scholarly journals Immune Responses to Gram-Negative Bacteria in Hemolymph of the Chinese Horseshoe Crab, Tachypleus tridentatus

2021 ◽  
Vol 11 ◽  
Author(s):  
Wei-Feng Wang ◽  
Xiao-Yong Xie ◽  
Kang Chen ◽  
Xiu-Li Chen ◽  
Wei-Lin Zhu ◽  
...  
Keyword(s):  
Immune Response ◽  
Horseshoe Crab ◽  
Mapk Signaling ◽  
Innate Immune ◽  
Coagulation Cascade ◽  
Gram Negative Bacteria ◽  
Fossil Species ◽  
Living Fossil ◽  
Gram Negative ◽  
Tachypleus Tridentatus

Chinese horseshoe crab, Tachypleus tridentatus, is an ancient marine arthropod with a long evolutionary history. As a kind of living fossil species, the pathogen defenses of horseshoe crabs entirely depend on the innate immune system. Although, there are abundant immune molecules found in the horseshoe crab hemolymph, the biological mechanisms underlying their abilities of distinguishing and defending against invading microbes are still unclear. In this study, we used high-throughput sequencing at mRNA and protein levels and bioinformatics analysis methods to systematically analyze the innate immune response to Gram-negative bacteria in hemolymph of Chinese horseshoe crab. These results showed that many genes in the complement and coagulation cascades, Toll, NF-κB, C-type lectin receptor, JAK-STAT, and MAPK signaling pathways, and antimicrobial substances were activated at 12 and 24 h post-infection, suggesting that Gram-negative bacteria could activate the hemolymph coagulation cascade and antibacterial substances release via the above pathways. In addition, we conjectured that Toll and NF-κB signaling pathway were most likely to participate in the immune response to Gram-negative bacteria in hemolymph of horseshoe crab through an integral signal cascade. These findings will provide a useful reference for exploring the ancient original innate immune mechanism.

scholarly journals Glycoconjugates of Gram-negative bacteria and parasitic protozoa – are they similar in orchestrating the innate immune response?

2019 ◽  
Vol 25 (1) ◽  
pp. 73-96 ◽  
Author(s):  
Magdalena A Karaś ◽  
Anna Turska-Szewczuk ◽  
Monika Janczarek ◽  
Agnieszka Szuster-Ciesielska
Keyword(s):  
Immune Response ◽  
Immune Cells ◽  
Intracellular Signaling ◽  
Inflammatory Responses ◽  
Mapk Signaling ◽  
Innate Immune ◽  
Gram Negative Bacteria ◽  
Parasitic Protozoa ◽  
Gram Negative ◽  
Immune Balance

Innate immunity is an evolutionarily ancient form of host defense that serves to limit infection. The invading microorganisms are detected by the innate immune system through germline-encoded PRRs. Different classes of PRRs, including TLRs and cytoplasmic receptors, recognize distinct microbial components known collectively as PAMPs. Ligation of PAMPs with receptors triggers intracellular signaling cascades, activating defense mechanisms. Despite the fact that Gram-negative bacteria and parasitic protozoa are phylogenetically distant organisms, they express glycoconjugates, namely bacterial LPS and protozoan GPI-anchored glycolipids, which share many structural and functional similarities. By activating/deactivating MAPK signaling and NF-κB, these ligands trigger general pro-/anti-inflammatory responses depending on the related patterns. They also use conservative strategies to subvert cell-autonomous defense systems of specialized immune cells. Signals triggered by Gram-negative bacteria and parasitic protozoa can interfere with host homeostasis and, depending on the type of microorganism, lead to hypersensitivity or silencing of the immune response. Activation of professional immune cells, through a ligand which triggers the opposite effect (antagonist versus agonist) appears to be a promising solution to restoring the immune balance.

scholarly journals The role of type 1 interferons in Gram-negative bacteria-induced coagulation

Blood ◽  
2020 ◽  
Author(s):  
Xinyu Yang ◽  
Xiaoye Cheng ◽  
Yiting Tang ◽  
Xianhui Qiu ◽  
Zhongtai Wang ◽  
...  
Keyword(s):  
Immune Responses ◽  
Bacterial Infection ◽  
Innate Immune ◽  
Coagulation Cascade ◽  
Outer Cell ◽  
Gram Negative Bacteria ◽  
Innate Immune Responses ◽  
Gram Negative ◽  
Type 1 Interferons

