Inhibitory effect of BMAP-28 on Leptospiral Lipopolysaccharide-Induced TLR2-Dependent Immune Response in Bovine Cells

Guo, Yi; Zhang, Bo; Xu, Jun; Meng, Xianhong; Xu, Jiru

doi:10.5812/jjm.33926

Cited by 6 publications

(7 citation statements)

References 28 publications

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“…Consistent with this result, whilst WT mice are largely asymptomatic, TLR4 deficient mice are highly sensitive to leptospirosis, and may die after intraperitoneal infection with virulent L. interrogans. In human, murine, bovine and pig cells, leptospiral LPS is also recognized by TLR2, which is the lipoprotein receptor [22,31,32]. Since leptospiral lipid A is not recognized by TLR2, the TLR2 recognition is most probably due to a non-identified lipopeptide tightly attached to the core or Oantigen part of the LPS.…”

Section: Toll-like Receptor (Tlr) and Nod-like Receptor (Nlr) Speciesmentioning

confidence: 99%

“…The recent finding that LL37 activates NET formation and reduces inflammation [68] may provide a potential mechanism for the observed protection of hamsters at the acute phase of infection, when both the bacterial load and inflammation are reaching their peak. BMAP, a bovine equivalent of LL37, has been shown to bind LPS and to decrease, in vitro, the leptospiral LPS induced signaling [31], which is important to elicit inflammation. Studies still need to determine whether LL37 can be used as a prophylactic treatment and/or, if it is active when administered after experimental infection.…”

Section: Antimicrobial Drugsmentioning

confidence: 99%

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Recent findings related to immune responses against leptospirosis and novel strategies to prevent infection

Vernel-Pauillac

Werts

2018

Microbes and Infection

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What are the new approaches and emerging ideas to prevent leptospirosis, a neglected bacterial re-emerging zoonotic disease? How do Leptospira interrogans escape the host defenses? We aim here to review and discuss the most recent literature that provides some answers to these questions, in particular data related to a better understanding of adaptive and innate immunity towards leptospires, and design of vaccines. This is an opinion paper, not a comprehensive review. We will try to highlight the new strategies and technologies boosting the search for drugs and vaccines. We will also address the bottlenecks and difficulties impairing the search for efficient vaccines and the many gaps in our knowledge of immunity against leptospirosis. Finally, we aim to delineate how Leptospira spp. escape the innate immune responses of Toll-Like receptors (TLR) and Nod-Like receptors (NLR). The rational use of TLR and NLR agonists as adjuvants could be key to design future vaccines against pathogenic leptospires.

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Section: Toll-like Receptor (Tlr) and Nod-like Receptor (Nlr) Speciesmentioning

confidence: 99%

Section: Antimicrobial Drugsmentioning

confidence: 99%

Recent findings related to immune responses against leptospirosis and novel strategies to prevent infection

Vernel-Pauillac

Werts

2018

Microbes and Infection

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“…Furthermore, in mice, TLR2 activation is dependent on TLR2/1 heterodimer formation (Nahori et al, 2005), leading to the recognition of tri-acylated lipoproteins. Another study reported TLR2-dependent activation of a bovine fibroblast cell line (Guo et al, 2016), suggesting that the bovine receptor could also be activated. The same group also suggested that porcine TLR2 could be activated in response to Leptospira infection (Guo et al, 2015).…”

Section: Leptospiral Recognition By Tlr2mentioning

confidence: 99%

Host and Species-Specificities of Pattern Recognition Receptors Upon Infection With Leptospira interrogans

Bonhomme

Werts

2022

Front. Cell. Infect. Microbiol.

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Leptospirosis is a zoonotic infectious disease affecting all vertebrates. It is caused by species of the genus Leptospira, among which are the highly pathogenic L. interrogans. Different mammals can be either resistant or susceptible to the disease which can present a large variety of symptoms. Humans are mostly asymptomatic after infection but can have in some cases symptoms varying from a flu-like syndrome to more severe forms such as Weil’s disease, potentially leading to multiorgan failure and death. Similarly, cattle, pigs, and horses can suffer from acute forms of the disease, including morbidity, abortion, and uveitis. On the other hand, mice and rats are resistant to leptospirosis despite chronical colonization of the kidneys, excreting leptospires in urine and contributing to the transmission of the bacteria. To this date, the immune mechanisms that determine the severity of the infection and that confer susceptibility to leptospirosis remain enigmatic. To our interest, differential immune sensing of leptospires through the activation of or escape from pattern recognition receptors (PRRs) by microbe-associated molecular patterns (MAMPs) has recently been described. In this review, we will summarize these findings that suggest that in various hosts, leptospires differentially escape recognition by some Toll-like and NOD-like receptors, including TLR4, TLR5, and NOD1, although TLR2 and NLRP3 responses are conserved independently of the host. Overall, we hypothesize that these innate immune mechanisms could play a role in determining host susceptibility to leptospirosis and suggest a central, yet complex, role for TLR4.

