference products in healthy male participants (GL-Asp and GL-Lis) or people with type 1 diabetes (GL-Gla). Study participants received 0.

Paramyosin Induces Colonic Regulatory T Cells to Mitigate Inflammatory Bowel Disease.

Helminth infection modulates host regulatory immune responses to maintain immune homeostasis. Our previous study identified paramyosin (Pmy) as a major immunomodulatory protein with the ability to induce regulatory T cells (Tregs). However, whether Pmy regulates gut Tregs and contributes to intestinal immune homeostasis remains unclear.

Calreticulin S-Domain Binds to Human Complement C1q to Interfere With C1q-Mediated Immune Functions.

Helminths develop strategies to escape host immune responses that facilitate their survival in the hostile host immune environment. , a tissue-dwelling nematode, has developed a sophisticated strategy to escape complement attack. Our previous study demonstrated that secretes calreticulin (CRT) to inhibit host classical complement activation through binding to C1q; however, the C1q binding site in CRT and the specific mechanism involved with complement-related immune evasion remains unknown.

Excretory/Secretory Products From Adult Worms Attenuated DSS-Induced Colitis in Mice by Driving PD-1-Mediated M2 Macrophage Polarization.

Helminth-modulated macrophages contribute to attenuating inflammation in inflammatory bowel diseases. The programmed death 1 (PD-1) plays an important role in macrophage polarization and is essential in the maintenance of immune system homeostasis. Here, we investigate the role of PD-1-mediated polarization of M2 macrophages and the protective effects of excretory/secretory products from adult worms (AES) on DSS-induced colitis in mice.

Excretory-Secretory Products Stimulate Host Regulatory T Cell Differentiation through Activating Dendritic Cells.

maintains chronic infections within its host, involving a variety of immunomodulatory properties, the mechanisms of which have not been completely elucidated. In this study, we found that infection induced strong regulatory T cell responses through parasite excretory-secretory (ES) products, characterized by increase of CD4CD25Foxp3 and CD4CD25Foxp3 Treg cells accompanied by high levels of IL-10 and TGF-β. adult worm excretory-secretory products (AES) and muscle larvae excretory-secretory products (MES) were both able to activate BMDCs in vitro to facilitate their maturation and to create regulatory cytokines IL-10 and TGF-β.

Mapping of the complement C1q binding site on Trichinella spiralis paramyosin.

Background: Trichinella spiralis is a tissue-dwelling parasite has developed the ability to evade the host immune attack to establish parasitism in a host. One of the strategies evolved by the nematode is to produce proteins that immunomodulate the host immune system. TsPmy is a paramyosin secreted by T.