Bacterial infection not only stimulates innate immune responses but also activates the coagulation cascades. Over-activation of the coagulation system in bacterial sepsis leads to disseminated intravascular coagulation (DIC), a life-threatening condition. However, the mechanisms by which bacterial infection activates the coagulation cascade are not fully understood. Here we show that type 1 interferons (IFNs), widely expressed family of cytokines that orchestrate innate antiviral and antibacterial immunity, mediate bacterial infection-induced DIC through amplifying the release of high mobility box group box 1 (HMGB1) into the blood stream. Inhibition of the expression of type 1 IFNs, disruption of their receptor IFN-α/βR or downstream effector (e.g., HMGB1) uniformly decreased Gram-negative bacteria-induced DIC. Mechanistically, extracellular HMGB1 markedly increased the pro-coagulant activity of tissue factor (TF) by promoting the externalization of phosphatidylserine (PS) to the outer cell surface, where PS assembles a complex of cofactor-proteases of the coagulation cascades. These findings not only provide novel insights into the link between innate immune responses and coagulation, but also open a new avenue for developing novel therapeutic strategies to prevent DIC in sepsis.

scholarly journals Caspase-11 Plays a Protective Role in Pulmonary Acinetobacter baumannii Infection

2017 ◽  
Vol 85 (10) ◽  
Author(s):  
Wei Wang ◽  
Yue Shao ◽  
Shengjun Li ◽  
Na Xin ◽  
Tingxian Ma ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Immune Response ◽  
Acinetobacter Baumannii ◽  
Pulmonary Infection ◽  
Protective Role ◽  
Innate Immune ◽  
Gram Negative Bacteria ◽  
Pathological Changes ◽  
Gram Negative ◽  
Content Type

ABSTRACT Activation of caspase-11 by some Gram-negative bacteria triggers the caspase-1/interleukin 1β (IL-1β) pathway, independent of canonical inflammasomes. Acinetobacter baumannii is a Gram-negative, conditionally pathogenic bacterium that can cause severe pulmonary infection in hospitalized patients. A. baumannii was revealed to activate canonical and noncanonical inflammasome pathways in bone marrow-derived macrophages (BMDMs). Pulmonary infection of caspase-11−/− mice with A. baumannii showed that caspase-11 deficiency impaired A. baumannii clearance, exacerbated pulmonary pathological changes, and enhanced susceptibility to A. baumannii. These data indicate that the caspase-11-mediated innate immune response plays a crucial role in defending against A. baumannii.

scholarly journals PtP38 May Increase the Immune Ability of Portunus trituberculatus Stimulated by LPS Imitating a Gram-Negative Bacterial Infection

2021 ◽  
Vol 8 ◽  
Author(s):  
Cheng-Peng Lu ◽  
Chao-Guang Wei ◽  
Jun-Quan Zhu ◽  
Dao-Jun Tang ◽  
Chun-Lin Wang ◽  
...  
Keyword(s):  
Immune Response ◽  
Antioxidant Enzymes ◽  
Bacterial Infection ◽  
Mapk Signaling ◽  
Mitogen Activated Protein Kinase ◽  
Portunus Trituberculatus ◽  
Gram Negative Bacteria ◽  
Gram Negative ◽  
Immune Ability ◽  
Immune Related Genes

The P38 mitogen-activated protein kinase (MAPK) signal transduction pathway is widespread in organisms and plays important roles in immune activities. The infection mechanism of environmental gram-negative bacteria on crustaceans is an important scientific problem. In this study, the cDNA full-length sequence of Portunus trituberculatus P38 (PtP38) was cloned and its structure was analyzed by bioinformatics methods. To study the function of the PtP38 gene after a Gram-negative bacterial infection, we injected P. trituberculatus with LPS to activate the immune response instead of directly infecting with Gram-negative bacteria. With LPS stimulation, the expression of the PtP38 gene in different tissues increased significantly. At the same time, the expression of immune-related genes (ALF and crustin) in the hepatopancreas, activities of antioxidant enzymes [superoxide dismutase (SOD), catalase (CAT), and inducible nitric oxide synthase (iNOS) enzymes], and expression of apoptosis-related genes (caspase2 and caspase3) were increased significantly. To further conform the function of PtP38 in the immune response, we injected P. trituberculatus with P38 inhibitor and subsequently injected with LPS. The results showed that the expression of immune-related genes was inhibited, the activity of antioxidant enzymes was decreased, and the expression of apoptosis-related genes were inhibited. Thus, we speculated that PtP38 may increase the immune ability by improving the expression of antimicrobial peptides, increasing the activity of oxidative stress-related enzymes, and promoting cell apoptosis in infected P. trituberculatus. This study also laid the foundation for further study of the P38 MAPK signaling pathway and immune mechanism of P. trituberculatus.

