International Journal of Molecular Sciences

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Advances in Lipopolysaccharide (LPS)

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Dear Colleagues,

Lipopolysaccharide (LPS) has previously been known as endotoxin, which was discovered about 100 years ago. It is a glycolipid that represents the major outer membrane component of Gram-negative bacteria. LPS is rarely released in the normal living state of bacteria, but is released after bacterial cell death and rupture, artificial lysis or active cell growth and reproduction. It is not toxic in itself.

However, when LPS enters the blood stream (e.g., by bacterial invasion in vivo), it binds to TLR4 receptors on host effector cells (mainly monocytes, macrophages, and neutrophils) as a nonspecific immune signal, and releases proinflammatory cytokines, such as tumor necrosis factor-α, interleukin 1 (IL-1), and other proinflammatory cytokines. Furthermore, persistent bacterial growth and the overproduction of LPS can cause fever, disseminated intravascular coagulation, multiple organ failure, and shock.

Recently, the physiological role of LPS through mucosa (e.g., the site of symbiotic bacteria) has been reviewed, and a wide variety of useful activities have been identified, such as anti-tumor, anti-radiation, anti-infection, alleviation of posterior cataract, and relieving asthma. It has also become clear that LPS regulates homeostasis through oral and/or transmucosal administration rather than vascular administration. A paradigm shift is indeed taking place regarding the physiological role of LPS. These activities of LPS could be due to its regulatory role of mainly innate immunity.

Dr. Gen-Ichiro Soma
Guest Editor

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Keywords

lipopolysaccharides
LPS
endotoxin
innate immunity
structure and functional relationship
oral administration
TLR-4
inflammation

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Research

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17 pages, 2186 KiB

Open AccessArticle

Oral Administration of Lipopolysaccharide Enhances Insulin Signaling-Related Factors in the KK/Ay Mouse Model of Type 2 Diabetes Mellitus

by Kazushi Yamamoto, Masashi Yamashita, Masataka Oda, Vindy Tjendana Tjhin, Hiroyuki Inagawa and Gen-Ichiro Soma

Int. J. Mol. Sci. 2023, 24(5), 4619; https://doi.org/10.3390/ijms24054619 - 27 Feb 2023

Cited by 5 | Viewed by 1903

Abstract

Lipopolysaccharide (LPS), an endotoxin, induces systemic inflammation by injection and is thought to be a causative agent of chronic inflammatory diseases, including type 2 diabetes mellitus (T2DM). However, our previous studies found that oral LPS administration does not exacerbate T2DM conditions in KK/Ay mice, which is the opposite of the response from LPS injection. Therefore, this study aims to confirm that oral LPS administration does not aggravate T2DM and to investigate the possible mechanisms. In this study, KK/Ay mice with T2DM were orally administered LPS (1 mg/kg BW/day) for 8 weeks, and blood glucose parameters before and after oral administration were compared. Abnormal glucose tolerance, insulin resistance progression, and progression of T2DM symptoms were suppressed by oral LPS administration. Furthermore, the expressions of factors involved in insulin signaling, such as insulin receptor, insulin receptor substrate 1, thymoma viral proto-oncogene, and glucose transporter type 4, were upregulated in the adipose tissues of KK/Ay mice, where this effect was observed. For the first time, oral LPS administration induces the expression of adiponectin in adipose tissues, which is involved in the increased expression of these molecules. Briefly, oral LPS administration may prevent T2DM by inducing an increase in the expressions of insulin signaling-related factors based on adiponectin production in adipose tissues. Full article

(This article belongs to the Special Issue Advances in Lipopolysaccharide (LPS))

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11 pages, 653 KiB

Open AccessReview

Utility of In Vitro Cellular Models of Low-Dose Lipopolysaccharide in Elucidating the Mechanisms of Anti-Inflammatory and Wound-Healing-Promoting Effects of Lipopolysaccharide Administration In Vivo

by Teruko Honda and Hiroyuki Inagawa

Int. J. Mol. Sci. 2023, 24(18), 14387; https://doi.org/10.3390/ijms241814387 - 21 Sep 2023

Cited by 1 | Viewed by 1153

Abstract

Lipopolysaccharide (LPS) is a bacterial component that activates intracellular signaling pathways upon binding to the Toll-like receptor (TLR)-4/MD-2 complex. It is well known that LPS injected into animals and high-dose (100 ng/mL to 1 μg/mL) LPS treatment to innate immune cells induce an inflammatory response. In contrast, LPS is naturally present in the gastrointestinal tract, respiratory tract, and skin of humans and animals, and it has been shown that TLR-4-deficient animals cannot maintain their immune balance and gut homeostasis. LPS from commensal bacteria can help maintain homeostasis against mucosal stimulation in healthy individuals. Oral LPS administration has been shown to be effective in preventing allergic and lifestyle-related diseases. However, this effect was not observed after treatment with LPS at high doses. In mice, oral LPS administration resulted in the detection of LPS at a low concentration in the peritoneal fluid. Therefore, LPS administered at low and high doses have different effects. Moreover, the results of in vitro experiments using low-dose LPS may reflect the effects of oral LPS administration. This review summarizes the utility of in vitro models using cells stimulated with LPS at low concentrations (50 pg/mL to 50 ng/mL) in elucidating the mechanisms of oral LPS administration. Low-dose LPS administration has been demonstrated to suppress the upregulation of proinflammatory cytokines and promote wound healing, suggesting that LPS is a potential agent that can be used for the treatment and prevention of lifestyle-related diseases. Full article

(This article belongs to the Special Issue Advances in Lipopolysaccharide (LPS))

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