Inflammatory Bowel Disease: How Effective Is TNF-α Suppression?

Lo, Wing-Cheong; Arsenescu, Violeta; Arsenescu, Razvan; Friedman, Avner

doi:10.1371/journal.pone.0165782

Cited by 11 publications

(16 citation statements)

References 45 publications

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“…Understanding the relationship between the patient's immune system and biological agents from this mathematical model is important for the treatment of patients. The mathematical model is based on the study of Lo et al [21]. In [21], the differential equation system was developed based on a network that integrates cytokines and transcription factors associated with Type 1 T helper cell(Th1), Type 2 T helper cell(Th2), Type 17 T helper cell(Th17) and regulatory T cell pathways.…”

Section: Methodsmentioning

confidence: 99%

“…The mathematical model is based on the study of Lo et al [21]. In [21], the differential equation system was developed based on a network that integrates cytokines and transcription factors associated with Type 1 T helper cell(Th1), Type 2 T helper cell(Th2), Type 17 T helper cell(Th17) and regulatory T cell pathways. Our model is substituted with an additional compartment for drug intervention.…”

Section: Methodsmentioning

confidence: 99%

“…In consideration of the characteristics of patients with IBD, [21] compared patients with Crohn's disease to a normal intestinal mucosa. Lo et al [21] also examined the activities of Th1 and Th2 with respect to the normal levels and classified them into four categories. Of the four categories, the first involved Th1 levels being higher and Th2 levels being lower than in healthy individuals.…”

Section: Plos Onementioning

confidence: 99%

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An immune therapy model for effective treatment on inflammatory bowel disease

et al. 2020

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Inflammatory bowel disease (IBD) is a disease that causes inflammation throughout the digestive tract. Repeated inflammation and frequent relapses cause intestinal damage and expose the patient to a higher risk. In this work, we proposed an immune therapy model for effective treatment strategy through mathematical modeling for patients with IBD. We evaluated the ability of the patient's immune system to recover during treatment. For this, we defined the interval of healthy individual, and examined the frequency of compartments such as T cells and cytokines considered in the model maintain the normal state. Based on the fact that each patient has a unique immune system, we have shown at the same drug works differently, depending on the individual immune system characteristics for every patient. It is known that IBD is related to an imbalance between pro-and anti-inflammatory cytokines as the cause of the disease. So the ratios of pro-to anti-inflammatory cytokines are used as an indicator of patient's condition and inflammation status in various diseases. We compared the ratios of pro-to anti-inflammatory cytokine according to patient's individual immune system and drugs. Since the effects of biological drugs are highly dependent on the patient's own immune system, it is essential to define the immune system status before selecting and using a biological drug.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Plos Onementioning

confidence: 99%

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An immune therapy model for effective treatment on inflammatory bowel disease

et al. 2020

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“…Activated and infected macrophages induce Th1 development through IL-12 [12,31] while Treg cells provide negative regulatory signals on Th1 cell activation [11,30]. On the other hand, Treg cell activation is induced by the two types of cytokine, IL-10 and IL-2, which are produced by activated macrophages and Th1 cells, respectively [1,10]. Similar to the equations for macrophages, we assume that the dynamics of cytokines are much faster than that of cells so that we simplify the processes by considering that Th1 and Treg cell activations are directly increased by the cell concentrations.…”

Section: Danyun He Qian Wang and Wing-cheong Lomentioning

confidence: 99%

“…k BM , then the above two possible ranges (10) and 12will have no intersection with nonzeroB, which means that there is no steady state solution with nonzero concentration of extracellular bacteria and (0, α Mr /µ Mr ) is the only steady state for the system. Now we first obtain the Jacobian matrix for local stability analysis, then the stability analysis will be investigated in the following three cases:…”

Section: Danyun He Qian Wang and Wing-cheong Lomentioning

confidence: 99%

Mathematical analysis of macrophage-bacteria interaction in tuberculosis infection

He¹,

Wang²,

Lo³

2018

Discrete &Amp; Continuous Dynamical Systems - B

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Tuberculosis (TB) is a leading cause of death from infectious disease. TB is caused mainly by a bacterium called Mycobacterium tuberculosis which often initiates in the respiratory tract. The interaction of macrophages and T cells plays an important role in the immune response during TB infection. Recent experimental results support that active TB infection may be induced by the dysfunction of Treg cell regulation that provides a balance between anti-TB T cell responses and pathology. To better understand the dynamics of TB infection and Treg cell regulation, we build a mathematical model using a system of differential equations that qualitatively and quantitatively characterizes the dynamics of macrophages, Th1 and Treg cells during TB infection. For sufficiently analyzing the interaction between immune response and bacterial infection, we separate our model into several simple subsystems for further steady state and stability studies. Using this system, we explore the conditions of parameters for three situations, recovery, latent disease and active disease, during TB infection. Our numerical simulations support that Th1 cells and Treg cells play critical roles in TB infection: Th1 cells inhibit the number of infected macrophages to reduce the chance of active disease; Treg cell regulation reduces the immune response to stabilize the dynamics of the system.

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Exopolysaccharide from Lactobacillus rhamnosusZFM231 alleviates DSS‐induced colitis in mice by regulating gut microbiota

et al. 2022

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BACKGROUND The exopolysaccharides (EPS) produced by Lactobacillus and other probiotics are associated with many benefits, such as immune regulation, antioxidant properties, antitumor effect, and regulation of intestinal microbe homeostasis. In the present study, the modulatory effect of EPS produced by Lactobacillus rhamnosus ZFM231 on the intestinal flora of mice with inflammatory bowel disease induced by dextran sulfate solution was investigated. RESULTS Results indicated that weight loss, colonic length, the disease activity index score and colonic tissue damage in mice were significantly improved by EPS treatment. Compared with the model group, in the EPS‐treated group, the diversity of and the composition of gut microbiota at both phylum and genus levels were found to recover to the levels of normal group, indicating the effective modulation on gut microbiota by EPS; short‐chain fatty acids, including acetic acid, propionic acid and butyric acid produced by intestinal microbial metabolism, increased significantly; the level of anti‐inflammatory factor transforning growth factor‐β significantly increased and the level of pro‐inflammatory factor tumor necrosis factor‐α significantly decreased in the colonic cells of EPS‐treated mice. CONCLUSION It is clear that EPS produced by L. rhamnosus ZFM231 could find application in functional foods with the property of anti‐ulcerative colitis. The experimental results provide new insights into the probiotic effect of EPS. © 2022 Society of Chemical Industry.

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Inflammatory Bowel Disease: How Effective Is TNF-α Suppression?

Cited by 11 publications

References 45 publications

An immune therapy model for effective treatment on inflammatory bowel disease

An immune therapy model for effective treatment on inflammatory bowel disease

Mathematical analysis of macrophage-bacteria interaction in tuberculosis infection

Exopolysaccharide from Lactobacillus rhamnosusZFM231 alleviates DSS‐induced colitis in mice by regulating gut microbiota

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