The interaction of macrophage receptors with bacterial ligands

2006 ◽  
Vol 8 (28) ◽  
pp. 1-25 ◽  
Author(s):  
Annette Plüddemann ◽  
Subhankar Mukhopadhyay ◽  
Siamon Gordon
Keyword(s):  
Immune Response ◽  
Early Recognition ◽  
Adaptive Immune Response ◽  
Innate Immune ◽  
Surface Proteins ◽  
Scavenger Receptors ◽  
Gram Negative Bacteria ◽  
Gram Positive ◽  
Gram Negative ◽  
Macrophage Receptors

Innate immune receptors play a key role in the early recognition of invading bacterial pathogens and initiate the crucial innate immune response. The diverse macrophage receptors recognise Gram-positive and Gram-negative bacteria via conserved structures on the bacterial surface and facilitate phagocytosis and/or signalling, providing the trigger for the adaptive immune response. These receptors include scavenger receptors, C-type lectins, integrins, Toll-like receptors and siglecs. The bacterial ligands generally recognised by these receptors range from lipopolysaccharides on Gram-negative bacteria to peptidoglycan and lipoteichoic acid on Gram-positive bacteria. However, emerging evidence indicates that bacterial proteins are also important ligands; for example, surface proteins from Neisseria meningitidis have been shown to be ligands for class A scavenger receptors. In addition, a group of cytosolic receptors, the NBS-LRR proteins, have been implicated in recognition of bacterial breakdown products. It is becoming increasingly apparent that macrophage receptors can act in conjunction with one another to deliver an appropriate response.

scholarly journals Advances in Understanding Activation and Function of the NLRC4 Inflammasome

2021 ◽  
Vol 22 (3) ◽  
pp. 1048
Author(s):  
Balamurugan Sundaram ◽  
Thirumala-Devi Kanneganti
Keyword(s):  
Immune Response ◽  
Cell Death ◽  
Innate Immune ◽  
Gram Negative Bacteria ◽  
Gram Negative ◽  
Immune Receptors ◽  
Caspase 1 ◽  
Cell Death Pathway ◽  
Molecular Patterns

Innate immune receptors initiate a host immune response, or inflammatory response, upon detecting pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs). Among the innate immune receptors, nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs) play a pivotal role in detecting cytosolic PAMPs and DAMPs. Some NLRs can form a multiprotein cytosolic complex known as the inflammasome. Inflammasome activation triggers caspase-1–mediated cleavage of the pore-forming protein gasdermin D (GSDMD), which drives a form of inflammatory cell death called pyroptosis. Parallelly, activated caspase-1 cleaves immature cytokines pro–IL-1β and pro–IL-18 into their active forms, which can be released via GSDMD membrane pores. The NLR family apoptosis inhibitory proteins (NAIP)-NLR family caspase-associated recruitment domain-containing protein 4 (NLRC4) inflammasome is important for mounting an immune response against Gram-negative bacteria. NLRC4 is activated through NAIPs sensing type 3 secretion system (T3SS) proteins from Gram-negative bacteria, such as Salmonella Typhimurium. Mutations in NAIPs and NLRC4 are linked to autoinflammatory disorders in humans. In this review, we highlight the role of the NAIP/NLRC4 inflammasome in host defense, autoinflammatory diseases, cancer, and cell death. We also discuss evidence pointing to a role of NLRC4 in PANoptosis, which was recently identified as a unique inflammatory programmed cell death pathway with important physiological relevance in a range of diseases. Improved understanding of the NLRC4 inflammasome and its potential roles in PANoptosis paves the way for identifying new therapeutic strategies to target disease.

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