scholarly journals Rupture, Invasion and Inflammatory Destruction of the Intestinal Barrier byShigella: The Yin and Yang of Innate Immunity

2006 ◽  
Vol 17 (2) ◽  
pp. 117-119 ◽  
Author(s):  
Philippe J Sansonetti
Keyword(s):  
Intestinal Inflammation ◽  
Bacterial Species ◽  
Adaptive Immune Response ◽  
Intestinal Barrier ◽  
Signalling Molecules ◽  
Adaptive Immune ◽  
Commensal Flora ◽  
The Family ◽  
Yin And Yang ◽  
Unified View

Shigellais a Gram-negative bacterial species of the family Enterobacteriaceae that causes bacillary dysentery in humans. This acute colitis reflects the capacity of the microorganism to disrupt, invade and cause the inflammatory destruction of the intestinal epithelium. The pathogenesis of theShigellainfection can be seen as a disruption of the homeostatic balance that protects the gut against inflammation in the presence of its commensal flora. This provides the unified view that enteroinvasive pathogens allow for the identification of key signalling molecules and pathways involved in the regulation of intestinal inflammation, and more generally, in the regulation of the innate and adaptive immune response.

scholarly journals Cathepsins in Bacteria-Macrophage Interaction: Defenders or Victims of Circumstance?

2020 ◽  
Vol 10 ◽  
Author(s):  
Lidia Szulc-Dąbrowska ◽  
Magdalena Bossowska-Nowicka ◽  
Justyna Struzik ◽  
Felix N. Toka
Keyword(s):  
Proteolytic Enzymes ◽  
Bacterial Species ◽  
Animal Health ◽  
Adaptive Immune Response ◽  
Direct Interaction ◽  
Adaptive Immune ◽  
Intracellular Digestion ◽  
Close Relationship ◽  
Recent Developments

Macrophages are the first encounters of invading bacteria and are responsible for engulfing and digesting pathogens through phagocytosis leading to initiation of the innate inflammatory response. Intracellular digestion occurs through a close relationship between phagocytic/endocytic and lysosomal pathways, in which proteolytic enzymes, such as cathepsins, are involved. The presence of cathepsins in the endo-lysosomal compartment permits direct interaction with and killing of bacteria, and may contribute to processing of bacterial antigens for presentation, an event necessary for the induction of antibacterial adaptive immune response. Therefore, it is not surprising that bacteria can control the expression and proteolytic activity of cathepsins, including their inhibitors – cystatins, to favor their own intracellular survival in macrophages. In this review, we summarize recent developments in defining the role of cathepsins in bacteria-macrophage interaction and describe important strategies engaged by bacteria to manipulate cathepsin expression and activity in macrophages. Particularly, we focus on specific bacterial species due to their clinical relevance to humans and animal health, i.e., Mycobacterium, Mycoplasma, Staphylococcus, Streptococcus, Salmonella, Shigella, Francisella, Chlamydia, Listeria, Brucella, Helicobacter, Neisseria, and other genera.

scholarly journals Netrin-1: A Modulator of Acute and Chronic Inflammation

2021 ◽  
Vol 23 (1) ◽  
pp. 275
Author(s):  
Laura Ziegon ◽  
Martin Schlegel
Keyword(s):  
Chronic Inflammation ◽  
Neuronal Development ◽  
Adaptive Immune Response ◽  
Immune Defense ◽  
Acute Injury ◽  
Biological Processes ◽  
First Line ◽  
Adaptive Immune ◽  
The Family ◽  
Acute And Chronic Inflammation

Netrins belong to the family of laminin-like secreted proteins, which guide axonal migration and neuronal growth in the developing central nervous system. Over the last 20 years, it has been established that netrin-1 acts as a chemoattractive or chemorepulsive cue in diverse biological processes far beyond neuronal development. Netrin-1 has been shown to play a central role in cell adhesion, cell migration, proliferation, and cell survival in neuronal and non-neuronal tissue. In this context, netrin-1 was found to orchestrate organogenesis, angiogenesis, tumorigenesis, and inflammation. In inflammation, as in neuronal development, netrin-1 plays a dichotomous role directing the migration of leukocytes, especially monocytes in the inflamed tissue. Monocyte-derived macrophages have long been known for a similar dual role in inflammation. In response to pathogen-induced acute injury, monocytes are rapidly recruited to damaged tissue as the first line of immune defense to phagocyte pathogens, present antigens to initiate the adaptive immune response, and promote wound healing in the resolution phase. On the other hand, dysregulated macrophages with impaired phagocytosis and egress capacity accumulate in chronic inflammation sites and foster the maintenance—and even the progression—of chronic inflammation. In this review article, we will highlight the dichotomous roles of netrin-1 and its impact on acute and chronic inflammation.