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“…The 32 articles selected for this review were published between 2001 and 2021, with 7 articles each from China and Taiwan, 5 from France, 3 from the United States, 2 from Brazil, India, Thailand, and Japan, and 1 each from Argentina and the Netherlands. The studies encompassed a range of experimental models, including 3 human [20][21][22], 5 in-vivo [23][24][25][26][27], 14 in-vitro [28][29][30][31][32][33][34][35][36][37][38][39][40][41], and 3 ex-vivo studies [42][43][44]. Additionally, four studies [9,10,45,46] used a combination of in-vivo and in-vitro models, while two studies [47,48] used a combination of human, in-vitro, and in-vivo models.…”

Section: General Characteristics Of the Included Studiesmentioning

confidence: 99%

Role of toll-like receptor 2 during infection ofLeptospiraspp.: A systematic review

Kappagoda,

Senavirathna,

Agampodi

2023

Preprint

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Background: Present systematic review was conducted to determine the role of the Toll-like receptor 2 during Leptospira infection in in-vitro, in-vivo, and ex-vivo experimental models and human studies. Methods: Original articles published in English up to March 2022 that examined the response of Toll-like receptor 2 during leptospirosis were selected. PubMed, Web of Science, Scopus, Trip, and Google Scholar were used to search the literature. The National Institute of Health Quality Assessment tool, Systematic Review Centre for Laboratory Animal Experimentation risk of bias tool, and Office of Health Assessment and Translation extended tool were used to assess the risk of bias and the quality of the studies. Results: Out of 2406 studies, only 32 were selected for the systematic review. These comprised 3 human studies, 14 in-vitro studies, 5 in-vivo studies, and 3 ex-vivo studies. 7 studies employed combined models that encompassed human, in-vivo, in-vitro, and ex-vivo. In our analysis, we assessed the response of Toll-like receptor 2 (TLR2) through various indicators, including TLR2 receptor/mRNA expression and indirect TLR2 involvement via the secretion/mRNA expression of cytokines, chemokines, and immune effectors. Notably, we identified increased TLR2 expression and the secretion/mRNA expression of several cytokines (IL6, IL8, IL-1beta, TNFalpha, IFNgamma, IL10, CCL2/MCP-1, CCL10, COX2, CXCL1/KC, CXCL2/MIP2) and immune effectors (hBD2, iNOS, Fibronectin, Oxygen, and Nitrogen reactive species) as key aspects of host TLR2 responses during leptospirosis. Besides the role of TLR2 in response to leptospirosis, the involvement of TLR4 and TLR5 was identified in in-vitro and in-vivo studies. IL6, IL10, IL-1beta, TNFalpha, MIP, CCL2, CCL10, COX2, MCP1, IFNgamma, iNOS, NO, anti-Leptospira IgG were triggered through TLR4. Furthermore, TNFalpha secretion was stimulated through TLR5. In addition to the role of TLR2, our review revealed the involvement of TLR4 and TLR5 in in-vitro and in-vivo studies. Specifically, the activation of TLR4 triggered responses including IL6, IL10, IL-1beta, TNFalpha, MIP, CCL2, CCL10, COX2, MCP1, IFNgamma, iNOS, NO, and anti-Leptospira IgG. Discussion: Recognition of pathogen-associated molecular patterns through TLR2 triggers the secretion of cytokines/chemokines and immune mediators, facilitating the eradication of Leptospira infection. However, excessive amounts of these compounds can harm host tissues; therefore, regulating immune mediators through TLR2 using agonists or antagonists at an optimal level is important for mitigating tissue damage and promoting effective immune responses. In addition to TLR2, TLR4 and TLR5 were found to play defensive roles in in-vitro and in-vivo studies against Leptospira infection.

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Inhibitory effect of BMAP-28 on Leptospiral Lipopolysaccharide-Induced TLR2-Dependent Immune Response in Bovine Cells

Cited by 6 publications

References 28 publications

Recent findings related to immune responses against leptospirosis and novel strategies to prevent infection

Recent findings related to immune responses against leptospirosis and novel strategies to prevent infection

Host and Species-Specificities of Pattern Recognition Receptors Upon Infection With Leptospira interrogans

Role of toll-like receptor 2 during infection ofLeptospiraspp.: A systematic review

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