For when bacterial infections persist: Toll-like receptor-inducible direct antimicrobial pathways in macrophages

Stocks, Claudia J.; Schembri, Mark A.; Sweet, Matthew J.; Kapétanovic, Ronan

doi:10.1002/jlb.4ri0917-358r

Cited by 51 publications

(41 citation statements)

References 230 publications

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“…One of the main strategies used by microorganisms to escape this macrophage activity involves altering the response profile of macrophages. 185,[235][236][237][238][239][240][241][242][243][244][245][246][247][248][249][250][251][252] The activation of a response profile mediated by M1 macrophages is commonly associated with a protective tissue environment and has been described for infections by pathogens such as Helicobacter pylori, M. tuberculosis, Mycobacterium leprae, Salmonella typhi, and Chlamydia. [253][254][255][256][257][258] M1 macrophages elicit an effective immune response against S. typhi and H. pylori, and in the response against H. pylori, the induction of iNOS associated with the M1 profile is closely related to the occurrence of gastric cancer.…”

Section: Autophagymentioning

confidence: 99%

Functional aspects, phenotypic heterogeneity, and tissue immune response of macrophages in infectious diseases

Sousa¹,

Vasconcelos²,

Quaresma³

2019

IDR

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Macrophages are a functionally heterogeneous group of cells with specialized functions depending not only on their subgroup but also on the function of the organ or tissue in which the cells are located. The concept of macrophage phenotypic heterogeneity has been investigated since the 1980s, and more recent studies have identified a diverse spectrum of phenotypic subpopulations. Several types of macrophages play a central role in the response to infectious agents and, along with other components of the immune system, determine the clinical outcome of major infectious diseases. Here, we review the functions of various macrophage phenotypic subpopulations, the concept of macrophage polarization, and the influence of these cells on the evolution of infections. In addition, we emphasize their role in the immune response in vivo and in situ, as well as the molecular effectors and signaling mechanisms used by these cells. Furthermore, we highlight the mechanisms of immune evasion triggered by infectious agents to counter the actions of macrophages and their consequences. Our aim here is to provide an overview of the role of macrophages in the pathogenesis of critical transmissible diseases and discuss how elucidation of this relationship could enhance our understanding of the host–pathogen association in organ-specific immune responses.

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Section: Autophagymentioning

confidence: 99%

Functional aspects, phenotypic heterogeneity, and tissue immune response of macrophages in infectious diseases

Sousa¹,

Vasconcelos²,

Quaresma³

2019

IDR

View full text Add to dashboard Cite

show abstract

“…Stimulation of TLR2, 4, and 9 results in the upregulation of hCAP expression in alveolar macrophages. Furthermore, TLR regulation of hCAP-18 is vitamin D dependent [60,62]. In case of human monocyte-derived macrophages, Salmonella does not induce cathelicidin hCAP-18 [61].…”

Section: Amp Responsementioning

confidence: 99%

Hoodwinking the Big-Eater to Prosper: The Salmonella-Macrophage Paradigm

2018

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Salmonella is a major cause of morbidity and mortality in the developing and underdeveloped nations. Being a foodborne disease, Salmonella infection is primarily contracted through the ingestion of contaminated food or water, or due to close contact with infected/carrier individuals. It is an intracellular pathogen, which can survive and replicate in various cells including macrophages, dendritic cells, epithelial cells, and other white blood cells. Once Salmonella crosses the intestinal barrier, it disseminates to various systemic sites by circulation via immune cells. One of the major cell types which are involved in Salmonella infection are host macrophages. They are the niche for intracellular survival and proliferation of Salmonella and a mode of dissemination to distal systemic sites. These cells are very crucial as they mediate the mounting of an appropriate innate and adaptive anti-Salmonella immune response. In this review, we have tried to concise the current knowledge of complex interactions that occur between Salmonella and macrophages.

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“…LPS is a PAMP that is recognized by the Toll-like receptor 4 (TLR4), which activates the downstream pyroptotic pathway [15]. LPS-stimulated cells are an established in vitro model of sepsis and simulate the first 24 hours [16].…”

Section: Introductionmentioning

confidence: 99%

Rapamycin Inhibited Pyroptosis and Reduced the Release of IL-1β and IL-18 in the Septic Response

Luo

Chen

Sun

et al. 2020

BioMed Research International

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Pyroptosis, an inflammatory form of programmed cell death, is the initiating event of sepsis and results in immune imbalance by releasing IL-1β and IL-18 in the early stages. Studies show that enhancing autophagy via genetic manipulation can inhibit pyroptosis and prolong the survival of a sepsis animal model, indicating a possible therapeutic strategy against sepsis. However, almost no study so far has achieved pyroptosis inhibition via pharmacological autophagy induction in a sepsis disease model. To this end, we established an in vitro sepsis model by stimulating primary human umbilical vein endothelial cells (HUVECs) with lipopolysaccharide (LPS), and analyzed the effect of the autophagy agonist rapamycin (RAPA) on pyroptosis. Phorbol 12-myristate 13-acetate- (PMA-) activated human THP-1 cells were used as the positive control. LPS significantly increased the levels of the pyroptotic protein Gasdermin D (GSDMD), cysteinyl aspartate-specific proteinase 1 (caspase-1), secreted LDH, IL-1β, and IL-18. RAPA treatment downregulated the above factors and enhanced autophagy in the LPS-stimulated HUVECs and THP-1 cells. This study shows that RAPA abrogates LPS-mediated increase in IL-1β and IL-18 by inhibiting pyroptosis and enhancing autophagy.

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For when bacterial infections persist: Toll-like receptor-inducible direct antimicrobial pathways in macrophages

Cited by 51 publications

References 230 publications

<p>Functional aspects, phenotypic heterogeneity, and tissue immune response of macrophages in infectious diseases</p>

<p>Functional aspects, phenotypic heterogeneity, and tissue immune response of macrophages in infectious diseases</p>

Hoodwinking the Big-Eater to Prosper: The <b><i>Salmonella</i></b>-Macrophage Paradigm

Rapamycin Inhibited Pyroptosis and Reduced the Release of IL-1β and IL-18 in the Septic Response

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