scholarly journals Strains of bacterial species induce a greatly varied acute adaptive immune response: The contribution of the accessory genome

2018 ◽  
Vol 14 (1) ◽  
pp. e1006726 ◽  
Author(s):  
Uri Sela ◽  
Chad W. Euler ◽  
Joel Correa da Rosa ◽  
Vincent A. Fischetti
Keyword(s):  
Immune Response ◽  
Bacterial Species ◽  
Adaptive Immune Response ◽  
Accessory Genome ◽  
Adaptive Immune

Is Alzheimer disease a failure of mobilizing immune defense? Lessons from cognitively fit oldest-old

2019 ◽  
Vol 21 (1) ◽  
pp. 7-19 ◽  
Keyword(s):  
Alzheimer Disease ◽  
Cognitive Aging ◽  
Oldest Old ◽  
Adaptive Immune Response ◽  
Effector T Cells ◽  
Immune Defense ◽  
Supporting Evidence ◽  
Therapeutic Approaches ◽  
Related Data ◽  
Adaptive Immune

Multifaceted evidence supports the hypothesis that inflammatory-immune mechanisms contribute to Alzheimer disease (AD) neuropathology and genetic association of several immune specific genes (TREM2, CR1, and CD33) suggests that maladaptive immune responses may be pivotal drivers of AD pathogenesis. We reviewed microglia-related data from postmortem AD studies and examined supporting evidence from AD animal models to answer the following questions: i) What is the temporal sequence of immune activation in AD progression and what is its impact on cognition? ii) Are there discordant, "primed", microglia responses in AD vs successful cognitive aging? iii) Does central nervous system (CNS) repair in aging depend on recruitment of the elements of cellular adaptive immune response such as effector T cells, and can the recruitment of systemic immune cells ameliorate AD neuropathology? iv) How effective are the immune-system-based therapeutic approaches currently employed for the treatment of AD?

scholarly journals BAFF Blockade Attenuates Inflammatory Responses and Intestinal Barrier Dysfunction in a Murine Endotoxemia Model

2020 ◽  
Vol 11 ◽  
Author(s):  
Runze Quan ◽  
Chaoyue Chen ◽  
Wei Yan ◽  
Ying Zhang ◽  
Xi Zhao ◽  
...  
Keyword(s):  
Barrier Function ◽  
Intestinal Inflammation ◽  
Inflammatory Responses ◽  
Survival Rates ◽  
Intestinal Barrier ◽  
Intestinal Barrier Function ◽  
Barrier Dysfunction ◽  
Protein Levels ◽  
Lps Challenge ◽  
Endotoxemia Model

B cell-activating factor (BAFF) production is increased in septic patients. However, the specific role of BAFF in sepsis remains unknown. This study was designed to investigate the expression and function of BAFF in an experimental endotoxemia model and to identify the potential mechanisms. We established an endotoxemia mouse (6–8 weeks, 20–22 g) model by administering 30 mg/kg lipopolysaccharide (LPS). BAFF levels in the circulating system and organ tissues were measured 4 and 8 h after LPS injection. Survival rates in the endotoxemia mice were monitored for 72 h after BAFF blockade. The effects of BAFF blockade on systemic and local inflammation, organ injuries, and intestinal barrier function were also evaluated 4 h after LPS treatment. BAFF production was systemically and locally elevated after LPS challenge. BAFF blockade improved the survival rate, systemic inflammation, and multi-organ injuries. Moreover, BAFF blockade attenuated both intestinal inflammation and impaired intestinal permeability. BAFF blockade upregulated ZO-1 and occludin protein levels via the NF-κB/MLCK/MLC signaling pathway. These results suggested that BAFF blockade protects against lethal endotoxemia at least partially by alleviating inflammation, multi-organ injuries, and improving intestinal barrier function and provides a novel focus for further research on sepsis and experimental evidence for clinical therapy.

Double positive CD4+CD8+ T cells are part of the adaptive immune response against Candida albicans

2019 ◽  
Vol 80 (12) ◽  
pp. 999-1005 ◽  
Author(s):  
Barbara Misme-Aucouturier ◽  
Adel Touahri ◽  
Marjorie Albassier ◽  
Francine Jotereau ◽  
Patrice Le Pape ◽  
...  
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Candida Albicans ◽  
Cd8 T Cells ◽  
Adaptive Immune Response ◽  
Double Positive ◽  
Adaptive Immune
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